Document Type : Review Article
Authors
1
Medical Physiology Department, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2
Medical Physiology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
3
Medical Biochemistry and Molecular Biology Department, Faculty of medicine, Helwan University, Egypt.
4
Anatomy and Embryology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
5
Clinical Pharmacology Department, Faculty of medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
6
Human Anatomy and Embryology Department, Faculty of Medicine, Ain Shams University, Ain Shams, Cairo, Egypt. Anatomy Department, IbnSina National College for Medical Studies, Jeddah
7
Internal Medicine department Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
8
Pathology department Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
9
Zoology Department - Faculty of Science, Menoufia University, Menoufia, Egypt.
10
Medical Physiology Department, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt.
Abstract
Background: Essential hypertension causes the kidney illness known as hypertensive nephropathy, which frequently results in both structural and functional renal impairment. 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 demonstrate the underlying mechanisms and renoprotective impact of MaR1 in rats with deoxycorticosterone acetate-salt-induced hypertension.
Material & Methods: Thirty Wister albino male rats divided into control, DOCA, DOCA+MaR1 groups. After 8 weeks rats were subjected to ABP, renal blood flow velocity (RBFV) and renal artery resistance (RAR) measurement and serum levels of urea, creatinine in addition to creatinine clearance, urinary albumin, renal MDA, SOD, TNF-α, IL-6, renal genes expression of TLR4 and NF κB were assessed. Renal tissue was evaluated histopathologically and immunohistochemically.
Results: The DOCA group's measured SBP, DBP, MABP, RAR, serum levels of urea, creatinine, renal MDA, renal TNF-α, renal IL-6, and renal genes TLR4 and NF-kB were all dramatically elevated than those of the control group, but their RBFV, renal SOD, and creatinine clearance values were significantly lower. MaR1 significantly enhanced the alterations brought about by DOCA.
Conclusion: MaR1 alleviated DOCA induced hypertensive nephropathy by anti-oxidant, anti-inflammatory, anti-apoptotic mechanisms and by down-regulation of TLR4 and NF κB renal genes expression.
Key words: Caspase-3, DOCA, Hypertension, Maresin-1, NF κB, TLR4
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