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目的:观察黄芩素对4种肝毒性物质诱导的人正常肝细胞株L-02细胞损伤的拮抗作用。方法:培养的L-02细胞分别给予10 mmol.L-1对乙酰氨基酚(AP),50μmol.L-1山岗橐吾碱(clivorine,CLI),2μmol.L-1川楝素(toosendanin,TSN)和100 mmol.L-1乙醇(EtOH)诱导肝细胞毒性。黄芩素1,10,25,50,100μmol.L-1分别与细胞预孵15 min后,加入肝毒性物质,48 h后MTT法检测细胞存活率。结果:与对照组相比,4种肝毒性物质均能显著降低肝细胞存活率(P<0.001)。经不同浓度黄芩素处理后,各浓度黄芩素均能显著提高AP,TSN,EtOH肝细胞损伤模型组的细胞存活率(P<0.01,P<0.001);10,25,50,100μmol.L-1黄芩素能显著提高CLI肝细胞损伤模型组的细胞存活率(P<0.05,P<0.001)。结论:黄芩素具有拮抗对乙酰氨基酚、山岗橐吾碱、川楝素和乙醇这些肝毒性物质诱导的肝细胞毒性的作用,且具有一定的浓度依赖性。
Objective: To observe the antagonistic effect of baicalein on four kinds of hepatotoxicity induced human normal liver cell line L-02 cell injury. Methods: The cultured L-02 cells were treated with 10 mmol·L -1 paracetamol (AP), 50 μmol·L -1 clivorine (CLI), 2 μmol·L -1 toosendanin , TSN) and 100 mmol. L-1 ethanol (EtOH) induced hepatotoxicity. Baicalin 1, 10, 25, 50 and 100μmol.L-1 were incubated with cells for 15 min, then hepatotoxic substances were added. After 48 h, the cell viability was detected by MTT assay. Results: Compared with the control group, all four hepatotoxic agents significantly reduced the survival rate of hepatocytes (P <0.001). After treatment with baicalein at different concentrations, baicalein at various concentrations significantly increased the cell viability (P <0.01, P <0.001) in the model group of AP, TSN and EtOH hepatocytes injury, while the levels of 10,25,50,100μmol.L-1 Baicalein could significantly increase the cell viability of the model group (P <0.05, P <0.001). CONCLUSION: Baicalein can antagonize the hepatotoxicity induced by hepatic toxicants such as acetaminophen, barnyardin, toosendanin and ethanol, and has certain concentration dependence.