Department of Pharmacology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Pharmacology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Drug Chem Toxicol. 2021 Jul;44(4):341-352. doi: 10.1080/01480545.2019.1591434. Epub 2019 Mar 25.
Chronic exposure to toxic inorganic arsenic results in the adverse health effects including skin lesions, cardiovascular diseases, diabetes, neurological disorders, and liver and kidney diseases. Gallic acid (GA) is an important phenolic compound, which could protect different tissues from oxidative stress induced damage. The present study investigated effects of GA against sodium arsenite (SA)-induced renal and hepatic toxicity. Thirty-five rats were randomly divided in to five groups; group 1 was treated with normal saline (2 ml/kg/day, p.o.; for 21 days); group 2 was exposed to SA (10 mg/kg/day, p.o.; for 14 days); groups 3 and 4 were treated with GA (10 and 30 mg/kg/day, respectively; for 7 days) prior to exposure to SA, and treatment was continued up to 21 days in parallel with SA administration; group 5 was treated with GA (30 mg/kg/day, p.o.; for 21 days). The level of MDA, IL-1β, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were evaluated in kidney and liver tissues. Histopathological parameters and serum levels of ALT, AST, ALP, Cr and BUN were also assessed. Treatment with GA remarkably improved SA-induced alteration of hematological and histopathological parameters; these protective effects were associated with the reduction of SA-induced elevation of MDA, IL-1β and NO levels as well as reduction of GSH level and GPx, SOD and CAT activity. Our results suggest that GA may inhibit SA-induced kidney and liver toxicity through scavenging reactive free radicals and increasing intracellular antioxidant capacity.
慢性暴露于有毒无机砷会导致皮肤损伤、心血管疾病、糖尿病、神经紊乱以及肝肾疾病等不良健康影响。没食子酸（GA）是一种重要的酚类化合物，可保护不同组织免受氧化应激引起的损伤。本研究探讨了 GA 对亚砷酸钠（SA）诱导的肾和肝毒性的作用。将 35 只大鼠随机分为五组；第 1 组给予生理盐水（2ml/kg/天，口服；21 天）；第 2 组给予 SA（10mg/kg/天，口服；14 天）；第 3 组和第 4 组在暴露于 SA 之前分别用 GA（10 和 30mg/kg/天）处理，并与 SA 给药同时持续 21 天；第 5 组给予 GA（30mg/kg/天，口服；21 天）。评估了肾和肝组织中 MDA、IL-1β、NO 和谷胱甘肽（GSH）的水平以及谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性。还评估了组织病理学参数以及血清 ALT、AST、ALP、Cr 和 BUN 水平。GA 处理显著改善了 SA 诱导的血液学和组织病理学参数的改变；这些保护作用与降低 SA 诱导的 MDA、IL-1β和 NO 水平以及降低 GSH 水平和 GPx、SOD 和 CAT 活性有关。我们的结果表明，GA 可能通过清除活性自由基和增加细胞内抗氧化能力来抑制 SA 诱导的肾和肝毒性。
