新疆医科大学学报

目的研究睡莲酚对H_2O₂致正常肝(LO2)细胞损伤的保护作用。方法将LO2细胞分为药物组(给予6.25、12.50、25.00、50.00、100.00μg/mL的睡莲酚)、空白组(给予完全培养液),置于37℃、5%CO₂环境下分别培养24、48和72 h后,采用MTT法检测样品对LO2细胞的毒性。0.6 mmol/L H_2O₂处理LO2细胞4 h构建H_2O₂损伤LO2细胞模型。用含6.25、12.50、25.00μg/mL的睡莲酚的培养液干预损伤肝细胞,MTT法测定细胞活力,并检测天冬氨酸氨基转移酶(AST)、谷氨酸氨基转移酶(ALT)、丙二醛(MDA)、氧化物歧化酶(SOD)和一氧化氮(NO)的水平。结果睡莲酚在6.50～25.00μg/mL的浓度范围内给药24、48和72 h,对正常人体肝(LO2)细胞无毒性作用。与空白组比较,给药组细胞的存活率达到90%以上,差异无统计学意义(P<0.01)。与对照组比较,给药组该范围内可抑制H_2O₂对LO2细胞的损伤,升高细胞活力,差异有统计学意义(P<0.05); H_2O₂致急性损伤肝细胞的ALT、AST、MDA和NO水平均降低, SOD活力升高,差异有统计学意义(P<0.05)。结论睡莲酚对氧化应激致肝细胞损伤有保护作用。

Objective To study the protective effect of isostrictiniin on LO2 cells damage. Methods The LO2 cells were divided into a series of drug groups(6.25, 12.50, 25.00, 50.00, 100.00 μg/mL isostrictiniin) and a normal group(administered with Culture medium), they were Incubate at 37℃ and 5% CO₂ for 24, 48 and 72 h, and the cytotoxicity of isostrictiniin was evaluated by MTT. Hepatocyte damage model was established by 0.6 mmol/L H_2O₂ treatment. After the oxidative stress hepatocyte was co-incubated with isostrictiniin at 6.25, 12.50, 25.00 μg/mL for 4 hours, the protective effect of isostrictiniin on H_2O₂-induced hepatocyte damage was assessed by MTT method. The contents of ALT, AST, MDA, SOD and NO in cell suspernatant were determined. Results Isostrictiniin has no cytotoxic effect on LO2 cells after administration for 24, 48 and 72 h in a concentration range of 6.50 to 25.00 μg/mL, and the cell survival rate was more than 90%, compared with the normal group, where the difference was statistically significant(P<0.01). Compared with the control group, injured by 0.6 mmol/L H_2O₂ treatment for 4 h were used as the hepatocyte damage model. Compared with the normal group. The concentration range of isostrictiniin was 6.25-25.00 μg/mL, isostrictiniin could inhibit H_2O₂-induced injury in LO2 cells and obviously reduced ALT, AST, MDA, and NO levels, improved SOD activity and the difference was statistically significant(P<0.05). Conclusion Isostrictiniin exhibits better protective effects on hepatocyte damage in vitro.