Inhibitory Effects of Differentially Cultivated Carrots on AOM/DSS-Induced Colorectal Cancer Via Modulation of Inflammation, Apoptosis, and Gut Microbiota | Chapter 1 | Molecular Mechanisms and Signaling Pathways of the Anti-inflammatory Effects of Functional Foods

 

Background: Carrot (Daucus carota) is a widely consumed vegetable rich in dietary fibre, vitamins, minerals, and antioxidant compounds. Carrots contain fibre and bioactive phytochemicals that have been associated with anti-inflammatory and anti-proliferative activities in preclinical settings. Beta-carotene, a prominent carotenoid in carrots, has been reported to modulate immune-related pathways in experimental models; however, the extent to which these observations translate to reduced colorectal cancer risk in humans remains to be determined.

 

Objective: This study investigated whether cultivation methods influence the bioactivity of carrot extracts in an azoxymethane/dextran sodium sulfate (AOM/DSS)-induced murine model of colitis-associated colon tumorigenesis, with emphasis on apoptosis-related markers, inflammatory responses, and gut microbiota alterations.

 

Methods: Six-week-old male C57BL/6 mice (~20 g) were maintained under SPF conditions (12-h light/dark cycle; 23 ± 2 °C; 50 ± 5% humidity). After one week of acclimatisation with ad libitum food and water, mice were randomly allocated to six groups (n = 10/group). The normal and AOM/DSS control groups received saline, whereas the Conventional Fertiliser Carrot (CFC), Seawater Fertiliser Carrot (SFC), Trace Element Fertiliser Carrot (TFC), and Deep-sea Water Mineral fertiliser carrot (NFC) groups received the respective carrot extracts (50 mg/mL). Total phenolic and total flavonoid contents were quantified and analysed using GraphPad Prism 9.4.1.

 

Results: Among the cultivation conditions tested, carrots produced with deep-sea water mineral fertiliser (NFC) were associated with increased expression of apoptosis-related genes and proteins in colon tissue, including p53, p21, Bim, Bad, Bax, Bak, Caspase-9, and Caspase-3. NFC treatment was also associated with lower levels of pro-inflammatory cytokines and mediators (TNF-α, IL-1β, IL-6, IFN-γ, NF-κB, and iNOS) measured across serum, spleen cells, and liver tissues. Gut microbiota profiling indicated a compositional shift in carrot-treated mice relative to controls, including increased relative abundance of taxa previously linked to anti-inflammatory or anti-tumour-associated profiles (e.g., Lachnospiraceae and Mucispirillum schaedleri).

 

Conclusion: In this AOM/DSS mouse model, carrot extracts—particularly those derived from carrots cultivated with deep-sea water mineral fertiliser—were associated with reduced tumour-related endpoints alongside coordinated changes in apoptotic and inflammatory markers and gut microbiota composition. These findings support further investigation into cultivation-dependent differences in carrot bioactivity and encourage additional studies to clarify mechanisms and assess translational relevance in humans.

 

 

Author(s) Details

Yanni Pan
Collaborative Innovation Center for Child Nutrition and Health Development, Chongqing Engineering Research Center of Functional Food, Chongqing Engineering Laboratory for Research and Development of Functional Food, Chongqing University of Education, Chongqing, China.

 

Yeon-Jun Lee
Department of Biotechnology, CHA University, Seongnam, Republic of Korea.

 

Jin Hyeop Kim
Department of Biotechnology, CHA University, Seongnam, Republic of Korea.

 

Min Ji Song
Department of Biotechnology, CHA University, Seongnam, Republic of Korea.

 

KyuBum Kwack

Department of Biomedical Science, CHA University, Seongnam, Republic of Korea.

 

Seung-Hwan Park
Organic Anti-Cancer Agriculture Institute, iCOOP Natural Dream Company, Goesan-gun, Chungcheongbuk-do, Republic of Korea.

 

Sin-Il Sin
Organic Anti-Cancer Agriculture Institute, iCOOP Natural Dream Company, Goesan-gun, Chungcheongbuk-do, Republic of Korea.

 

Ji Hyung Chung
Department of Biotechnology, CHA University, Seongnam, Republic of Korea.

 

Kun-Young Park
Graduate School of Integrative Medicine, CHA University, Seongnam, Republic of Korea.

 

Please see the book here :- https://doi.org/10.9734/bpi/mono/978-81-998509-0-3/CH1

Anticancer Mechanisms and Therapeutic Potential of Garlic (Allium sativum) Derived Allicin and Z-Ajoene | Chapter 3 | Medical Science: Recent Advances and Applications Vol. 9

 

Garlic (Allium sativum) derives much of its anticancer properties from sulfur-containing metabolites generated when cloves are crushed, including Allicin and its more stable rearrangement product Z‑Ajoene. Despite its rapid degradation, Allicin induces mitochondrial-driven apoptosis, changes the Nrf2 pathway to alter cellular redox balance, and inhibits drug efflux proteins (such as P glycoprotein) to render chemotherapy-resistant cancer cells more susceptible. Z‑Ajoene has multiple effects, including triggering endoplasmic reticulum stress_(upregulating BiP/GRP78 and activating the PERK/ATF4/CHOP axis blocking Wnt/β_catenin signaling through CK1α-mediated β-catenin phosphorylation, reducing oncogenic drivers like c-Myc, disrupting vimentin filaments to impair invasion, and selectively targeting cancer stem cells through AKT, TGF_β, Notch, and ERK/p38 pathways. Recent translational efforts include nanoformulation of Allicin for better stability and delivery, as well as combination regimens matching these drugs with traditional chemotherapeutics (e.g., 5-FU, paclitaxel), which demonstrate synergistic tumour suppression and lower systemic toxicity. Nanocage-based delivery systems, such as Al₁₂N₁₂ and B₁₂N₁₂, enhance allicin’s stability, bioavailability, and targeted delivery, significantly improving its therapeutic potential.

