尤瑞克林对大鼠脑缺血再灌注损伤Bcl-2和Bax表达的影响

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，24 h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±0.084]，比假手术组[(7.58±0.97)个/HP、0.324±0.042]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±0.037]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±0.096]，Bax阳性细胞数和mRNA的表达下调[(18.54±2.38)个/HP、0.359±0.053],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。

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

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 immunohistochemical 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±0.053] 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.