Ameliorative Impact of Tecoma stans on Streptozotocin-Induced Diabetic Cardiomyopathy in Wistar Rats | Chapter 2 | Advanced Concepts in Pharmaceutical Research Vol. 1

 The objective concerning this study was to visualize how an ethanolic extract of Tecoma stans overwhelmed diabetic cardiomyopathy in wistar rats after streptozotocin-inferred diabetes.  The pathogenesis of diabetic cardiomyopathy (DCM) is complex, and the therapeutic alternatives available to treat DCM are restricted. A single intravenous portion of drug or other consumable of (Streptozotocin 45 mg/kg) produced diabetes in male wistar rats. Blood pressure, antitoxin lactate dehydrogenase (LDH), hydrogen apolipoprotein B, and lipids were measured, in addition to heart pressure, caspase-3, sodium potassium adenosine triphosphatase (Na + -K + ATPase), and DNA laddering.  The obtained result granted that the administration of ethanolic extract of Tecoma stans (120 mg/kg/p.o.) considerably (P < 0.01) reduced myocyte deficit by suppressing the levels of cardiac caspase-3, DNA laddering; mean unmodified blood pressure and heart rate in addition to serum LDH, organic compound composed of carbon, apolipoprotein B and lipids levels. Further, it augmented the soul weight and cardiac Na+ K + ATPase activity in diabetic rats. Finally, an flammable liquid extract of Tecoma stans was found to have important anti-apoptotic potential in Streptozotocin-inferred diabetic cardiomyopathy.

Author(s) Details:

S. Kameshwaran,
Department of Pharmacology, SSM College of Pharmacy, Bhavani (Tk), Erode (Dt), Tamilnadu - 638 312, India.

M. Ravisankar,
Department of Pharmacy, Vinayaka Mission’s College of Pharmacy, Vinayaka Mission’s Research Foundation (Deemed to be a University), Salem, Tamilnadu - 636 308, India.

P. Srinivasan,
Department of Pharmacology, Vivekanandha Pharmacy College for Women, Sankari West, Salem -637303, India.

V. Suresh,
Department of Pharmacology, Arunai College of Pharmacy, Tiruvannamalai 606 603, India.

Please see the link here: https://stm.bookpi.org/ACPR-V1/article/view/12073

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

 Background information: The current study looked at the potential cardioprotective benefits of GLP1 and SGLT2i against diabetic cardiomyopathy (DCM) in type 2 diabetic rats, as well as the mechanisms behind them. The existence of heart failure in the absence of coronary artery disease is referred to as DCM.

 Methods: Forty-two male Sprague Dawley rats were randomized into four equal groups at random; a) DM+ GLP1, as DM group with GLP1 analogue (liraglutide) at a dose of 75 g/kg for 4 weeks, and DM+ SGLT2i: as DM group with SGLT2 inhibitor (dapagliflozin) at a dose of 1 mg/kg for 4 weeks. Serum blood glucose, HOMA-IR, insulin, and cardiac enzymes (LDH, CK-MB) were all tested at the end of the four-week treatment.

Myocardial oxidative stress markers (MDA, GSH, and CAT) as well as norepinephrine (NE), myocardial fibrosis, and the expression of caspase-3, TGF-, TNF-, and tyrosine hydroxylase (TH) in myocardial tissues were all assessed. As a result, T2DM resulted in a considerable increase in blood sugar levels. (p 0.05) serum glucose, HOMA-IR, serum CK-MB, and LDH In addition, DM resulted in severe myocardial damage and fibrosis, as well as an increase in myocardial MDA, NE, and upregulation of myocardial caspase-3, TNF, TGF, and TH, as well as a substantial drop in serum insulin, myocardial GSH, and CAT (p0.05). All examined indicators improved significantly (p 0.05) after administration of either GLP1 analog or SGLT2i. Conclusion: We found that both GLP1 and SGLT2i had cardioprotective effects against DCM in T2DM, with SGLT2i having the upper hand. This could be related to fibrosis, oxidative stress, apoptosis (caspase-3), sympathetic nerve activity, and other factors.

Author (s) Details

Prof. Dr. Abdelaziz M. Hussein
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt

Elsayed A. Eid
Department of Internal Medicine and Endocrinology, Delta University for Science and Technology, Gamasa, Egypt

Medhat Taha
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.

Rami M. Elshazli
Department of Biochemistry, Faculty of Physical Therapy, Horus University-Egypt, New Damietta, Egypt.

Raouf Fekry Bedir
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.


Lashin Saad Lashin
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt and Department of Medical Physiology, Horus University, Damietta, Egypt.

View Book :- https://stm.bookpi.org/HMMR-V9/article/view/1021