 

 

Author(s) Details

Shivani L. Bhuse
Department of Pharmaceutical Chemistry, PES Modern College of Pharmacy, Nigdi-411044, Pune, Maharashtra, India.

 

Pallavi M. Patil
Department of Pharmaceutical Chemistry, PES Modern College of Pharmacy, Nigdi-411044, Pune, Maharashtra, India.

 

Rajat R. Durbule
Department of Quality Assurance Technique, PES Modern College of Pharmacy, Nigdi-411044, Pune, Maharashtra, India.

 

Prathmesh B. Parkale
Department of Quality Assurance Technique, PES Modern College of Pharmacy, Nigdi-411044, Pune, Maharashtra, India.

 

 

Please see the book here:- https://doi.org/10.9734/bpi/msraa/v9/6041

HIV and Alcohol Synergistically Disrupt Lysosomal Function in Hepatocytes, Driving Extracellular Vesicle Release and Liver Injury | Chapter 11 | Disease and Health: Research Developments Vol. 10

Although the etiologies of hepatic complications among people living with HIV who consume alcohol are multifactorial, alcohol remains a relatively understudied contributor to the progression of HIV-related liver injury. Here, we investigated whether metabolically derived acetaldehyde impairs lysosomes and releases exosomes to enhance HIV-induced hepatotoxicity. Cytochrome P450 2E1 (CYP2E1)-expressing Huh 7.5 (also known as RLW) cells were exposed to an acetaldehyde-generating system (AGS) for 24 h. We then infected (or not) the cells with HIV-1ADA, then exposed them again to AGS for another 48 h. Lysosome damage was assessed by galectin 3/LAMP1 co-localisation and cathepsin leakage. Additionally, we measured the co-localisation of DRAM 1 and Bax in lysosomes, indicating the contribution of HIV-AGS-triggered lysosomal damage to apoptosis induction in hepatocytes. Expression of lysosome biogenesis–transcription factor, TFEB, was measured by its protein levels and in situ immunofluorescence. Exposure of cells to AGS + HIV caused the greatest amount of lysosome leakage and impaired lysosomal biogenesis, leading to intrinsic apoptosis. Furthermore, AGS exposure impaired the microtubule-dependent translocation of TFEB from the cytosol to the nucleus. This appeared to result from the acetylation of α-tubulin.

Moreover, ZKSCAN3, a repressor of lysosome gene activation by TFEB, was amplified by AGS. Both these changes contributed to AGS-elicited disruption of lysosome biogenesis and promoted exosome release from hepatocytes. These results demonstrate that acetaldehyde impairs lysosomal integrity and repair, promotes exosome release, and exacerbates HIV-induced hepatotoxicity, offering mechanistic insight into alcohol’s role as a co-factor in liver damage among people with HIV.

 

Author (s) Details

Moses New-Aaron
Department of Environmental Health, Occupational Health and Toxicology, College of Public Health, University of Nebraska Medical Center, Omaha, NE 68198, USA and Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University, 615 Michael St. (Suite 205), Atlanta, GA 30322, United States of America.

 

Paul G. Thomes

Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA and Auburn University, Auburn, Alabama, United States of America.

 

Raghubendra Singh Dagur
Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA.

 

Kharbanda K. Kusum
Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA and Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, USA.

 

Larisa Y. Poluektova
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68105, USA.

 

Natalia A. Osna
Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA and Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68105, USA.

 

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v10/5390

Centella asiatica in Oncology: An Ancient Herb with Modern Anticancer Promise | Chapter 9 | Pharmaceutical Science: New Insights and Developments Vol. 5

Centella asiatica (L.) Urban, also known as Gotu Kola, has been traditionally used in Asian medicine for wound healing, neurological disorders, and skin conditions. In recent years, emerging scientific evidence has illuminated its remarkable anticancer properties. This chapter provides a critical review of the phytochemical constituents of Centella asiatica, their underlying mechanisms of action in various cancer types, in vitro and in vivo experimental findings, and the challenges associated with clinical translation. Emphasis is placed on the herb’s molecular targets and potential synergism with conventional chemotherapeutic agents (James & Dubery, 2009).

 

Author (s) Details

 

Sharmeen Shaikh
Siddhi’s Institute of Pharmacy, Thane 421401, India.

 

Pratiksha Salunkhe
Siddhi’s Institute of Pharmacy, Thane 421401, India.

 

Harshada Jadhav
Siddhi’s Institute of Pharmacy, Thane 421401, India.

 

Shoheb Shaikh
RSM’s NN Sattha College of Pharmacy, Ahilyanagar 414001, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/psnid/v5/5282

Role of Caspase-12 in Hepatocyte Apoptosis Induced by Carbon Tetrachloride in Mice | Chapter 13 | Medical Science: Trends and Innovations Vol. 10

Toxic liver damage can lead to acute liver failure, hepatic fibrosis, and even carcinogenesis. This study aimed to explore the role of caspase-12 and its downstream targets in hepatocyte apoptosis induced by carbon tetrachloride (CCl₄). To determine the role of caspase-12, caspase-12 knockout mice were used. Wild-type and caspase-12 knockout mice received a single intraperitoneal injection of either CCl₄ (300 μl/kg BW) or vehicle (corn oil). The animals were sacrificed 24 hours after treatment, and blood samples were collected to assess liver function through alanine aminotransferase activity. Liver samples were analyzed for reactive oxygen species (ROS) levels using plasma malondialdehyde as a biomarker, hepatocyte apoptosis via TUNEL assay and morphological analysis, and cytochrome C release and caspase activation through western blotting.

