Document Type : Original Article
Authors
1
Medical physiology department, faculty of Medicine, Menoufia University
2
Medical Biochemistry and Molecular Biology Department, Faculty of medicine, Mansoura University, Egypt. Medical Biochemistry and Molecular Biology Department, Faculty of medicine, New Mansoura University, Egypt.
3
Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
4
Clinical Pharmacology, Faculty of Medicine, Mansoura University, Egypt. 35516
5
Anatomy and Embryology Department, Faculty of Medicine, Portsaid University, Portsaid, Egypt
6
Pathology Department, Faculty of Medicine, Menoufia University Shebin El-Kom, Menoufia, Egypt.
7
Internal Medicine and Nephrology department, Faculty of Medicine, Menoufia University Shebin El-Kom, Menoufia, Egypt.
8
Medical Physiology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
9
Medical Physiology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
10.21608/besps.2025.347094.1193
Abstract
Introduction: One serious health issue is diabetic nephropathy (DN). A lipid mediator that is naturally produced from omega-3 fatty acids, maresin-1 (MaR1), may be able to considerably lessen the symptoms of a number of inflammatory illnesses.
Objective: to assess the potential underlying processes and the protective impact of Maresin-1 in DN caused by STZ
Materials and Methods: Thirty adult male albino rats were divided into: control, DN group, and DN+MaR1 group (10/group). levels of urine albumin, renal SOD, creatinine clearance, renal MDA, renal TNF-α, renal IL-6, and renal genes expression of nuclear factor E2-related factor 2 (Nrf2) and heme-oxygenase 1 (HO-1) in addition to serum levels of glucose, glycosylated Hb A1c, urea, and creatinine. Furthermore, renal histopathology and immunohistochemical analyses were performed.
Results Along with urinary albumin, renal MDA, renal TNF-α, and renal IL-6, DN significantly increased serum levels of glucose, glycosylated Hb A1c, urea, and creatinine when compared to the control. Additionally, it dramatically reduced the expression of the renal genes Nrf2 and HO-1, renal SOD, and creatinine clearance levels. In addition, the DN group's NF-kB immunoreaction and Caspase-3 were both upregulated in comparison to the control. The DN+MaR1 group showed a considerable improvement in STZ-induced DN changes.
Conclusion: Through anti-oxidant and anti-inflammatory mechanisms, apoptosis suppression, and the up-regulation of Nrf2 and HO-1 renal gene expressions, MaR1 provides significant protective benefits against STZ-induced DN.
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