FGF-2对大鼠心肌细胞保护作用的机制  

The mechanism of FGF-2-induced cardioprotection in rats

作　　者：李婷[1] 何璐[2] 颜斌[3] 

机构地区：[1]南华大学附属第一医院功能科,湖南衡阳421000 [2]南华大学附属第一医院妇产科,湖南衡阳421000 [3]南华大学附属第一医院内分泌科,湖南衡阳421000

出　　处：《暨南大学学报（自然科学与医学版）》2016年第1期60-65,共6页Journal of Jinan University(Natural Science & Medicine Edition)

基　　金：湖南省教育厅基金资助项目(2014C0981)

摘　　要：目的:探讨碱性成纤维细胞生长因子(FGF-2)在内质网(ER)应激中对心肌的保护作用.方法:建立SD大鼠心肌细胞缺氧/复氧模型,使用衣霉素(TM)建立SD大鼠心肌细胞内质网应激模型.观察对照组与FGF-2及牛磺熊去氧胆酸(TUDCA)治疗组细胞凋亡情况,并使用乳酸脱氢酶(LDH)试剂盒检测各组心肌细胞活力.Western blot和实时荧光定量核酸扩增(q-RTPCR)检测各组内质网应激相关分子的表达.结果:缺氧/复氧可引起心肌细胞内质网应激增加,与缺氧/复氧组相比,FGF-2预处理组及TUDCA预处理组内质网应激减弱;FGF-2和TUDCA均能改善缺氧/复氧引起的心肌细胞凋亡及活力减弱;FGF-2能够抑制TM诱导的内质网应激;与TM处理组相比,FGF-2预处理组心肌细胞凋亡减弱,细胞活力改善.结论:缺氧/复氧及TM均可以通过内质网应激诱导心肌细胞损伤,而FGF-2可以通过抑制内质网应激而保护心肌细胞.Aim：To study the mechanism of growth factor-2-induced cardioprotection in rats. Meth- ods： Arat cardiac myocyteshypoxia/reoxygenation model was made to study the role of FGF-2 and TUD- CA in myocardial damage. Flow cytometrywas used to evaluate the myocardium cell apoptosis of each group. The levels of LDH was studied to assess cardiocyte viability. Western blot and qPCR were used to detect the expression of ERS related genes. A rat cardiac myocytesERS model was made to study the effect of FGF-2 on ERS. Methods mentioned above were used to study apoptosis, cardioeyte viability and the expression of ERS related genes. Results： Compared with intact group, FGF-2 and TUDCA can sig- nificantly improve the apoptosis and cell activity and reduce ER stressor myocardial cell. Compared with- TM treated group, TM ＋ FGF-2 double-treated group has reduced apoptosis and ER stress and improved cell activity. Thus, FGF-2 and TUDCA contributed to cardioprotectionand repressed ER stress, and FGF- 2 also protected myocardial cellfrom TM induced apoptosis and inhibited ER stress. Conclusion：FGF-2 act as a cardioprotection factor by repressing ER stress.

关 键 词：碱性成纤维细胞生长因子-2 内质网应激 缺氧/复氧损伤 心肌保护 

分 类 号：TP391.41[自动化与计算机技术—计算机应用技术]