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6(5H)-菲啶酮对化学诱导的肝小叶中央坏死的肝保护作用。

Hepatoprotective effects of 6(5H)-phenanthridinone from chemical-induced centrilobular necrosis.

作者信息

Banasik Marek, Stedeford Todd, Ueda Kunihiro, Muro-Cacho Carlos, Su Phi-Huynh, Tanaka Seigo, Harbison Raymond D

机构信息

Center for Environmental and Occupational Risk Analysis and Management, Department of Environmental and Occupational Health, College of Public Health, University of South Florida, Tampa, Florida 33612, USA.

出版信息

Res Commun Mol Pathol Pharmacol. 2004;115-116:15-20.

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme involved in the detection of DNA strand termini. Extensive cellular damage can overactivate PARP-1, which rapidly depletes the cellular stores of NAD+ and ATP, resulting in necrotic cell death. The purpose of the present study was to determine whether 6(5H)-phenanthridinone, a potent inhibitor of PARP-1, could attenuate the hepatotoxicity of carbon tetrachloride (CCl4). Male ICR mice treated via the intraperitoneal route with CCl4 exhibited severe necrotic centrilobular lesions and significantly elevated serum transaminases. In contrast, the histopathology and serum biochemistry of animals treated concomitantly with CCl4 and 6(5H)-phenanthridinone were not significantly different versus controls. In conclusion, the results of this study demonstrate that the hepatotoxicity of CCl4 can be blocked independently of its metabolism and suggest the predominant role of PARP-1 overactivation in chemical-induced toxicity.

摘要

聚(ADP - 核糖)聚合酶 -1(PARP -1)是一种参与检测DNA链末端的核酶。广泛的细胞损伤会过度激活PARP -1,从而迅速耗尽细胞内的NAD +和ATP储备,导致坏死性细胞死亡。本研究的目的是确定PARP -1的强效抑制剂6(5H)-菲啶酮是否能减轻四氯化碳(CCl4)的肝毒性。经腹腔注射CCl4处理的雄性ICR小鼠表现出严重的坏死性小叶中心病变,血清转氨酶显著升高。相比之下,同时用CCl4和6(5H)-菲啶酮处理的动物的组织病理学和血清生化指标与对照组相比无显著差异。总之,本研究结果表明,CCl4的肝毒性可以独立于其代谢而被阻断,并提示PARP -1过度激活在化学诱导毒性中起主要作用。

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