蚓激酶对缺血再灌注大鼠脑内 JAK-STAT 通路的作用

 目的 研究大鼠局灶性脑缺血再灌注损伤后脑组织 JAK1 和 STAT1 蛋白及 mRNA 的表达以及给予蚓激酶（ lumbrokinase ）后二者的变化。 方法 线拴法制备大鼠大脑中动脉阻塞模型，随机分为蚓激酶高剂量组（ 1.2 mg·kg^-1 ）、蚓激酶中剂量组（ 0.6 mg·kg^-1 ）、蚓激酶低剂量组（ 0.3 mg·kg^-1 ）、阳性药脉络宁组（ 1.1 mL·kg^-1 ）、模型组和假手术组。再灌注开始时给予蚓激酶，连续给药 3 d ，用免疫荧光染色法检测 JAK1,STAT1 蛋白的表达，半定量 RT-PCR 方法检测 JAK1 mRNA,STAT1 mRNA 的表达。 结果 模型组 JAK1, STAT1 蛋白和 mRNA 的表达均较假手术组显著升高；蚓激酶 1.2 mg·kg ^-1 组和蚓激酶 0.6 mg·kg ^-1 组 JAK1 蛋白和 mRNA 的表达均高于模型组；蚓激酶 1.2 mg·kg^-1 组 STAT1 蛋白和 mRNA 的表达均低于模型组。 结论 JAK1 有抗神经细胞凋亡作用， STAT1 有促进神经细胞凋亡作用，蚓激酶可能通过增加脑组织 JAK1 蛋白和 mRNA 表达、减少 STAT1 蛋白和 mRNA 的表达起到对脑组织的保护作用。

Effect of Lumbrokinase on JAK-STAT Pathway in Rat Brain during Cerebral Ischemia and Reperfusion

OBJECTIVE To study the expressions of JAK1 and STAT1 protein and mRNA, and the effect of lumbrokinase(LK) after focal cerebral ischemia-reperfusion injury in the brain tissue of rats. METHODS The model of local cerebral ischemia-reperfusion injury was induced by reversible middle cerebral artery occlusion (MCAO) with inserting a thread. The rats were randomly divided into 6 groups: lumbrokinase 1.2 mg·kg-1 group, lumbrokinase 0.6 mg·kg -1 group, lumbrokinase 0.3 mg·kg-1 group, mailuoning1.1 mL·kg-1 group, model group and sham group. Lumbrokinase was administrated after the reperfusion began initiation, once daily for 3 d. The expression of JAK1 and STAT1 protein was assayed by immunofluorescence stainin. The expression of JAK1 and STAT1mRNA was assayed by RT-PCR. RESULTS JAK1 and STAT1 protein and mRNA were increased in model group compared with those in from sham-operation group. JAK1 protein and mRNA were increased significantly in lumbrokinase 1.2 mg·kg -1 group and lumbrokinase 0.6 mg·kg-1 group compared with those in model group. STAT1 protein and mRNA were decreased in lumbrokinase 1.2 mg·kg-1 group compared with those in model group. CONCLUSION JAK1 shows antiapoptosis effect on neurons. STAT1 shows apoptosis effect on neurons. Lumbrokinase maybe protect the brain from cerebral ischemia reperfusion injury through improving the JAK1 protein and mRNA and decreasing STAT1 protein and mRNA.