In wild-type mice, low-dose CCl₄ administration caused hepatocyte apoptosis and acute liver injury, accompanied by increased ROS production and endoplasmic reticulum (ER) stress in the liver. These events triggered the activation of caspases-12, -9, and -3, along with the release of small amounts of cytochrome C. However, in CCl₄-treated caspase-12 knockout mice, the activation of caspases-9 and -3 was significantly reduced, while cytochrome C release remained unaffected. Compared to wild-type mice, CCl₄-induced apoptosis and liver damage were substantially attenuated in caspase-12 knockout mice (p < 0.05). Notably, the active form of caspase-8 was not detected in either wild-type or knockout mice. Additionally, there was no significant difference in ROS formation between the two groups following CCl4 treatment.

These findings demonstrate that caspase-12 plays a critical role in CCl₄-induced hepatic apoptosis by directly or indirectly activating effector caspase-3 downstream, with partial involvement of caspase-9 activation. In conclusion, prolonged exposure to even low levels of CCl₄ could cause liver pathology in humans, warranting further clinical and animal studies to investigate the long-term consequences of minimal exposure.

 

Author (s) Details

Hua Liu
Division of Pediatric Gastroenterology, Department of Pediatrics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.

 

Madison Nicole Burton
University of Mississippi Medical Center, Jackson, MS 39216, USA.

 

Neha Dhaliwal
William Carey University, 710 William Carey Pkwy, Hattiesburg, MS 39401, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/msti/v10/4801

Targeting JNK-1 with Small Interfering RNA: Induction of Apoptotic Pathways in PC-3 Prostate Cancer Cells | Chapter 5 | Research Perspectives of Microbiology and Biotechnology Vol. 9

Jun-N-terminal kinase-1 (JNK-1) has been implicated in the transformation of primary fibroblasts and the regulation of tumor cell growth. Emerging evidence suggests that JNK-1 functions as a growth-promoting factor in prostate cancer cells, making it a potential therapeutic target. In this study, we utilized small interfering RNA (siRNA) to selectively suppress JNK-1 expression in the prostate cancer cell line PC-3. The targeted siRNA effectively reduced JNK-1 levels, leading to alterations in the expression of key apoptotic and cell cycle regulatory proteins, including p21, XIAP, and Bcl-2, while VEGF expression remained unaffected. In contrast, a control scramble siRNA did not impact the expression of these proteins. The silencing of JNK-1 was confirmed at the mRNA and protein levels via RT-PCR and western blot analysis. Functional assays revealed significant inhibition of cell proliferation, with apoptosis induction validated through flow cytometry, DNA fragmentation, and caspase activity assays. Notably, siRNA-mediated downregulation of JNK-1 led to a cell death rate of 52%, an apoptotic rate of 26%, and a viability rate of 22% after five days of treatment. These findings highlight the potential of JNK-1-targeting siRNA as a novel therapeutic strategy for prostate cancer. Further research is warranted to explore its clinical applicability.

 

Author (s) Details

 

Eduardo Parra
Department of Biomedical Sciences, Faculty of Medicine, Saucache Campus, University of Tarapacá, Ave. Senator Luis Valente Rossi-2223, Arica, Chile.

 

Víctor Rojas
Department of Biomedical Sciences, Faculty of Medicine, Saucache Campus, University of Tarapacá, Ave. Senator Luis Valente Rossi-2223, Arica, Chile and Doctorate Program in Translational Biotechnology, Faculty of Agricultural and Forestry Sciences, Catholic University of Maule, 3480112, Talca, Chile.

 

Pedro Hecht
Department of Biomedical Sciences, Faculty of Medicine, Saucache Campus, University of Tarapacá, Ave. Senator Luis Valente Rossi-2223, Arica, Chile.

 

Please see the book here:- https://doi.org/10.9734/bpi/rpmab/v9/3718

DNA Damage in Peripheral Blood Mononuclear Cells and Neutrophils of Dairy Cows during the Transition Period: Experimental Investigation | Chapter 14 | Advanced Research in Biological Science Vol. 5

 The purpose concerning this study was to examine the apoptotic process in peripheral ancestry mononuclear cells (PBMC) and polymorphonuclear neutrophil leukocytes (PMN) in creamery cattle all the while the transition ending. This period is from marked changes in the endocrine rank of the animals that are much more moving than at any different time in the removal of liquid gestation era, and by a reduction in feed consumption when nutrient demand for the evolving conceptus and the impending lactogenesis are increasing. Blood samples were captured from four dairy cows three weeks before discharged parturition (wk -3), all the while parturition (ww 0), and three weeks subsequently parturition (wk +3). The meteor test was used to assess the DNA damage of PBMC and PMN utilizing visual notch (arbitrary wholes). Undamaged DNA remained in the gist (score 0), while broken DNA well-traveled from the core to the anode, create a comet tail (cut 1-4).  Significantly higher scores in PBMC were stated at wk 0 and wk +3 compared to PMN, in spite of no significant changes in scores in either container type across the study period. It has happened suggested that the apoptotic rate of PBMC is faster than that of PMC all along the transition ending.

