复方茵柏颗粒对四氯化碳致急性肝损伤大鼠MAPK信号通路的影响

Effects of Complex Yinbai Granule on MAPK Signaling Pathway of Acute Liver Injury Induced by Carbon Tetrachloride in Rats

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 effects of Complex Yinbai Granule on MAPK signaling pathway of acute liver injury induced by carbon tetrachloride in rats. Methods： Rats were randomly divided into 6 groups： normal control group,model group,Complex Yinbai Granule low,middle and high dose groups（ 2. 16 g·kg- 1,4. 32 g·kg- 1,8. 64 g·kg- 1）,positive control（ Complex Yinbai mixture 8. 64 g·kg- 1）. Acute liver injury was induced by 40% carbon tetrachloride in rats. JNK,ERK and p38 MAPK phosphorylations were detected by Western- blotting and the liver morphology change of rat in each group was observed. Results： As compared with the control group,p38 MAPK phosphorylation was decreased markedly and JNK and ERK phosphorylations were increased in the liver tissue of the model group with statistical significance（ P 〈0. 01 or P 〈0. 05）. Compared with the model group,low and middle dose groups obviously inhibit JNK,ERK and P38 MAPK phosphorylations with significance（ P 〈0. 01 or P 〈. 05）. Conclusion： The protection mechanism of Complex Yinbai Granule on acute liver injury in rats may be to suppress the activation of JNK,ERK and P38 of the MAPK signal pathways.