目的 研究萱草花总黄酮(HCTF)对氧化应激引起的肝细胞损伤的改善作用,并探讨其作用机制.方法 采用CCl₄诱导小鼠肝氧化损伤和H₂O₂诱导体外肝细胞损伤2种模型,HCTF给药后检测肝组织抗氧化指标,HE染色观察肝组织形态学改变,应用MTT法测定肝细胞存活率,ELISA法检测肝细胞中丙氨酸转氨酶(ALT)、乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST)活性,实时荧光定量PCR(RT-PCR)和Western blotting法检测LXRα、FAS mRNA及蛋白的表达.结果 HCTF可以明显降低CCl₄肝损伤小鼠肝组织内MDA水平,提高肝组织GSH-Px和SOD活性,保护肝组织;HCTF可以明显提高H₂O₂损伤的HL-7702细胞存活率(P<0.01):使HL-7702细胞中MDA水平降低(P<0.05、0.01),GSH-Px和SOD活性升高(P<0.01),ALT、LDH、AST活性降低(P<0.05、0.01),LXRα和FAS mRNA及蛋白的表达水平下降(P<0.05、0.01).结论 HCTF可能通过提高机体抗氧化能力而起到对CCl₄肝损伤小鼠的保护作用;同时可能通过降低氧化反应、减少LXRa和FAS的转录及蛋白表达,从而抑制H₂O₂对HL-7702细胞的损伤.

Objective To study the protective effects of Hemerocallis citrina total flavonoids (HCTF) on oxidative damage of liver cells HL-7702, and explore its possible mechanism. Methods The liver cell damage model was induced by H₂O₂, and the proliferation of liver cells was examined by MTT assay, and the changes of ALT, LDH, and AST were dectected by ELISA assay, the levels of LXRα and FAS were determined by RT-PCR and Western blotting assay. Results HCTF (5 and 10 μg/mL) could significantly improve the proliferation of liver cells (P < 0.01), the content of NO increased and the content of MDA decreased (P < 0.01 or 0.05), the activity of SOD increased (P < 0.05), the levels of mRNA, and protein of LXRα and FAS decreased (P <0.01 or 0.05). Conclusion HCTF could inhibit the transcription and protein expression of LXRα and FAS through anti-oxidation, and repair the damage of HL-7702 liver cells caused by H₂O₂.

吉林省教育厅基金资助课题(2013359)