HLECs-B3 were incubated in the fresh media containing so-dium salicylate at different concentrations for different durations, and allowed to be recovered in fresh 哪里 medium

without sodium salicylate for different durations with or without pretreatment with p38MAPK inhibitor (SB203580), ERK1/2 inhibitor (PD98059) and JNK/SAPK inhibitor (SP600125). The expression of P38MAPK, ERK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 was detected by Western blot. The expression of HSP27 mRNA and protein was detected by RT-PCR and immunohistochemistry respectively. It was found there was only weak expression of HSP27 in normal HLECs. The expression Sorafenib细胞系 of HSP27 was not detectable in HLECs-B3 that were exposed to sodium salicylate (55 mmol/L) for 1-5 h. It was indicated that recovery from sodium salicylate (>35 mmol/L) significantly increased the synthesis of HSP27. The expression of HSP27 was up-regulated in HLECs-B3 under sodium salicylate recovery for 3 h, reached the peak level for 6 h, and returned to the level of

control cells by 24 h. Activation of P38MAPK from sodium salicylate stimulation occurred KRX-0401订单 at 30th min, and increased significantly at 1st h, then declined and returned to baseline level at 3rd h under sodium salicylate recovery. Activation of ERK1/2 occurred at 1st h and reached the peak level at 6th h under sodium salicylate recovery. However, JNK/SAPK was inactivated by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059 jointly. It is concluded

that sodium salicylate can induce the expression of HSP27 in HLECs-B3. The effects are mediated, at least in part, through the activation of P38MAPK and ERK1/2 signaling pathway.
目的探讨p38丝裂原激活的蛋白激酶(p38MAPK,p38)和心锚重复蛋白(cardiac ankyrin repeat protein,CARP)与心肌梗死后心肌重塑的关系,及辛伐他汀改善心肌梗死后心肌重塑的机制。方法结扎大鼠冠脉前降支致心肌梗死,术后24h存活大鼠随机分为心肌梗死组(MI组)、p38抑制剂SB203580组(SB组)、辛伐他汀组(Sim组)和假手术组(sham组)。7d后测定左心室重量指数(LVWI),心肌细胞横切面面积(CSA),RT-PCR和免疫组化法测定p38和CARP在非梗死区心肌中的表达。结果与Sham组相比,MI组LVWI和CSA明显增加(P<0.01),磷酸化p38(P-p38)和CARP表达明显增加(P<0.05)。与MI组相比,SB组和Sim组LVWI和CSA明显降低(P<0.01),SB组CARP表达低于MI组(P<0.01),Sim组p38和CARP表达明显低于MI组(P<0.