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目的研究玉郎伞多糖(YLSPS)对抗结核药诱导的肝细胞损伤的保护作用。方法将不同浓度的利福平、异烟肼及吡嗪酰胺合用(RFP+INH+PZA)作用于人张氏肝细胞,用MTT法检测肝细胞的存活率,以80%~85%存活率的药物浓度为最佳浓度建立肝细胞损伤模型;给予YLSPS处理后,检测细胞培养上清液中丙氨酸氨基转移酶(ALT)、天门冬氨酸转移酶(AST)和乳酸脱氢酶(LDH)和细胞内丙二醛(MDA)和超氧化物歧化酶(SOD)的浓度。结果与模型组比较,YLSPS各剂量可明显降低肝细胞培养上清液中的AST、ALT、LDH水平及肝细胞中MDA的含量,升高SOD的水平,且呈剂量依赖性。结论YLSPS对RFP+INH+PZA合用诱导张氏肝细胞损伤具有保护作用,其机制可能与抗氧化和清除自由基的作用有关。
Objective To study the protective effect of YLSPS against tuberculosis-induced hepatocyte injury. Methods Different concentrations of rifampicin, isoniazid and pyrazinamide (RFP + INH + PZA) were applied to human hepatocytes. The viability of hepatocytes was detected by MTT assay. The survival rate of hepatocytes was 80% ~ 85% (P <0.05), the model of hepatocyte injury was established at the optimal concentration of the drug. After treatment with YLSPS, the alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase LDH) and intracellular concentrations of malondialdehyde (MDA) and superoxide dismutase (SOD). Results Compared with the model group, each dose of YLSPS could significantly reduce the levels of AST, ALT, LDH and the content of MDA in hepatocytes, and increase the level of SOD in a dose-dependent manner. Conclusion YLSPS can protect HepG2 cells from injury induced by RFP + INH + PZA, and its mechanism may be related to the effects of antioxidation and free radical scavenging.