抑肽酶对脑缺血再灌注大鼠c-Jun氨基末端激酶信号转导通路的影响

目的探讨抑肽酶对脑缺血再灌注大鼠c—Jun氨基末端激酶（c-Jun NH2 terminal kinases，JNK）信号转导通路的影响。方法将30只健康雄性SD大鼠完全随机分为假手术组、模型组、抑肽酶组，每组10只。采用4-VO法建立大鼠全脑缺血模型，在预定时间行灌注、固定、取脑、石蜡包埋切片；免疫组化法检测p-JNK的表达，DNA断端末端标记法检测CA1区凋亡细胞。结果p-JNK在模型组大鼠海马CA1区大量表达（239．17±2．74），抑肽酶组p-JNK则无明显表达（176．53±O．36），2组比较，差异有统计学意义（P〈0．05）；抑肽酶组细胞凋亡指数（27．06±3．16）明显低于模型组（62．13±1．04），差异有统计学意义（P〈0．05）。结论JNK信号通路在大鼠脑缺血再灌注损伤中发挥重要作用，抑肽酶能够抑制JNK信号转导通路的激活，对脑缺血再灌注损伤导致的细胞损伤起到保护作用。

Effect of Aprotinin on C-Jun NH_2 terminal kinases signaling pathway in rats of brain ischemia-reperfusion

Objectives To study the effect of Aprotinin on C-Jun NH_2 terminal kinases signaling pathway in mrs of brain ischemia/reperfusion. Methods Healthy rats were randomly divided into 3 group: sham operated group, model group and Aprotinin group. The brain tissue were removed, embedded and sliced up. The p-JNK was detected by immunohistochemistry and TUNEL in the hippocampal CA1 region was counted. Results The p-JNK in model group was significantly expressed (239.17±2.74). The level of p-JNK in Aprotinin group (176.53±0.36) was much lower than that in model group (P <0.05). In Aprotinin group, the apoptotic index (27.06±3.16) was much lower than that in model group (62.13±1.04) (P<0.05). Conclusions In the process of brain ischemia/reperfusion injury, JNK signaling pathway plays an important role. Aprotinin may help protect neurons against apop-tosis by inhibiting of JNK signaling pathway.