Naringin ameliorates sodium arsenite-induced renal and hepatic toxicity in rats: decisive role of KIM-1, Caspase-3, TGF-β, and TNF-α

Abstract

Chronic exposure of a naturally occurring metal arsenic leads to renal and hepatic diseases. Naringin, a flavanone glycoside, possesses anti-inflammatory and anti-oxidant potential. The aim of this investigation was to evaluate the protective effect of naringin against arsenic-induced renal and hepatic toxicity in rats. Renal and hepatic toxicity was induced in rats by sodium arsenite (5 mg/kg, p.o.). Rats were treated orally with either vehicle or naringin (20, 40, and 80 mg/kg) or Coenzyme Q10 (10 mg/kg) for 28 days. Various biochemical, histological, and molecular biomarkers were assessed in kidney and liver. Treatment with naringin (40 and 80 mg/kg) significantly and dose-dependently restored (p < 0.01 and p < 0.001) altered levels of kidney (serum creatinine, urine creatinine, BUN, uric acid, and creatinine clearance) and liver function test (AST and ALT) induced by sodium arsenite. Elevated levels of oxido-nitrosative stress in renal and hepatic tissue was significantly and dose-dependently decreased (p < 0.01 and p < 0.001) by naringin (40 and 80 mg/kg) treatment. It significantly and dose-dependently down-regulated (p < 0.01 and p < 0.001) renal KIM-1, Caspase-3, TGF-β, and TNF-α mRNA expression. Histopathological alteration induced in kidney and liver by sodium arsenite was reduced by naringin (40 and 80 mg/kg) treatment. In conclusion, naringin treatment ameliorates arsenic-induced renal and hepatic damage in rats due its antioxidant and anti-inflammatory properties via down-regulation of elevated oxido-nitrosative stress, KIM-1, Caspase-3, TGF-β, and TNF-α levels.

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“…Furthermore, nitric oxide (NO) is an unconventional intracellular messenger in the nervous system and its elevated level associated with sensitized spinal as well as central neurons (Lin et al, 1999[58]). NO reacts with ROS and acts as an oxidant (Adil et al, 2015[4]; Badole et al, 2015[9]; Kamble et al, 2013[36]). Reaction with deficient superoxide dismutase leads to the production of notorious peroxynitrite, which affects any cell molecule (Honmore et al, 2015[29], 2016[30]).…”

Flax lignan concentrate reverses alterations in blood pressure, left ventricular functions, lipid profile and antioxidant status in DOCA-salt induced renal hypertension in rats

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Naringin, a natural dietary compound, prevents intestinal tumorigenesis in Apc Min/+ mouse model

“…It mitigates cardiac hypertrophy by reducing oxidative stress and inactivating c-Jun nuclear kinase (JNK-1) protein in type I diabetes (Adeniyi et al 2015). Naringin ameliorates sodium arsenite-induced renal and hepatic toxicity in rats by modulating the activities of KIM-1, caspase-3, TGF-β and TNF-α (Adil et al 2015). Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model (Qi et al 2015).…”