摘要
目的研究β2-AR过表达对心力衰竭大鼠心肌细胞IL-18分泌的影响。方法采用腹主动脉缩窄法建立慢性心力衰竭大鼠模型,胶原酶消化法分离大鼠心肌细胞,用携带β2-AR基因的重组腺病毒转染大鼠心肌细胞,培养48 h后,Western blot法检测心肌细胞β2-AR蛋白的表达及ELISA法测定IL-18的含量。经筛选后心力衰竭大鼠随机分为心力衰竭对照组(HF组)、转染EGFP组(HF+EGFP组)、转染β2-AR-EGFP组(HF+β2组);假手术组也相应随机分为对照组(sham组)、转染EGFP组(sham+EGFP组)、转染β2-AR-EGFP组(sham+β2组)。结果与假手术组相比,心力衰竭组左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)均升高(P<0.05),左心室短轴缩短率(FS)及射血分数(EF)均降低(P<0.05)。Western blot结果显示HF+β2组心肌细胞β2-AR蛋白表达量高于HF+EGFP组及HF组(P<0.05)。与sham组相比,HF组IL-18含量显著升高(P<0.05);HF+β2组IL-18含量明显低于HF+EGFP组及HF组(P均<0.05)。结论心力衰竭大鼠心肌细胞分泌炎症因子IL-18增加,β2-AR过表达后能抑制心肌细胞IL-18的分泌。
Objective To investigate the effects of β2-AR overexpression on IL-18 content secreted by cardiomyocytes of heart failure rats. Methods The rats model of chronic heart failure was established by partially banding abdominal aorta and the cardiomyocyte was isolated with collagenase IL then the cardiomyocyte was transfected with Ad5-ADRbeta2-EGFP for 48 h to observe the changes of β2-AR protein expression in Western Blot and IL-18 content in ELISA. The experiment was divided into six groups： HF group, HF＋EGFP group, HF＋ β2 group,sham group, sham＋EGFP group and sham＋β2 group. Results Compared with the sham-operated group, left ventricular diastolic dimension （LVEDD）, left ventricular systolic dimension（LVESD） were all increased（P〈0.05）, ejection fraction（EF）and fxactional shortening （FS） were decreased（P〈0.05） in HF group. Compared with HF group and I-IF＋EGFP group, the expression of β2-AR protein of cardiomyocytes was increased in HF＋β2 group（P〈0.05）. Compared with sham group, IL-18 content secreted by cardiomyocytes in HF group was significantly increased（P〈0.05）. Compared with HF group and HF＋EGFP group, IL-18 content in HF＋β2 group were both increased（P〈0.05）. Conclusion The exmtent of IL-18 is incav.ased in the cardiomyocytes of heart failure rats. The overexpressed β2-AR protein can decrease the IL-18 content secreted by cardiomyocytes of heart failure rats.
出处
《中华临床医师杂志（电子版）》
CAS
2013年第16期80-83,共4页
Chinese Journal of Clinicians(Electronic Edition)
基金
江苏省生命健康科技专项资金(BL2012019)
