锰对吲哚美辛诱导Wistar大鼠肝肾氧化应激的抑制作用

T. Abiola, O. O. David, Farombi Ebenezer Olatunde
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引用次数: 1

摘要

目的:锰(Mn)是许多细胞过程中必需的微量元素。但关于其对吲哚美辛所致肝肾损害的影响,文献报道较少。因此,本研究旨在探讨锰对吲哚美辛致大鼠肝肾损害的影响。方法:将大鼠分为4组,每组8只,分别为对照组、单用吲哚美辛(IND) (20 mg/kg)、单用Mn (10 mg/kg)和共给药组,连续口服14 d。治疗24小时后,戊巴比妥麻醉下采血,切除肝脏,制备匀浆,进行组织学染色。肝肾功能检测:天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、碱性磷酸酶(ALP)、谷氨酰转移酶(GGT)、乳酸脱氢酶(LDH)、苹果酸脱氢酶(MDH)、谷氨酰胺脱氢酶(GLDH)、山梨醇脱氢酶(SDH)、葡萄糖-磷酸脱氢酶(G6PD)、胆红素(BIL)、尿素、肌酐、胆固醇(CHOL)、原始研究文章Abiola等;生物工程学报,29(9):79- 90,2020;文章no.IJBCRR。评估了621580种甘油三酯(TG)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)、电解质和氧化应激超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽(GSH)和脂质过氧化(LPO)生物标志物。结果:吲哚美辛引起大鼠肝肾损害,表现为血清肝肾功能标志物升高。但IND与Mn合用显著降低了肝肾生物标志物水平(p < 0.05)。此外,IND与Mn的联合使用改善了抗氧化状态,同时降低了LPO,并在组织学上恢复了肝脏和肾脏的完整性。结论:本研究结果强调IND与Mn联合给药可减轻IND诱导的大鼠肝肾毒性和氧化应激。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Manganese Inhibits Indomethacin-Induced Hepatorenal Oxidative Stress in Wistar Rats
Aim: Manganese (Mn) is an essential trace element in many cellular processes. However, there is dearth of literature on its influence on indomethacin-induced hepatorenal damage. Therefore, this study was conducted to investigate the effect of manganese on indomethacin-induced hepatorenal damage in rats. Methods: Rats were divided into four groups of eight rats consisting of control group, indomethacin (IND) alone (20 mg/kg), Mn alone (10 mg/kg) and co-treated group that were treated orally for 14 consecutive days. Twenty four hours after treatment, under pentobarbital anesthesia, blood was collected and liver was excised to prepare homogenate and histology staining. Liver and kidney function tests aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), glutamine dehydrogenase (GLDH), sorbitol dehydrogenase (SDH), glucose6-phosphate dehydrogenase (G6PD), bilirubin (BIL), urea, creatinine, cholesterol (CHOL), Original Research Article Abiola et al.; IJBCRR, 29(9): 79-90, 2020; Article no.IJBCRR.62152 80 triglycerides (TG), low and high density lipoprotein (LDL and HDL), electrolytes and oxidative stress superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and lipid peroxidation (LPO) biomarkers were assessed. Results: The results showed that indomethacin caused hepatorenal damage in rats manifested with increase in serum hepatic and renal function biomarkers. But co-administration of IND with Mn significantly (p < 0.05) decreased the level of hepatorenal biomarkers. Additionally, coadministration of IND with Mn improved the antioxidant status with concomitant reduction of LPO and restored the integrity of the liver and kidney histologically. Conclusion: The results of this study emphasize that co-administration of IND with Mn to rats alleviated IND-induced hepatorenal toxicities and oxidative stress in rats.
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