CAJ | 학술논문

目的：通过分析丝裂原和应激激活蛋白激酶1（MSK1）在实验性自身免疫性脑脊髓炎（EAE）中的表达情况探讨中药复方益肾达络饮保护小鼠损伤脑组织的机制。方法利用蛋白印迹技术，检测小鼠脑组织中MSK1、CREB 的含量。结果脑组织中MSK1表达显示，正常组和中药组、激素组、抑制剂组均有显著性差异（均P＜0.01）；模型组和抑制剂组有显著性差异（均P＜0.01）；中药组和激素组、抑制剂组有显著性差异（ P＜0.01）；中药组和模型组、中药加激素组有差异（均P＜0.05）。 CREB表达显示：中药组CREB的表达与其余各组相比均显著升高（P＜0.01）；中药组、中药加激素组和激素组的CREB水平依次降低。结论复方益肾达络饮治疗EAE与MSK1升高有关，p38MAPK信号通路下游因子 MSK1表达与其底物CREB表达呈相同态势。
목적：통과분석사렬원화응격격활단백격매1（MSK1）재실험성자신면역성뇌척수염（EAE）중적표체정황탐토중약복방익신체락음보호소서손상뇌조직적궤제。방법이용단백인적기술，검측소서뇌조직중MSK1、CREB 적함량。결과뇌조직중MSK1표체현시，정상조화중약조、격소조、억제제조균유현저성차이（균P＜0.01）；모형조화억제제조유현저성차이（균P＜0.01）；중약조화격소조、억제제조유현저성차이（ P＜0.01）；중약조화모형조、중약가격소조유차이（균P＜0.05）。 CREB표체현시：중약조CREB적표체여기여각조상비균현저승고（P＜0.01）；중약조、중약가격소조화격소조적CREB수평의차강저。결론복방익신체락음치료EAE여MSK1승고유관，p38MAPK신호통로하유인자 MSK1표체여기저물CREB표체정상동태세。
Objective To explore the effect of Yishendaluo Decoction on expression of MSK 1 in experimental autoimmune encepha-lomyelitis ( EAE) mice and its mechanism .Methods Western blot was used to determine the expression levels of MSK 1 and CREB protein in the brain tissue of EAE mice .Results Compared with that of normal group ,the expression of MSK1 protein in mice brain tissue was im-proved in Yishendaluo Decoction-treated group, hormone-treated group and SB203580-treated group(all P<0.01);compared with that of model group, it was improved in SB203580-treated group (P<0.01);compared with Yishendaluo Decoction-treated group, the contents in hormone-treated and SB203580-treated groups were improved (all P<0.01);compared with Yishendaluo Decoction-treated group, the con-tents in model group and Yishendaluo Decoction-hormone treated group were higher (all P<0.05).Compared with Yishendaluo Decoction-treated group,the content of CREB in brain was highest than that of other groups (all P<0.01);The level of CREB was declining in Yishen-daluo Decoction-treated, Yishendaluo Decoction-hormone treated,hormone-treated groups in order .Conclusions The mechanism of Yishen-daluo Decoction in EAE mice might be associated with the rising level of MSK 1.The expression of MSK1, the downstream factor of p38MAPK signaling pathways, shows the same trend with its substrate CREB .