Author(s) Details:

Mohamed Tharwat,
Department of Animal Medicine, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt and Department of Veterinary Medicine, College of Agriculture and Veterinary Medicine, Qassim University, Saudi Arabia.

Shin Oikawa,
Veterinary Herd Health, Department of Veterinary Medicine, School of Veterinary Medicine, Rakuno Gakuen University, Japan.

Please see the link here: https://stm.bookpi.org/ARBS-V5/article/view/12587

Alpha-mangostin-loaded PLGA Nanoparticles for Cholangiocarcinoma | Chapter 1 | Current Innovations in Disease and Health Research Vol. 1

 The present study proposed to formulate and typify the AM-loaded PLGA nanoparticles (AM-PLGA-NPs) and further evaluated their antiproliferative and proapoptotic endeavors, including inhibitory actions on CCA cell invasion and migra-tion. Alpha-mangostin, a instinctive xanthone mainly culled from the pericarp of Garcinia mangostana, has existed shown to have promising anticancer features in many types of cancer. PLGA MW 7,000-17,000 and 38,000-54,000 were used to create the AM-PLGA-NPs using the fit displacement method. Physical (piece size and makeup, polydispersity index, and zeta potential) and pharmaceutical (encapsulation efficiency, stowing efficiency, and drug release description) parameters were evaluated for the optimised AM-PLGA-NPs. . The morphology of the AM-PLGA-NPs and PLGA-NPs were examined under a broadcast electron microscope (TEM). The MTT assay, flow-cytometry, QCM ECMatrix container migration and container invasion assays were used to evaluate antiproliferative and proapoptotic endeavors, including inhibitory actions on CCA cell (CL-6 and HuCCT-1) invasion and movement, respectively. The inhibitory actions of AM-PLGA-NPs on the migration and attack of both CCA cell lines were aggregation- and time-reliant, while no inhibitory effect was found accompanying OUMS-36T-1F cells. AM-PLGA-NPs showed comparably potent and discriminating antiproliferative and proapoptotic activities in both CCA container lines in a concentration- and opportunity-dependent tone. Results revealed that PLGA nanoparticles could be a appropriate nanocarrier to encapsulate AM for allure delivery to CCA containers. The underlying molecular methods of AM-PLGA-NPs involved in these endeavors should be further investigated.

Author(s) Details:

Kesara Na-Bangchang,
Center of Excellence in Pharmacology and Molecular Biology of Malaria and Cholangiocarcinoma, Chulabhorn International College of Medicine, Thammasat University (Rangsit Campus), Klongneung, Klongluang District, Pathumthani, Thailand and Drug Discovery and Development Center, Office of Advanced Science and Technology, Thammasat University (Rangsit Campus), Klongneung, Klongluang District, Pathumthani, Thailand.

Tullayakorn Plengsuriyakarn,
Center of Excellence in Pharmacology and Molecular Biology of Malaria and Cholangiocarcinoma, Chulabhorn International College of Medicine, Thammasat University (Rangsit Campus), Klongneung, Klongluang District, Pathumthani, Thailand.

Chuda Chittasupho,
Faculty of Pharmacy, Chiang Mai University, Thailand.

Please see the link here: https://stm.bookpi.org/CIDHR-V1/article/view/11057

Inhibitory Effect of Burmannic Acid for Proliferation and Oxidative Stress Induce Responses of Oral Cancer Cells | Chapter 10 | New Advances in Medicine and Medical Science Vol. 3

 The present inquiry evaluated the antiproliferation effects of C. burmannii-derive BURA on oral malignancy cells for the first time. Oral tumor cell lines came from gin-gival, tongue, and buccal covering layer tissues (Ca9-22, CAL 27, and OC-2) were selected for testing the natural response to BURA. Oxidative stress in spoken disease is related to added systemic ailments in the body such as periodontitis, cardiovascular, pancreatic, stomachic, and liver diseases. In the review, we discuss the various pathways that intervene oxidative cellular damage. In terms of machine, BURA per- turbed cell phase distribution, upregulated mitochondrial superoxide, induced mitochondrial depo- larization, prompted γ H2AX and 8-hydroxy-2-deoxyguanosine DNA damage, and induced apop- tosis and caspase 3/8/9 incitement in oral cancer containers. N-acetylcysteine treatment confirmed oxidative stress as a key determinant in promoting antiproliferation, apoptosis, and DNA damage in spoken cancer cells.  The study showed that BURA generates oxidative stress and causes apoptosis and DNA damage that prevents oral cancer container proliferation.

Author(s) Details:

Su-Ling Liu,
Experimental Forest College of Bioresources and Agriculture, National Taiwan University, Zhushan Township, Nantou County-55750, Taiwan.

Kun-Han Yang,
Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.

Che-Wei Yang,
Graduate Institute of Natural Products, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.

Min-Yu Lee,
Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.

Ya-Ting Chuang,
Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.

Yan-Ning Chen,
Department of Biomedical Science and Environmental Biology, College of Life Science, Kaohsiung Medical University, Kaohsiung-80708, Taiwan.

Chung-Yi Chen,
School of Medical and Health Sciences, Fooyin University, Kaohsiung-83102, Taiwan.

