摘要
目的 探讨缺血预处理对大鼠缺血再灌注心肌细胞凋亡及相关基因 Bcl- 2和 Bax蛋白表达的影响。方法 制备缺血预处理 (IP)和缺血再灌注损伤 (I/ R)模型 ,采用末端标记技术 (TU NEL )检测心肌细胞凋亡 ,应用免疫组织化学方法检测 Bcl- 2和 Bax的蛋白表达。结果 缺血再灌注组心肌细胞凋亡率明显比正常对照组高 (P<0 .0 5 ) ,而缺血预处理组心肌细胞凋亡率明显比缺血再灌注组低 (P<0 .0 5 )。缺血再灌注组 Bcl- 2表达阳性细胞率明显比正常组低 (P<0 .0 5 ) ,而缺血预处理组 Bcl- 2表达阳性细胞率明显较缺血再灌注组高 (P<0 .0 5 )。缺血再灌注组 Bax表达阳性细胞率明显较正常组高 ,而缺血预处理组 Bax表达阳性细胞率明显较缺血再灌注组低 (P<0 .0 5 )。结论 缺血再灌注可诱导心肌细胞凋亡 ,缺血预处理可减少心肌细胞凋亡 ;Bcl- 2和 Bax的蛋白表达在心肌凋亡发生中起重要作用 ,缺血预处理可上调 Bcl- 2蛋白表达和下调
? Objective To study the effects of ischemic preconditioning (IP) on the apoptosis and Bcl-2, Bax expression of myocardial cells in myocardial ischemic reperfusion (I/R). Methods IP and I/R models were established in rats. Apoptotic myocytes were detected with TUNEL, and Bcl-2, Bax expression was detected with immunohistochemistry. Results The rate of apoptosis was significantly higher in the I/R group than in the NC group ( P <0 05), but significantly lower in the IP group than in the I/R group ( P <0 05), Bcl-2 expreession positive cells were significantly fewer in I/R than in NC ( P <0 05), but significantly more in IP than in I/R ( P <0 05). Bax expression positive cells were significantly more in I/R than in NC ( P <0 05), but significantly fewer in IP than in I/R ( P <0 05). Conclusion I/R could induce while IP could reduce myocyte apoptosis in rats. The myocyte apoptosis might be related to the expression of Bcl-2 and Bax. IP could increase the Bcl-2 expression and decrease the Bax myocardial cells in myocardial ischemic reperfusion in rats.\;〔
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2002年第1期85-88,共4页
Chinese Journal of Histochemistry and Cytochemistry
基金
湖北省教育厅科研基金 (No.2000B44009)
