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石榴籽油对氯化汞诱导的大鼠肝毒性的保护作用

PROTECTIVE EFFECT OF POMEGRANATE SEED OIL AGAINST MERCURIC CHLORIDE-INDUCED HEPATOTOXICITY IN RAT.

作者信息

Boroushaki Mohammad Taher, Hosseini Azar, Dolati Karim, Mollazadeh Hamid, Rajabian Arezoo

出版信息

Acta Pol Pharm. 2016 Jul;73(4):991-997.

PMID:29648725
Abstract

Mercuric chloride (HgCL2) is an environmental and industrial toxicant that affects many tissues. Considering oxidative stress is an important component of mercury induced hepatotoxicity, antioxidants are expected to play a protective role against it. The present study was designed to investigate the probable effects of pomegranate seed oil (PSO) on hepatotoxicity induced by HgCL₂, administration in rats. Rats were divided into five groups. Group 1 and 2 received corn oil (1 mL/kg, i.p.) and PSO (0.8 mL/kg, i.p.), respectively. Group 3 was treated with HgCl, (5 mg/kg, i.p.) for 3 days. In groups 4 and 5 PSO (0.4 and 0.8 mL/kg i.p., respectively) was given 1 h before HgCl2 administration. Twenty four hours after last injection of HgCl2, blood samples and specimens of liver were taken. HgCl2 administration led to significant increase in liver malondialdehyde level, significant reduction in total sulfhydryl content and significant changes in serum alanine aminotransferase (ALT) and aspartate aminotransferase activity (AST), compared to control group. The histopathological changes such as necrosis, inflammatory cell infiltration and hepatocellular vacuolization were observed. PSO administration (0.8 mL/kg i.p.) improved the liver function in HgCL2 intoxicated animals as indicated by the significant decline in increased levels of AST, ALT in serum, MDA level and significant elevation in decreased total sulfhydryl content. Histological studies revealed milder hepatic lesions in PSO treated samples. The results indicated that oxidative stress may be an important mechanism of HgCl₂ induced hepatic injury and dysfunction and PSO may be a useful agent for the prevention of HgCl₂ induced oxidative damage in rat liver.

摘要

氯化汞(HgCL2)是一种影响多种组织的环境和工业毒物。考虑到氧化应激是汞诱导肝毒性的重要组成部分,抗氧化剂有望对其发挥保护作用。本研究旨在探讨石榴籽油(PSO)对大鼠体内HgCL₂诱导的肝毒性的可能影响。将大鼠分为五组。第1组和第2组分别接受玉米油(1 mL/kg,腹腔注射)和PSO(0.8 mL/kg,腹腔注射)。第3组用HgCl₂(5 mg/kg,腹腔注射)处理3天。在第4组和第5组中,在给予HgCl2前1小时分别腹腔注射PSO(0.4和0.8 mL/kg)。在最后一次注射HgCl2后24小时,采集血样和肝脏标本。与对照组相比,给予HgCl2导致肝脏丙二醛水平显著升高,总巯基含量显著降低,血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶活性(AST)发生显著变化。观察到坏死、炎性细胞浸润和肝细胞空泡化等组织病理学变化。PSO给药(0.8 mL/kg,腹腔注射)改善了HgCL2中毒动物的肝功能,表现为血清中AST、ALT水平升高以及MDA水平显著下降,总巯基含量降低显著升高。组织学研究显示PSO处理的样本中肝脏病变较轻。结果表明,氧化应激可能是HgCl₂诱导肝损伤和功能障碍的重要机制,PSO可能是预防大鼠肝脏中HgCl₂诱导的氧化损伤的有用药物。

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