Please see the link here: https://stm.bookpi.org/NAMMS-V3/article/view/10778

Segmental Arterial Mediolysis a Norepinephrine Induced Multi-guised Vasospastic Arteriopathy: Pathogenesis, Pathology and Clinical Presentations | Chapter 14 | Research Developments in Medicine and Medical Science Vol. 9

 Definition: Segmental arterial mediolysis (SAM) is a exceptional vasospastic, multiguised arteriopathy that affects the power arteries innervated by the minor sympathetic central nervous system. It typically manifests in aging people as destructive abdominal and retroperitoneal haemorrhages.Pathogenesis: SAM is initiated for one coupling of norepinephrine to plastically derivative hyper thick foci of alpha-1 adrenergic receptors on the sarcolemma of arterial influence. This ligand is created by provocation signaled by iatrogenic sympathomimetic agonists, some Beta-2 agonists, or an overdone release of adrenal catecholamines. Coupling of this ligand accompanying cytoplasmic heterotrimeric Gq protein excessively signals a cascade of biochemical events create the two principal lesions of hurtful phase SAM.Pathology: These are the shearing of the outer news from the adventitia and an overload of cytoplasmic calcium ions poisonous to mitochondria causing mediolysis and/or apoptosis. The transmedial misfortune of the medial muscle causes breach-aneurysms, which burst and cause the tremendous haemorrhages. The rapid development of a norepinephrine-supervised reparative answer either heals angiographic injury lesions or generates a frame of vascular illnesses, the new guises of SAM, accompanying ischemic clinical descriptions. These present in the epicardial, vertebral, intestinal, and retroperitoneal arteries, frequently in younger women as fibromuscular dysplasia, dissecting hematomas, and persistent aneurysms. Norepinephrine can cross talk accompanying serotonin and histamine to create SAM lesions and endothelin-1 in a field effect that produce venous fibromuscular dysplasia. Norepinephrine participates in the collateral development of mesangial hyperplasia with pertaining to a focus segmental glomerulosclerosis and myocardial mediolysis and apoptosis in subjects accompanying markedly elevated essence rates.Conclusion: Norepinephrine coupling accompanying plastically elevated beginning-1 adrenoceptor or other pressor agents produce SAM, a histologically recognizable vasospastic arteriopathy, that accompanying repair is transformed into several various standardized arterial ailments that alter SAM’s clinical characterization from a hemorrhagic to an ischemic disease.

Author(s) Details:

Richard E. Slavin,
1793 Childs Rd, Lake Oswego, Oregon, USA.

Please see the link here: https://stm.bookpi.org/RDMMS-V9/article/view/10428

7-hydroxicoumarin Exposure Induces Prompt Activation of caspase-3 in A-549 Cancer Cells through Single Cell Microinjection | Chapter 4 | Current Overview on Pharmaceutical Science Vol. 7

 Coumarins and their apoptogenic belongings have arisen obvious   interest in recent years.  The present division aims to determine either 7-hydroxycoumarin (7-HC) induces changes in caspase-3 (C-3) activity in A549 human lung malignant growth cells.The belongings of 7-HC were investigated utilizing a variety of analytical approaches, containing colorimetric and fluorometric assays, western blotting, distinct-cell microinjection, fluorescence microscopy, and concept analysis. After being unprotected to 1.85 mM 7-HC for 24 hours, C3 activity raised by 65%, procaspase-3 was significantly converted to C-3, and poly(ADP-ribose) polymerase was cleaved. Additionally, semantic modifications linked to apoptosis were seen. The calcium conductance of the cells raised by 27% after being unprotected to 7HC for 3 or 6 hours. Single-cell microinjection of a distinguishing fluorescent substrate of C-3 into cells that had earlier been unprotected to 7-HC allowed for the identification of a usual enzymatic energetic profile of C-3 incitement several hours before the morphological and biochemical changes related to the observation of apoptosis. These judgments imply that 7-HC, the most main biotransformation product of coumarin in crowd, is what causes the rapid in vivo activation of C-3.

Author(s) Details:

Maribel Soto-Núñez,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

Karen Azucena Díaz-Morales,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

Patricia Cuautle-Rodríguez,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

Víctor Torres-Flores,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

José Sullivan López-González,
Department of Chronic Degenerative Diseases, National Institute of Respiratory Diseases ‘Ismael Cosío Villegas’, Mexican Ministry of Health, Mexico City, Mexico.

Juan José Mandoki Witzner,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

Juan Arcadio Molina-Guarneros,
Department of Pharmacology, School of Medicine, National University of Mexico, Mexico City, Mexico.

Please see the link here: https://stm.bookpi.org/COPS-V7/article/view/9695

Synthesis, Characterization and Biocompatibility of Maltodextrin-coated Cadmium Sulfide Quantum Dots in Experimental Models| Chapter 8 | Recent Progress in Science and Technology Vol. 1

