Joint Remodeling Molecules and Complement Components in Septic Arthritis | Chapter 5 | Recent Progress in Microbiology and Biotechnology Vol. 6

 Septic arthritis (SA), also known as infectious arthritis, is caused by viruses, bacteria, and fungi, as opposed to other inflammatory joint diseases. These microorganisms spread to the joints through the bloodstream from an existing focus in the body or enter through a wound in the case of joint injury or surgical intervention. SA pathogenesis is caused by specific interactions between the microorganism and the host, particularly its immune system. We examined the available literature data on some Infections in which molecular factors are produced, which are also known to be involved in arthritis remodeling processes. We looked at the role of complement system components and joint remodeling markers like TGF-, BMP, osteoprotegerin/receptor activator of nuclear factor B/receptor activator of nuclear factor B ligand (OPG/RANK/RANKL) and sclerostin in the pathogenesis of septic arthritis. We discuss potential treatment strategies based on the targeting of these molecules in order to reduce the inflammatory destructive response in the joints during infections.

Author (S) Details

Lyudmila Belenska-Todorova
Department of Biology, Medical Genetics and Microbiology, Faculty of Medicine, Sofia University “St. Kliment Ohridsky”, Sofia, Bulgaria.

Nina Ivanovska
Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria.

View Book :- https://stm.bookpi.org/RPMB-V6/article/view/1679

 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