组织型激肽释放酶对脑缺血再灌注大鼠细胞凋亡和炎性反应的影响

The effect of TK on apoptosis and inflammatory reaction in rat models of cerebral ischemia-reperfusion

目的探讨组织型激肽释放酶(TK)对脑缺血再灌注大鼠的治疗作用和对细胞凋亡、炎性反应的影响。方法将36只SD大鼠随机分为3组,A组:假手术;B组:生理盐水2ml·kg-1·d-1干预;C组:脑缺血再灌注后8h给予TK17.5×10-3U·kg-1·d-1治疗,每组12只。连续给药3天后分别进行神经功能缺损评分,脑梗死体积测定,梗死组织HE染色。对脑梗死组织进行TUNEL染色和细胞凋亡蛋白酶-3(caspase-3)、TNF-α、白细胞介素-1(IL-1)免疫组织化学检测。结果与A组和B组比较,C组能明显降低神经功能缺损,使脑梗死的体积变小(P<0.05);减轻脑梗死的病理改变;使缺血区内TUNEL、caspase-3、TNF-α、IL-1阳性细胞减少(P<0.05)。结论TK对脑缺血再灌注大鼠有治疗作用,能明显减轻缺血区内的细胞凋亡和炎性反应。

Objective To explore the therapeutic effectiveness of tissue kallikrein（TK） in rat models of ischemia-reperfusion induced by middle cerebral artery occlusion and the effect of TK on apoptosis and inflammatory reaction in the cerebral infarction. Methods Thirty-six rats were randomly divided into three groups. Group A underwent sham operation;group B was administrated with normal saline（2 ml· kg^-1·d^-1）;group C was administrated with TK（17. 55〈10^-3U· kg^-1· d ^-1）after ischemia-reperfusion for 8 hours. All rats received intraperitoneal injection for three days. After three days, neurological function was appraised and infarct volume was determined. The pathology of ischemic tissue was examined. TUNEL staining and immunohistochemical examination of caspase-3,TNF-α,IL-1 in ischemic tissue were carried out. Results Compared with group A and group B,deficit of neurological function and the infarct volume （P 〈0.05） were reduced significantly, pathological change in ischemic tissue was improved, the positive cells of TUNEL staining, caspase-3, TNF-α and IL-1 in ischemic tissue were reduced in group C （P〈0.05）. Conclusion TK has therapeutical effect on cerebral infarction and can obviously relieve the apoptosis and inflammatory reaction in the cerebral infarct area.