研究卷丹百合醇提物矢车菊素对CCl4诱导的小鼠急性肝损伤的保护作用及相关机制。将50只昆明小鼠随机分为空白对照组（S），CCl4组（M），CCl4+卷丹百合矢车菊素低（25 mg/kg，LLC）、中（50 mg/kg，MLC）、高（100 mg/kg，HLC）剂量组。给药组每日灌胃给予相应剂量药物，连续给药7 d，末次给药2 h后，腹腔注射0.3 mL 1% CCl4花生油溶液造模。24 h后处死小鼠，测定血清ALT、AST、ALP水平，肝脏称重后行HE染色，且匀浆测定SOD、CAT、MDA，Westren-blot检测肝脏组织中Ｎrf2、HO-1和NQO1蛋白的表达。实验结果发现，与M组比较，高剂量卷丹百合花矢车菊素能显著使血清中ALT、AST、ALP水平分别降低至（15.67±5.38）U/L，（35.58±8.68）U/L和（31.38±8.57）U/L，肝组织SOD、CAT酶活力增加至（36.67±5.47 U/mg pro）和（21.58±4.62 U/mg pro），MDA生成减少到（4.67±1.42 nmol/mg pro） （p<0.05）；同时使肝脏组织中Ｎrf2、HO-1和NQO1蛋白表达明显上调（p<0.05）。可见，卷丹百合醇提物矢车菊素具有一定保护肝损伤的作用，其机制可能是通过Nrf2/OH-1/NQO1信号通路介导了氧化应激反应，清除自由基、减轻脂质过氧化、保护肝细胞膜结构和功能起效。

The protective effects of Lilium lancifolium cyanidin on the acute liver injury in mice caused by CCl4 were investigated. Fifty mice were randomly divided into blank control group (S), CCl4 group (M), CCl4 + Lilium lancifolium cyanidin low (25 mg/kg, LLC), medium (50 mg/kg, MLC), high (100 mg/kg, HLC) dose groups. Drug groups were given different dose drugs for days. After 2 h in last day, model was developed with the intraperitoneal injection of 0.3 mL 1% CCl4 peanut oil solution. Then, all mice were executed after 24 h, and the serum was collected for the determination of ALT, AST and ALP levels. Liver was weighed and triturated for detecting SOD, CAT and MDA. HE staining was also examined. Western blot was employed to examine the expression of Ｎrf2、HO-1 and NQO1 protein in the liver tissue. Compared with M group, our experimental results showed that Lilium lancifolium cyanidin could significantly reduce the levels of ALT, AST and ALP in serum, increase SOD and CAT enzyme activity of liver tissue and reduce MDA content (p<0.05). At the same time, the Nrf2、HO-1 and NQO1 protein expression of the liver tissue also significantly raised (p<0.05). The results suggest that, Lilium lancifolium cyanidin exhibited a protection against liver damage, and the underlying mechanism may be associated with its mediation of the oxidative stress reaction, antioxidant activities (e.g., scavenging free radical activity, and inhibiting lipid peroxidation activity), and the protection of liver cell membrane structure and function through the Nrf2/OH-1/ NQO1 signaling pathways.

湖北省卫生和计划生育委员会(WJ2017F023)；武汉市卫计委重点项目(WX17A04)