Effect of tumor necrosis factor alpha inhibition with etanercept on renal functions in L-NAME induced hypertensive rats: insights into the possible mechanisms | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 3, Volume 42, Issue 2, April 2022, Page 163-179 PDF (779.43 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2021.93323.1111 | ||||
View on SCiNiTO | ||||
Authors | ||||
Mona AbdelAzim Said 1; Reham Mohammed Ibrahim2; Mona Maher Allam2 | ||||
1Physiology department, faculty of Medicine, Benha University, Egypt. | ||||
2Physiology department, Faculty of Medicine, Benha University, Egypt | ||||
Abstract | ||||
Many studies suggest the dominant role of the inflammatory cytokine, tumor necrosis factor alpha (TNF-α) in the prognosis of hypertension and end stage renal disease (ESRD). The objective of this study was to investigate the effects of TNF-α inhibition on renal functions in Nω-nitro-L-arginine methyl ester (L-NAME) induced hypertensive rats and the potential underlying mechanisms. Four groups of rats were used in the study for 3 weeks period; normal control group, TNF- α inhibitor (etanercept) group, L-NAME-induced hypertensive group and L-NAME + etanercept group. L-NAME group showed elevated systolic and diastolic blood pressure, plasma urea, creatinine, plasma renin activity, angiotensin II, kidney tissue nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, TNF- α and malondialdehyde (MDA) together with decreased creatinine clearance rate and renal antioxidants. Treatment with etanercept affords antihypertensive effect and ameliorates L-NAME induced renal impairment by improving renin–angiotensin system (RAS) and NADPH oxidase as well as by attenuating oxidative stress. | ||||
Keywords | ||||
TNF-α; Etanercept; Hypertension; Renin – angiotensin system; Oxidative stress | ||||
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