 Semiconductor Quantum dots (QDs) have win quite a bit of recognition due to their characteristics and extensive application in organic and biomedical research. However, these very same features present further troubles in comprehending, thinking, and controlling possible antagonistic health results after exposure. These past few age, QDs have rapidly enchant and novel tools for theragnostic purposes; their use entails the contributing safety studies. Cadmium and selenium, that are the main components in the majority of quantity dots, are known expected acutely and chronically toxic to containers and organisms, but insulating the core of nanoparticles can, to some degree, control toxicity had connection with cadmium and selenium leakage. Our research has proved that CdS-maltodextrin (CdS-MDx) QDs are biocompatible and nontoxic to containers and animals. However, QDs can still induce embryotoxic belongings. This study successfully combined and characterized maltodextrin coated cadmium sulfide semiconductor nanoparticles (CdS-MDx QDs) and the results presented that, in low concentrations (4.92 and 6.56 nM), these gently increased the number of HepG2 cells. We likewise observed a decline in MDA-MB-231 cells under concentrations higher than 4.92 nM in a measurement-response form, while Caco-2 cells significantly raised starting at 1.64 nM. CdS-MDx QDs persuaded cell death by apoptosis and loss in MDA-MD-231 cells offset at 8.20 nM concentrations in a dose-response conduct. CdS-MDx QDs biodisposition was evaluated established an analysis of the pharmacokinetic parameters of various tissues following the administration of a alone i.p. dose to rodents at several opportunity points. We analyzed fabric images utilizing fluorescence microscopy and tissue homogenates utilizing spectroscopy to identify and measure CdS MDx QD content and resolve QD concentration in each tissue at prearranged time breaks. Our data clearly granted that CdS-MDx QDs were not completely emptied from in vivo systems after 360 h. Liver and sort tissues took up ultimate QDs, but their Ke and MRT evidenced rapid energetic elimination, suggesting these tools might eliminate QDs. Therefore, in an work to further address this issue, we studied the belongings of CdS-MDx QDs on embryos via an embryotoxicity assay on chicken embryos. Chicken embryos unprotected to CdS-MDx QDs (0.001, 0.01, 0.1 and 1 µg/kg) in ovo for 72 h showed tumor and developmental alterations during the inception and at the end of their incident in a dose-weak manner. Current studies have also proved that CdS-MDx QDs induce embryotoxicity, moving mainly the CNS, the neural hose and somites. The nature of the noticed abnormalities suggests that these belongings could be straightforwardly associated with QD concentrations affecting somitogenesis. Our results display that CdS-MDx QDs induce container death in human container lines. The pharmacokinetic properties of CdS-Mdx QDs can have healing and diagnostic use but, as per current results, remain conceivably harmful to fetus and fetus development. Further studies utilizing mammalian variety are required to discard supplementary toxic belongings.

Author(s) Details:

Rodríguez-López Anahi,
Departamento de Fisica, CINVESTAV – I.P.N, Mexico, D.F., Mexico.

Ayala-Calvillo Erick,
Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, México.

Rodríguez-Fragoso Patricia,
Departamento de Fisica, CINVESTAV – I.P.N, Mexico, D.F., Mexico.

Gerardo González De la Cruz,
Departamento de Fisica, CINVESTAV – I.P.N, Mexico, D.F., Mexico.

Lourdes Rodríguez-Fragoso,
Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, México.

Please see the link here: https://stm.bookpi.org/RPST-V1/article/view/9095

Evaluating the Effect of Monocyte Locomotion Inhibitory Factor a Natural Anti-Inflammatory Produced by E. histolytica on Apoptosis in Human CD4+ T Lymphocytes| Chapter 6 | Challenges and Advances in Pharmaceutical Research Vol. 6

 The study assessed how MLIF affected human CD4+ T cells' intrinsic and extrinsic apoptotic pathways. For 24 hours, cells were either cultured in RPMI-1640 media alone (control), or in RPMI medium with actinomycin D, MLIF, PMA, or any combination of the four. According to annexin V/propidium iodide-stained cells, cells treated with MLIF or PMA + MLIF did not significantly differ from control cells in medium during early apoptosis; in contrast, cells treated with PMA or PMA + MLIF displayed significant differences from the control during delayed apoptosis. Cells treated with PMA and PMA + MLIF showed a considerable rise in cytochrome c and caspase 3 levels when compared to the control, showing that this ineffective activation of cell death is governed by the intrinsic route of apoptosis. In comparison to control cells, MLIF-treated cells did not significantly differ in their levels of cytochrome c or caspase 3. The lack of Fas receptor identification in cell culture in response to any of the treatments used suggests that the extrinsic mechanism of apoptosis is not activated. When treated to MLIF, human CD4+ T lymphocytes may not undergo apoptosis; nevertheless, PMA and MLIF may also affect the minor quantities of cell death seen during the late apoptosis phase. MLIF is an intriguing candidate for possible clinical uses because of its small size and ability to act as a natural, biological anti-inflammatory chemical produced in Entamoeba histolytica axenic cultures.

Author(s) Details:

Sara Rojas-Dotor,
Unidad de Investigación Médica en Inmunología, Hospital de Pediatría, Centro Médico Nacional Siglo XXI Instituto Mexicano del Seguro Social (IMSS), México City, México.

Marco Julio Sánchez Rojas,
Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), México City, México.

Please see the link here: https://stm.bookpi.org/CAPR-V6/article/view/8094

Methyl-donors Induce Apoptosis and Attenuate Proliferation Pathways Mediated by Akt and Erk1/2 in Breast and Lung Cancer Cell Lines| Chapter 5 | Current Practice in Medical Science Vol. 9

 We expected to investigate what methyl-contributor therapies mean for the development, expansion, apoptosis and the connected pathways in chemical positive obtrusive bosom disease (MCF7 and T47D) and NSCLC cellular breakdown in the lungs (A549 and H1650) cell lines. Methyl-givers are utilized as an adjunctive help in oncotherapy and assume basic parts in physiological cycles catalyzed by coenzymes of the B nutrients. Our hypothesis was that methyl-benefactors may straightforwardly hinder growth advancement and expansion as well as assisting patients with enduring disease treatment. Methyl-giver treatment essentially decreased the expansion in undeniably examined cell lines, perhaps through the downregulation of MAPK/ERK and AKT flagging. These were joined by the upregulation of the supportive of apoptotic Bak, Bax both in MCF7 and H1650 cells, at diminished enemy of apoptotic Mcl-1 and Bcl-2 levels in MCF7 and H1650 cells, separately. The treatment actuated downregulation of p-p53(Thr55) was probably going to add to safeguarding the atomic limitation and apoptosis inciting elements of p53. The highlights that are being offered are known to build the responsiveness of disease treatment. Considering this, the perceptions are predictable with the hypothesis that methyl-givers might safeguard p53 exercises by advancing apoptotic announcing downregulating both the MAPK/ERK and the AKT pathways in bosom and cellular breakdown in the lungs cell lines. Our outcomes can stress the significance and advantages of the proper dietary backings in malignant growth medicines. Notwithstanding, further examinations are expected to affirm these impacts with next to no antagonistic result in clinical settings.

