紫苏提取物对化学性肝损伤保护作用的研究

目的研究紫苏提取物(Perilla frutescens extract,PE)对急性化学性肝损伤的保护作用。方法80只雄性KM小鼠(体重20±2g)随机分为8组:正常对照组(NC),模型对照组(MC),阳性药联苯双酯(DDB)组(200mg/kg),迷迭香酸(rosmarinic acid,RAD)低、高剂量预防组(11、44mg/kg),PE低、中、高剂量预防组(30、60、120mg/kg)。NC、MC组灌胃生理盐水,其它各组灌胃同等容量的相应药物,每天给药1次。实验20d后,用四氯化碳(CCl4 0.05ml/kg)和乙酰氨基酸(APAP 250mg/kg)腹腔注射分别制作急性化学性肝损伤模型。测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性、甘油三酯(TG)含量,肝组织匀浆超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性、丙二醛(MDA)含量,并观察肝脏病理改变。结果PE(120mg/kg)能显著降低CCl4与APAP诱导的肝损伤小鼠血清ALT、AST活性、TG含量,升高肝脏SOD、GSH-Px活性,降低MDA含量能明显减轻肝组织损伤程度;PE对正常小鼠血清ALT、AST、TG无影响。结论PE对CCl4或APAP诱导的小鼠急性化学性肝脏氧化损伤具有显著保护作用。

STUDY ON THE PROTECTIVE EFFECT OF PERILLA FRUTESCENS EXTRACT ON CHEMICAL LIVER INJURY IN MICE

Objective To study the protective effect of Perilla frutescens extract (PE) on acute chemical liver injury in mice. Method Eighty mice were randomly divided into eight groups: normal control group (NC), model control group (MC), positive control group treated with 200 mg/kg bifendate (DDB), prevention groups treated with 11 or 44 mg/kg rosmarinic acid (RAD), prevention groups treated with 30, 60, or 120 mg/kg PE. Normal saline was given to NC and MC group daily and the other groups were given corresponding drugs at the same volume and same way for successive 20d. The model of acute chemical liver injury was set up in mice respectively by carbon tetrachloride (CCl4) and acetaminophen (APAP) after last administration. The activities of alanine aminotransferase (ALT), aspartate aminotran- sferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the content of malondia- dehyde (MDA) and triglyceride (TG) were detected respectively in serum and liver. Results PE significantly reduced the activities of ALT, AST, level of TG in serum and level of MDA in liver, and increased the activities of SOD, GSH-Px in liver in acute chemical liver injury induced by CCl4 and APAP. The pathologic changes in liver in PE groups were slighter than in MC group. Conclusion PE showssignificant antioxidative effect in protecting acute chemical liver injury induced by CCl4 and APAP in mice.