6(5H)-phenanthridinone对化学诱导小叶中心坏死的肝保护作用。

Marek Banasik, Todd Stedeford, Kunihiro Ueda, Carlos Muro-Cacho, Phi-Huynh Su, Seigo Tanaka, Raymond D Harbison
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引用次数: 0

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。广泛的细胞损伤可过度激活PARP-1,迅速耗尽细胞内储存的NAD+和ATP,导致坏死细胞死亡。本研究的目的是确定PARP-1的有效抑制剂6(5H)-phenanthridinone是否可以减轻四氯化碳(CCl4)的肝毒性。经腹腔注射CCl4的雄性ICR小鼠表现出严重的小叶中心坏死病变和血清转氨酶显著升高。与对照组相比,CCl4和6(5H)-菲蒽醌联合治疗的动物的组织病理学和血清生化无显著差异。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的毒性中起主导作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hepatoprotective effects of 6(5H)-phenanthridinone from chemical-induced centrilobular necrosis.

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.

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