尤瑞克林对大鼠脑缺血再灌注损伤Bcl-2和Bax表达的影响

The effects of urinary kallidinogenase on the expression of Bcl-2 and Bax in rats with focal cerebral ischemia-reperfusion

目的观察大鼠脑缺血再灌注损伤后脑组织中Bcl-2和Bax的表达及尤瑞克林的影响。方法48只SD大鼠，随机分为假手术组、模型组、生理盐水对照组和尤瑞克林治疗组。线栓法制作大鼠大脑中动脉脑缺血再灌注模型，缺血2h后再灌注，24h后行神经功能评分，采用免疫组织化学法和反转录聚合酶链反应（RT—PCR）法观察脑组织Bcl-2和Bax表达的变化。结果大鼠脑缺血再灌注损伤后，模型组和生理盐水对照组Bcl-2阳性细胞数和mRNA的表达分别为[（14．28±2．54）个／HP、0．551±0．068和（16．54±1．84）个／HP、0．585±0．0843，比假手术组[（7．58±0．97）个／HP、0．324±0．0423增多（P〈0．05）；模型组和生理盐水对照组Bax阳性细胞数和mRNA的表达分别为[（24．38±3．58）个／HP、0．540±0．076和（26．74±4．04）个／HP、0．527±0．065]，比假手术组[（8．24±1．95）个／HP、0．309±0．0373增多（P〈0．05）。尤瑞克林干预后，Bcl-2阳性细胞数和mRNA的表达显著上调[（25．61±3．41）个／HP、0．791±0．0963，Bax阳性细胞数和mRNA的表达下调[（18．54士2．38）个／HP、0．359±0．0533，与模型组和生理盐水对照组相比，差异均有统计学意义（P〈0．05）。结论尤瑞克林可上调脑组织中Bcl-2的表达，下调Bax的表达，从而抑制细胞凋亡，这可能是其发挥脑保护作用的机制之一。

Objective To investigate the effect of urinary kallidinogenase on the expression of Bcl-2 and Bax in cerebral ischemia-reperfusion injury of rats. Methods Forty eight male adult Sprague-Dawley rats were randomly assigned into four groups： sham operation group, model group, normal saline group and urinary kallidinogenase group. The middle cerebral artery occlusion reperfusion model was made by the suture method. After focal cerebral ischemia-reperfusion, the animals were neurologically assessed on a 5 point scale. The levels of Bcl-2 and Bax expression were measured by immunohistochemieal and RT-PCR. Results In model and normal saline group, the expressions of positive Bcl-2 neurocytes and mRNA [（14.28±2.54）/HP, 0. 551±0. 068 and （16.54 ± 1.84）/HP, 0. 585±0. 084] were significantly increased compared with the sham operation group [（7.58±0.97）/HP, 0. 324±0. 042] （P〈 0.05）; The expressions of Bax positive neurocytes and mRNA[（ 24. 38 ±3.58）/HP, 0.540±0.076 and （26.74 ± 4.04） /HP, 0. 527±0. 065 ] were significantly increased than the sham operation group（（8.24 ± 1.95）个/HP, 0. 309 ± 0. 037] （P〈 0.05）. After treatment with urinary kallidinogenase, the expressions of Bcl-2 positive neurocytes and mRNA [（25.61±3.41）/HP, 0. 791±0. 096] were upregulated （P〈0.05）, and the expressions of Bax positive neurocytes and mRNA [（18.54±2.38）/HP, 0. 359±0. 0533 were down regulated （P〈 0.05）, compared with model group and normal saline group. Conclusions Urinary kallidinogenase is significantly related to the upregulation of Bcl-2 expression and the downregulation of Bax expression, which suggest that urinary kallidinogenase could be related with the inhibitory effects on ischemic neurocyte apoptosis.