中文摘要：

目的将与脂肪肝疾病在老鼠的 Kupffer 房间在 c6 月 N 终端 kinase (JNK ) 的激活上观察不同治疗学的方法的效果和中国药(厘米) 的配方并且探索这些治疗学的方法的机制。由使用一个随机的数字的方法搁置， 98 只老鼠随机被划分成 7 个组：控制组，模型组，和 5 处理组织，包括劝慰肝(轧) 配方组，鼓舞的怒气(Pi ) 配方组，驱散的潮湿配方组，提拔的血配方组，和复杂配方组织。在控制组的老鼠用正常食物被喂并且由胃的灌注提取了水，当在模型组的老鼠用高脂肪的食物被喂并且由胃的灌注提取了精神时。在 5 个治疗组的老鼠被胃的灌注用高脂肪的食物和相应配方喂。12 个星期以后，所有老鼠被牺牲，肝纸巾为 pathohistological 观察被染色。Kupffer 房间从老鼠的肝被孤立由西方的弄污计算 JNK 和 phospho-JNK 表达式。结果肝的脂肪变性的等级比控制组在模型组是更高的(P < 0.05 ) 。与模型组相比，在劝慰肝配方组和鼓舞的怒气配方组的丰满的退化的等级显著地被改善(P < 0.05 ) 。在 Kupffer 房间的 JNK 和 phospho-JNK 的表情比在控制组的那些在模型组是显著地更高的(P < 0.05， P < 0.01 ) 。与模型组相比，在所有处理组的 JNK 的表情减少了，特别在鼓舞怒气配方组和提拔的血配方组(P < 0.05 ) 。与模型组相比，在所有处理组的 phospho-JNK 的表情显著地衰退了(P < 0.01 ) ，特别在现场劝慰，配方组和鼓舞的怒气配方组织。在 Kupffer 房间的 JNK 和 phospho-JNK 的高表情可能在老鼠在脂肪肝疾病的致病起一个重要作用的结论。厘米，特别鼓舞的脾配方和劝慰的肝配方的配方，可能由减少全部的 JNK 蛋白质内容并且在脂肪肝模型老鼠的 Kupffer 房间禁止 JNK 蛋白质的激活保护肝免于损害，它在脂肪肝上显示出有益的效果疾病。

英文摘要：

Objective： To observe the effects of different therapeutic methods and the recipes of Chinese medicine （CM） on the activation of c-Jun N-terminal kinase （JNK） in Kupffer cells of rats with fatty liver disease and to explore the mechanisms of these therapeutic methods. Methods： By using a random number table, 98 rats were randomly divided into 7 groups： control group, model group, and 5 treatment groups, including soothing Liver （Gan） recipe group, invigorating Spleen （Pi） recipe group, dispelling dampness recipe group, promoting blood recipe group, and complex recipe group. Rats in the control group were fed with normal food and distilled water by gastric perfusion, while rats in the model group were fed with high-fat food and distilled spirits by gastric perfusion. Rats in the 5 treatment groups were fed with high-fat food and corresponding recipes by gastric perfusion. Twelve weeks later, all rats were sacrificed and liver tissues were stained for pathohistological observation. Kupffer cells were isolated from livers of rats to evaluate JNK and phospho-JNK expressions by Western blotting. Results： The grade of hepatic steatosis was higher in the model group than the control group （P〈0.05）. Compared with the model group, the grade of fatty degeneration in soothing Liver recipe group and invigorating Spleen recipe group were significantly ameliorated （P〈0.05）. Expressions of JNK and phospho-JNK in Kupffer cells were significantly higher in the model group than those in the control group （P〈0.05, P〈0.01）. Compared with the model group, expressions of JNK in all treatment groups decreased, especially in invigorating Spleen recipe group and promoting blood recipe group （P〈0.05）. Compared with the model group, expressions of phospho-JNK in all treatment groups declined significantly （P〈0.01）, especially in soothing Live recipe group and invigorating Spleen recipe group. Conclusions： The high expressions of JNK and phospho-JNK in Kupffer cells might play an imp