The effects of urinary kallidinogenase on the expression of Bcl-2 and Bax in rats with focal cerebral ischemia-reperfusion
10.3760/cma.j.issn.0254-9026.2011.09.019
- VernacularTitle:尤瑞克林对大鼠脑缺血再灌注损伤Bcl-2和Bax表达的影响
- Author:
Guoqian LI
;
Jiehua WANG
;
Xiaoxia YANG
;
Zhuquan HONG
- Publication Type:Journal Article
- Keywords:
Brain ischemia;
Reperfusion;
Gene expression
- From:
Chinese Journal of Geriatrics
2011;30(9):770-773
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo 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 andurinary 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.ConclusionsUrinary 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.
