4.6 Article

Naringenin ameliorates streptozotocin-induced diabetic rat renal impairment by downregulation of TGF-1 and IL-1 via modulation of oxidative stress correlates with decreased apoptotic events

Journal

PHARMACEUTICAL BIOLOGY
Volume 54, Issue 9, Pages 1616-1627

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.3109/13880209.2015.1110599

Keywords

Catalase; diabetes; histopathology; immunohistochemistry; terminal dUTP nick end-labeling; reduce glutathione; malondialdehyde

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Context: Naringenin, a flavonone and a nutritive antioxidant which is mostly obtained from grapefruit, orange or tomato skin, has been extensively studied due to its radical scavenging activity.Objective: The present study investigates the protective effect of naringenin on rat kidney after streptozotocin-induced diabetes.Materials and methods: Sixty male Wistar rats were divided into six groups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (50mg/kg) in groups II, III and IV. Naringenin 5mg/kg body weight was given to groups III and V, but 10mg/kg was given to groups IV and VI, orally once a day for 10 weeks. After which all animals were sacrificed, and the biochemical, histopathological, immunohistochemical and apoptotic assays were conducted.Results: Naringenin treatment with 5 and 10mg/kg significantly decreased (p<0.05) the serum biochemical parameters, elevated tissue malondialdehyde levels and increased (p<0.01) the reduced superoxide dismutase, catalase and reduced glutathione enzyme activities in the diabetic kidney. Diabetes-induced naringenin-treated groups showed an improved histology and revealed a significant reduction in apoptosis activity (7.20.01 and 1.8 +/- 0.05) and in expression of TGF-1 (18.9 +/- 3.4 and 10.2 +/- 2.1) at a dose of 5 and 10mg/kg, respectively. Similarly, in contrast to the diabetic group, a significant difference was observed in the IL-1 expression (15.68 +/- 4.3) in 5mg/kg and (9.85 +/- 2.1) in 10mg/kg naringenin-treated groups.Conclusion: Naringenin acts as a protective agent in diabetic renal impairment by altering oxidative stress, modulation of cytokines expression and apoptotic events.

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