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为阐明LPS诱导全身炎症反应失控的信号转导机制 ,采用Westernblot检测LPS刺激对枯否细胞ERK、JNK、p38MAPK蛋白表达及磷酸化水平的影响。结果显示 ,LPS刺激后 ,枯否细胞内ERK、JNK、p38MAPK蛋白表达无明显变化 ,但其磷酸化水平均发生了显著变化 ,刺激后 5min即明显升高 ,并分别于 30、45、2 0min达到高峰 ,然后逐渐下降 ,2h后基本恢复至正常水平 ,其中以p38MAPK变化最快且变化幅度最大。LPS浓度在 10pg/ml～ 10 0ng/ml范围内时 ,ERK、JNK、p38MAPK的磷酸化水平与LPS刺激浓度呈明显的剂量依赖性。提示ERK、JNK、p38MAPK均是LPS信号转导途径中的重要信号分子 ,其中p38MAPK在LPS所介导的枯否细胞早期反应中可能较ERK和JNK有着更为重要的作用。
To clarify the signal transduction mechanism of LPS-induced systemic inflammatory response out of control, the effect of LPS stimulation on the protein expression and phosphorylation of ERK, JNK and p38MAPK in Kupffer cells was detected by Western blot. The results showed that the expressions of ERK, JNK and p38MAPK in Kupffer cells did not change significantly after LPS stimulation, but the phosphorylation levels of Kupffer cells were significantly changed, which were significantly increased at 5 min after stimulation, and were significantly increased at 30, 45 and 20 min Reached the peak, and then gradually decreased, returned to normal after 2h, of which p38MAPK changes the fastest and the largest changes. The phosphorylation levels of ERK, JNK and p38MAPK were significantly dose-dependent when compared with LPS at a concentration of 10pg / ml ~ 10 0ng / ml. These results suggest that ERK, JNK and p38MAPK are both important signaling molecules in LPS signaling pathway. Among them, p38MAPK may play a more important role in ERK and JNK than LPS-mediated early Kupffer cell reaction.