用16只 SD 大白鼠建立缺血再灌流心肌损伤模型,其中8只预先静脉注射吗啡以抗心律失常。此外,再用8只大鼠开胸作正常对照。其心脏标本进行 HE 染色及抗肌动蛋白单克隆抗体(HHF_(35))免疫组化观察:对照组心肌呈均匀一致的棕褐色染色;注射...用16只 SD 大白鼠建立缺血再灌流心肌损伤模型,其中8只预先静脉注射吗啡以抗心律失常。此外,再用8只大鼠开胸作正常对照。其心脏标本进行 HE 染色及抗肌动蛋白单克隆抗体(HHF_(35))免疫组化观察:对照组心肌呈均匀一致的棕褐色染色;注射吗啡后再灌流组心肌呈小灶性分布的 HHF_(35)染色缺染区;未注射吗啡组心肌缺染呈广泛大面积分布。结果表明,HHF_(35)免疫组化法对显示实验性心肌缺血再灌流损伤有重要价值,且心肌缺血再灌流损伤程度与心律失常有关。展开更多
Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was...Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion （I/R） injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation （H/R）.Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo （24.4％ ± 9.4％ vs.2.2％ ± 1.9％,P ＜ 0.01,n =5） and in vitro （14.12％ ±0.92％ vs.2.22％ ± 0.08％）.The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.展开更多
文摘Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion （I/R） injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation （H/R）.Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo （24.4％ ± 9.4％ vs.2.2％ ± 1.9％,P ＜ 0.01,n =5） and in vitro （14.12％ ±0.92％ vs.2.22％ ± 0.08％）.The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.
