摘要
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.
出处
《中华老年医学杂志》
CAS
CSCD
北大核心
2011年第9期770-773,共4页
Chinese Journal of Geriatrics
关键词
脑缺血
再灌注
基因表达
Brain ischemia
Reperfusion
Gene expression