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J Adv Pharm Technol Res. 2019 Jul-Sep;10(3):132-137. doi: 10.4103/japtr.JAPTR_386_18.

Effect of Tribulus terrestris in mercuric chloride-induced renal accumulation of mercury and nephrotoxicity in rat.

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Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, India.


Mercury generates free radicals and subsequently increases oxidative stress, which leads to renal injury. Tribulus terrestris (TT) has good anti-inflammatory and antioxidant properties. Hydroalcoholic extract of different dose of TT was evaluated against mercuric chloride-induced nephrotoxicity. Rats (n = 6) were treated with TT at doses of 100, 200, and 300 mg/kg. Drugs were administered orally for 7 days. Single dose of mercuric chloride (5 mg/kg, intraperitoneal) on the 5th day caused significant elevation of blood urea nitrogen, serum creatinine, malondialdehyde, liver fatty acid binding protein, kidney injury molecule-1, and kidney mercury level and fall in glutathione, superoxide dismutase, glutathione peroxidase, and histopathological changes in disease control as compared to normal control group (P < 0.001). Dose of TT 200 and 300 mg/kg significantly (P < 0.001) prevented the renal injury, and mercury accumulation in kidney tissues significantly decreases in higher dose, i.e., 300 mg/kg as compared to control group. Our result indicates that the treatment of TT exerted significant protection against renal damage induced by mercuric chloride possibly due to its antioxidant and anti-inflammatory properties and by decreasing the renal accumulation of mercury.


Antioxidant; Tribulus terrestris; kidney injury molecule-1; liver fatty acid binding protein; mercuric chloride; nephrotoxicity

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