摘要
目的:观察硫化氢对于扑热息痛引起肝损伤的保护作用及相关机制。方法:将正常雄性C57小鼠20只随机分为正常组、扑热息痛组、硫化氢预处理组以及单纯硫化氢处理组。在分别给予相应的处理后,于扑热息痛处理后8 h处死小鼠并检测各组小鼠血生化指标,观察各组小鼠肝脏组织病理学变化以及相关关键蛋白的变化。结果:扑热息痛引能够引起小鼠血清ALT、AST明显升高,光镜下小鼠肝脏呈现大面积坏死。而在硫化氢预处理后,相较于模型组前者小鼠ALT、AST的表达明显下降、肝脏损伤显著减轻。于此同时,扑热息痛损伤后,小鼠肝内凋亡相关蛋白Cleaved-Caspase3、Bax明显上调,Bcl-2的表达下降,MAPK/JNK信号通路被激活。而在H_2S预处理以后,小鼠肝内Cleaved-Caspase3、Bax的表达下降、Bcl-2的表达升高。同时,MAPK/JNK信号通路的活化受到抑制。结论:H_2S可以通过抑制MAPK/JNK信号途径从而减少肝细胞的损伤。
Objective:To explore the effect of H2S on liver injury caused by acetaminophen(APAP).Methods:Male C57BL/6J mice(n=20)were divided randomly into control group,APAP group,APAP+H2S group and H2S group.Eight hours they were treated with APAP,serum biochemical levels,the changes of morphological structure and the expression of related proteins were tested in all the groups.Results:After APAP treated,the level of ALT,AST were increased and massive necrosis could be observed under the pathologic microscope.Compared with APAP group,mice had lower ALT and AST,shown less tissue necrosis after H2S treatment.Meanwhile,APAP increased the expression of apoptotic proteins Cleaved-Caspase3 and Bax,inhibited the expression of Bcl-2 and activated MAPK/JNK signaling pathway.After H2S treatment,the expression of Cleaved-Caspase3 and Bax were reduced,Bcl-2 was increased and MAPK/JNK signaling pathway was supreessed.Conclusion:H2S can attenuate the APAP induced liver damage by inhibiting MAPK/JNK signaling pathway.
作者
黄海进
施洋
仲艳阳
陈大六
焦峰
HUANG Hai-jin;SHI Yang;ZHONG Yan-yang;CHEN Da-liu;JIAO Feng(Department of General Surgery,Hongze District People's Hospital,Huai an 223001,China;Department of General Surgery,The 82nd Hospital of the People's Liberation Army of China,Huai an 223001,China)
出处
《东南大学学报（医学版）》
CAS
2018年第1期1-5,共5页
Journal of Southeast University(Medical Science Edition)
基金
国家自然科学基金(81600689)
