Protective Effect of Platycodin D on Acetaminophen Induced L02 Cell Injury and Its Molecular Mechanism
张若冰 1王士杰 2沈琼 1李伟 2王梓1
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作者信息
1. 吉林农业大学中药材学院,长春 130118
2. 吉林农业科技学院中药学院,吉林 132101
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摘要
为研究桔梗皂苷(Platycodin D,PD)拮抗对乙酰氨基酚(Acetaminophen,APAP)致L02人源肝细胞损伤的保护作用与分子机制.建立L02肝细胞损伤的体外模型,筛选PD最佳给药剂量及时间,试剂盒测定细胞中谷胱甘肽(GSH)的含量,利用免疫荧光和 Western Blot技术检测 CYP2E1,iNOS,Nrf2,HO-1,Bax,Bcl-2,Caspase 3等蛋白的表达水平.PD在0.25,0.5,1 μmol/L剂量时改善APAP引起的细胞活力,增加CYP2E1和iNOS的荧光强度(P＜0.05或P＜0.01),抑制过量GSH消耗,上调Nrf2依赖性抗氧化酶,Bcl-2及下调Bax、Caspase 3的表达(P＜0.05或P＜0.01).PD可能部分通过调控Nrf2/HO-1信号通路发挥拮抗APAP致L02细胞损伤作用.
Abstract
To investigate the protective effect and molecular mechanism of platycodin D(PD)against acetaminophen(APAP)-induced injury of L02 human hepatocytes.We established the hepatocyte injury model of L02 in vitro,screened the optimal dose and time of PD administration,determined the content of glutathione(GSH)in the cell with a kit,and detected the expression levels of CYP2E1,iNOS,Nrf2,HO-1,Bax,Bcl-2 and Caspase-3 by immunofluorescence and Western blot.PD amelio-rated APAP induced cell viability in the dose range of 0.25,0.5 and 1 µmol/L,increased the fluores-cence intensity of CYP2E1 and iNOS(P＜0.05 or P＜0.01),inhibited excessive GSH consumption,upregulated Nrf2 dependent antioxidant enzyme,Bcl-2 and down-regulated the expression of Bax and Caspase 3(P＜0.05 or P＜0.01).PD may antagonize the damage of L02 cells induced by APAP partly by regulating Nrf2/HO-1 signaling pathway.
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