Author(s) Details:

Eva Kiss,
Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest-1083, Hungary.

Gertrud Forika,
Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.

Reka Mohacsi,
Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest-1083, Hungary.

Magdolna Dank,
Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest-1083, Hungary.

Tibor Krenacs,
Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.

Istvan Takacs,

Department of Internal Medicine and Oncology, Semmelweis University, Budapest-1083, Hungary.

Zsuzsanna Nemeth,

Department of Internal Medicine and Oncology, Semmelweis University, Budapest-1083, Hungary.

Please see the link here: https://stm.bookpi.org/CPMS-V9/article/view/8012

Determination of Cisplatin Effect on Head and Neck Squamous Cell Carcinoma Modulated by Erk1/2 Protein Kinases | Chapter 14 | Current Practice in Medical Science Vol. 8

The aim of this study was to investigate the role of extracellular signal-regulated kinases (ERK1/2) and/or p53 activation in the apoptotic process induced by cisplatin-CisPT treatment on two head and neck squamous cell carcinoma cell lines (FaDu and PE/CA-PJ49) and how curcumin (CRM) used as an adjuvant supports it. According to data, CRM enhances CisPt activity. In both cell lines, CRM raised the phosphorylation of the p53 protein. CisPt altered the phosphorylation of the p53 protein in PE/CA-PJ49 cells but enhanced it in FaDu cells. The constitutive expression of activated ERK1/2 protein-kinase varied in the two tumour cell lines under investigation. The activation status of ERK1/2 was a factor in the cell processes that CisPt and/or CRM induced, including cell proliferation and death. Our results suggest that the phosphorylation of p53 during the apoptotic response to CRM treatment may need ERK1/2. In both tumour cell lines, combination treatments (CisPt and CRM) resulted in apoptosis that was dependent on p53 phosphorylation and ERK1/2 activation. Finally, ERK1/2 may affect cell proliferation and/or death depending on the type of therapeutic drug, the properties of the cells, and the level of ERK1/2 activation.

 

Author (s) Details

Marinela Bostan

Stefan S. Nicolau Institute of Virology, Center of Immunology, Bucharest, Romania and  Victor Babes National Institute of Pathology, Bucharest, Romania.

Georgiana Gabriela Petrica-Matei

Department of Cytogenetics, Personal Genetics - Medical Genetics Center, Bucharest, Romania.

Gabriela Ion

Stefan S. Nicolau Institute of Virology, Center of Immunology, Bucharest, Romania.

Nicoleta Radu

University of Agronomic Sciences and Veterinary Medicine of Bucharest, Biotechnology Dept.& National Institute for Chemistry and Petrochemistry R&D of Bucharest, Romania.

Mirela Mihaila

Stefan S. Nicolau Institute of Virology, Center of Immunology, Bucharest, Romania.

Razvan Hainarosie

Prof. Dr. Dorin Hociota Institute of Phonoaudiology and Functional ENT Surgery, Bucharest, Romania.

Lorelei Irina Brasoveanu

Stefan S. Nicolau Institute of Virology, Center of Immunology, Bucharest, Romania.

Viviana Roman

Stefan S. Nicolau Institute of Virology, Center of Immunology, Bucharest, Romania.

Carolina Constantin

Victor Babes National Institute of Pathology, Bucharest, Romania.

Monica Teodora Neagu

Victor Babes National Institute of Pathology, Bucharest, Romania.

 

Please see the link here:-  https://stm.bookpi.org/CPMS-V8/article/view/7803

Methyl Donors Inhibit Panc-1 Cell Proliferation by Decreasing NFkB and Erk Signaling Levels and Raising E-Cadherin Expression | Chapter 11 | Current Practice in Medical Science Vol. 8

The physiology of cancer patients, particularly those with pancreatic cancer, may be improved by dietary methyl donors, which may also be utilised as intervention treatment. In this study, an aggressive pancreatic adenocarcinoma cell line (Panc-1) was treated with methyl-donors (L-methionine, choline chloride, folic acid, and vitamin B12), which significantly increased the levels of p21WAF1/Cip1 cyclin dependent kinase inhibitor and the SubG1 fractions while significantly decreasing the levels of phospho-Erk1/2 and the proliferation rate. Diet is one of the lifestyle-related factors in the genesis of pancreatic cancer, an aggressive malignancy with a high chance of metastasizing. Methyl-donors are dietary micronutrients that function as bioactive food ingredients by delivering methyl groups as cofactors and substrates for critical metabolic pathways. Pathological disorders have recently been related to methyl-donors' unbalanced nutritional status. Although Bak, Puma, and Caspase-9 levels were likewise raised by methyl donor treatments, cleaved Caspase-3 levels were not. The production of the transcription factor NFkB and the pro-inflammatory cytokine IL-17a was also markedly decreased by the therapy. After methyl-donor treatments, SDF-1a and VEGF levels were found to be much lower, which may indicate a reduced risk of metastatic dissemination. As was anticipated, E-cadherin expression increased following the methyl-donor therapy and was negatively correlated with these changes. It is determined that methyl-donors may have the ability to lessen Panc-1 cells' aggressive and proliferative character. This implies a potential function for dietary methyl-donors in enhancing

 

Author (s) Details

Eva Kiss

Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Gertrud Forika

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.0

Istvan Takacs

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Tibor Krenacs

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.

