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目的:探讨复方茵柏颗粒对四氯化碳诱导的急性肝损伤的肝MAPK信号通路的影响。方法:将大鼠随机分为6组:正常对照组、模型组、复方茵柏颗粒低、中、高剂量组(2.16、4.32、8.64 g·kg-1)、阳性对照组(复方茵柏合剂8.64 g·kg-1),SD大鼠腹腔单次注射40%CCl4玉米油制备急性肝损伤模型,Western blotting方法测定肝脏MEK、ERK、p38MAPK磷酸化水平,并做大鼠肝脏组织形态学观察。结果:与正常对照组比较,模型组大鼠肝组织JNK、ERK磷酸化明显增加,P38MAPK磷酸化有所降低,具有统计学意义(P<0.01或P<0.05)。与模型对照组比较,复方茵柏颗粒高、中、低剂量组显著抑制JNK、ERK、P38MAPK磷酸化,具有统计学意义(P<0.01或P<0.05),并呈现明显正相剂量的药-效关系。结论:复方茵柏颗粒对急性肝损伤大鼠的肝脏保护作用机制可能是与抑制MAPK信号通路中的ERK、JNK和p38的激活有关。
Objective: To investigate the effect of compound Yinbai granules on hepatic MAPK signaling pathway induced by CCl4 in acute liver injury. Methods: The rats were randomly divided into 6 groups: normal control group, model group, compound Yinbai granules low, medium and high dose groups (2.16,4.32,8.64 g · kg-1), positive control group 8.64 g · kg-1). The acute liver injury model was induced by a single intraperitoneal injection of 40% CCl4 corn oil into the abdominal cavity of SD rats. The phosphorylation of MEK, ERK and p38 MAPK in the liver was detected by Western blotting and the liver morphology was observed. Results: Compared with the normal control group, the phosphorylation of JNK and ERK increased significantly and the phosphorylation of P38MAPK decreased in the model group, with statistical significance (P <0.01 or P <0.05). Compared with the model control group, compound Yinbai granules significantly inhibited the phosphorylation of JNK, ERK and P38MAPK in high, medium and low dose groups (P <0.01 or P <0.05), and showed obvious positive phase dose of drug- Effective relationship. Conclusion: The mechanism of hepatic protective effect of compound Yinbai granules on acute liver injury in rats may be related to the inhibition of the activation of ERK, JNK and p38 in MAPK signaling pathway.