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ROS激活P53调控线粒体凋亡途径在α-鹅膏毒肽中毒肝损害中作用的研究进展
作者:赖福平1  胡杰2  陆元兰1  杨登会1  詹江珊1  吴瑾1  王庭刚1  谢智慧3 
单位:1. 遵义医科大学附属医院 急诊科, 贵州 遵义 563003;
2. 遵义医科大学附属医院 重症医学科, 贵州 遵义 563003;
3. 遵义医科大学附属医院 高压氧科, 贵州 遵义 563003
关键词:α-鹅膏毒肽 P53 活性氧 线粒体凋亡途径 肝损害 综述 
分类号:R575.3;R155.32
出版年·卷·期(页码):2022·41·第五期(734-739)
摘要:

α-鹅膏毒肽(α-AMA)是含鹅膏毒肽类毒蘑菇最常见的毒素种类,现已成为我国食物中毒最主要致死因素,但α-AMA中毒肝损害的具体机制尚未清楚,且无特异性解毒剂,因此成为人们关注的焦点。α-AMA中毒导致氧化还原平衡失调产生过多活性氧(ROS)是肝损害重要因素之一,ROS作为凋亡上游信号分子激活P53表达,向线粒体内易位促进细胞色素C释放,抑制B细胞淋巴瘤-2(Bcl-2)家族基因和促进Bcl-2相关X蛋白(Bax)基因表达,进而使含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)级联反应触发线粒体凋亡途径,最终导致肝细胞异常凋亡造成肝脏严重损害。作者就ROS激活P53调控线粒体凋亡途径与α-AMA中毒肝损害之间的关系作一综述,进一步阐述α-AMA中毒肝损害的机制,展望α-AMA中毒肝损害治疗新方向。

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