东菱迪芙对大鼠局灶性脑缺血再灌注后JNK和ERK活性的影响

目的探讨东菱迪芙对局灶性脑缺血再灌注大鼠脑内c-Jun氨基末端激酶(JNK)和胞外信号调节酶(ERK)活性的影响。方法采用大脑中动脉线栓法(MCAO)建立大鼠局灶性脑缺血再灌注模型,用免疫组织化学法和免疫印迹法检测ERK和JNK的活性,同时观察缺血侧脑组织形态学变化、脑梗死体积比、凋亡细胞数。结果东菱迪芙可下调脑缺血再灌注大鼠脑组织JNK蛋白的活性,上调ERK蛋白的活性,并降低梗死体积、坏死和凋亡细胞数。结论东菱迪芙对大鼠局灶性脑缺血再灌注损伤有保护作用,抑制JNK凋亡通路、促进ERK生存通路, 从而减轻细胞凋亡是其脑保护机制之一。

Effects of batroxobin on the activation of JNK and ERK after focal cerebral ischemia-reperfusion injury in rats

Objective To investigate the effect of Batroxobin on activation of C-Jun NH2-terminal kinase (JNK) and extracelluar-regulated protein kinases (ERK) after focal cerebral ischemia reperfusion (IR) injury in rats. Methods The rats subjected to middle cerebral artery occlusion with intranall filament occlusion were injected intraperitoneally with Batroxobin before reperfusion. Neuroprotective effect of Batroxobin on IR was evaluated in terms of TTC staining,morphology,and TUNEL assay. In addition,immunohistochemistry and immunoblotting were used to detect JNK and ERK expression. Results Compared with the sham group,the cerebral infarct volume ratio, necrosis, and apoptotic cell death were more evident in IR-treated rats at 22h. Batroxobin significantly decreased all of the above parameters compared with the IR group. At a molecular basis,IR significantly increased JNK and ERK immunoreactivity and expression. Batroxobin decreased JNK but increased ERK expression at 6h after reperfusion. Conclusions These findings suggest that Batroxobin treatment have neuroprotective effect against IR injury in rats,and that this may be associated with differentialy regulation of ERK and JNK expression.