Zsuzsanna Nemeth

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

 

Please see the link here:-  https://stm.bookpi.org/CPMS-V8/article/view/7800

Post-Translational Modification of SUMOylation and Cancer: A Brief Review | Chapter 09 | New Horizons in Medicine and Medical Research Vol. 3

 SUMOylation is a reversible post-translational modification that plays a role in DNA damage repair, immunological responses, carcinogenesis, cell cycle progression, and apoptosis. SUMO1, SUMO2/3, and SUMO4 are the four SUMO isoforms that have been identified. In complicated protein regulatory networks, many levels of regulation or SUMOylation may play a crucial role. SUMOylation dysfunction can lead to the development of illnesses and malignancies. As a result, SUMO could be employed as a cancer treatment target. The small ubiquitin-like modifier (SUMO) pathway is found in all eukaryotes and is involved in gene regulation, cellular signalling, and the preservation of genomic integrity. Maturation, activation, conjugation, ligation, and de-modification are all part of the SUMO catalytic cycle. The SUMO system has been related to a number of disorders, the most prominent of which being cancer. Carcinogenesis, DNA damage response, cancer cell proliferation, metastasis, and apoptosis are all affected by SUMOylation. SUMO has the potential to be a cancer treatment target. To better comprehend the role of SUMO in human disease, we present the basic concepts of the SUMO system and summarise the involvement of SUMO proteins in cancer cells in this review.

Author(S) Details

ZhI-Jian Han
Key Laboratory of the Digestive System Tumors of Gansu Province, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Yan-Hu Feng
Key Laboratory of the Digestive System Tumors of Gansu Province, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Bao-Hong Gu
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Yu-Min Li
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

Hao Chen
Department of General Surgery, Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R., China.

View Book:- https://stm.bookpi.org/NHMMR-V3/article/view/6338

Recent Trends in Ethylene Glycol Monomethyl Ether Research | Chapter 09 | New Innovations in Chemistry and Biochemistry Vol. 6

 Ethylene glycol monomethyl ether (EGME) is a solvent that has a wide range of applications. The results of studies on EGME in humans and animals undertaken over the previous two decades are presented in this chapter. The documentation supports EGME's classification as a gonadotoxicant, with implications for haematological, oxidative state, apoptosis, inflammation, gene expression, and metabolism.

Author (S) Details

Oluwatoyin Adenike Adeyemo-Salami
Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.

View Book:- https://stm.bookpi.org/NICB-V6/article/view/5302

Lectin-positive Spherical Deposits (SPD) in Molecular Layer of Hippocampal Dentate Gyrus of Dementia, Down's Syndrome, and Schizophrenia: Mini Review | Chapter 15 | Recent Developments in Medicine and Medical Research Vol. 8

 Lectins are proteins that bind (or crosslink) carbohydrates in a specific way. Recent research has revealed the role of glycosylation in disease aetiology. In dementia, Down's syndrome, and schizophrenia, we found lectin-positive spherical deposits (SPD) in the molecular layer of the dentate gyrus of the hippocampus, measuring 3-10 micron in diameter. The goal of this research is to better understand the nature and significance of SPD in the aetiology of neuropsychiatric disorders. SPD was detected in all cases of schizophrenia, regardless of previous medication. Single strand DNA was found co-localized with lectins in the hippocampus SPD of schizophrenia, including GSI-B4 for galactose and UEA-I for fucose, using multi-labeling histochemical methods, implying that SPD formation in schizophrenia is linked to apoptotic events. The biochemical basis of SPD development in brains with neuropsychiatric diseases should be studied further.

Author(S) Details

Keiko Ikemoto
Department of Psychiatry, Iwaki City Medical Center, Iwaki, 973-8555, Japan.

Akiyoshi Nishimura
Department of Forensic Medicine, Health Bioscience Institute, University of Tokushima Graduate School, Tokushima, 770-8503, Japan.

View Book:- https://stm.bookpi.org/RDMMR-V8/article/view/4574

Assessing the Effects of Thermal Stimulation on Skeletal Muscle-Derived Cell Density | Chapter 10 | Recent Developments in Medicine and Medical Research Vol. 7

 We looked into whether thermal stimulation could help prevent atherosclerotic cardiovascular disease in the past (ASCVD). Variations in the expression of associated genes were validated in studies utilising human skeletal muscle-derived cells (SMDC). A small decrease in the number of cells was also verified. The application of thermal stimulation to cultured cells has long been connected with apoptosis. Although various research have confirmed the above, such as promoting apoptosis and decreasing apoptosis with heat stimulation, the precise effects of thermal stimulation on apoptosis have yet to be determined. In order to safely use heat stimulation for the prevention of ASCVD in vivo, we reexamined the effects of thermal stimulation on human skeletal muscle cells. We hypothesised that thermal stimulation of SMDC causes apoptosis based on our previous findings. This suggested that in order to prevent ASCVD in vivo, heat stimulation should be moderate.

Author(S) Details

Masayo Nagai
Department of Nursing Faculty of Health Science, Aino University, Japan.

Hidesuke Kaji
Division of Physiology and Metabolism, University of Hyogo, Division of Pathophysiology, Kobe Women’s University, Japan.

View Book:- https://stm.bookpi.org/RDMMR-V7/article/view/4535