Behvandi Mohammad Mehdi, Sabbagh Susan, Rostami Reza, Moradipour Ayat, Karami Marzieh, Jafarian Ashkan, Jafarian Marjan, Jafaripour Leila, Norouzirad Reza
School of Allied Medical Sciences, Dezful University of Medical Sciences, Dezful, Iran.
Department of Anatomy, Faculty of Medicine, Dezful University of Medical Sciences, Dezful, Iran.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Jun 28. doi: 10.1007/s00210-025-04382-7.
Gentamicin (GEN) causes liver and kidney toxicity by generating free radicals and inflammation. This study tested gallic acid (GA) as an antioxidant to reduce this oxidative stress. Thirty-five male rats were divided into five groups: sham, GEN, and three GEN + GA groups with doses of 60, 90, and 120 mg/kg. After 10 days, the rats were euthanized, and their serum, kidneys, and livers were analyzed. Results showed that GEN significantly increased serum BUN, creatinine, AST, ALT, and ALP (p < 0.05). It also raised malondialdehyde (MDA) levels and the expression of TNF-α and caspase-3 genes, with notable histopathological injuries in the kidneys and liver (p < 0.05). GA demonstrated potential protective effects against GEN-induced damage. GEN reduced antioxidant enzyme activities (GPX, CAT, and GSH) in the organs (p < 0.05). Conversely, GA at all doses lowered BUN, creatinine, ALT, AST, ALP, and MDA levels and decreased TNF-α and caspase-3 gene expression in the liver and kidneys (p < 0.05). It also protected against tissue injuries and boosted antioxidant enzyme levels in both organs (p < 0.05). The study shows that gallic acid (60, 90, 120 mg/kg) significantly mitigates gentamicin-induced hepatorenal toxicity by reducing oxidative stress, inflammation, and apoptosis. Notably, doses of 90 and 120 mg/kg were especially more effective in minimizing tissue damage and improving antioxidant activity.
庆大霉素（GEN）通过产生自由基和引发炎症导致肝脏和肾脏毒性。本研究测试了没食子酸（GA）作为一种抗氧化剂来减轻这种氧化应激。35只雄性大鼠被分为五组：假手术组、GEN组以及三个GEN + GA组，GA剂量分别为60、90和120 mg/kg。10天后，将大鼠安乐死，并对其血清、肾脏和肝脏进行分析。结果显示，GEN显著增加了血清尿素氮、肌酐、天冬氨酸转氨酶、丙氨酸转氨酶和碱性磷酸酶（p < 0.05）。它还提高了丙二醛（MDA）水平以及肿瘤坏死因子-α（TNF-α）和半胱天冬酶-3（caspase-3）基因的表达，同时在肾脏和肝脏出现明显的组织病理学损伤（p < 0.05）。GA对GEN诱导的损伤表现出潜在的保护作用。GEN降低了器官中的抗氧化酶活性（谷胱甘肽过氧化物酶、过氧化氢酶和谷胱甘肽）（p < 0.05）。相反，所有剂量的GA均降低了血清尿素氮、肌酐、丙氨酸转氨酶、天冬氨酸转氨酶、碱性磷酸酶和MDA水平，并降低了肝脏和肾脏中TNF-α和caspase-3基因的表达（p < 0.05）。它还预防了组织损伤并提高了两个器官中的抗氧化酶水平（p < 0.05）。该研究表明，没食子酸（60、90、120 mg/kg）通过减轻氧化应激、炎症和细胞凋亡，显著减轻庆大霉素诱导的肝肾毒性。值得注意的是，90和120 mg/kg的剂量在最小化组织损伤和提高抗氧化活性方面尤其更有效。
