摘要
目的:观察β-肾上腺素能刺激与缺氧/复氧损伤对离体小鼠心脏细胞凋亡的影响。方法:逆行灌注离体小鼠心脏,观察不同剂量异丙基肾上腺素(Iso)和不同时间缺氧/复氧心肌细胞凋亡率的变化,并观察β1-肾上腺素能受体阻滞剂、caspase-拮抗剂、Bcl-2对其凋亡率的影响,以TUNEL法检测心肌细胞凋亡率。结果:单独Iso未引起心肌细胞凋亡率的变化,但可增加缺氧/复氧所诱导的细胞凋亡率;Bcl-2转基因鼠细胞凋亡率明显低于正常小鼠;β1-受体拮抗剂(美托洛尔)及caspase-拮抗剂(zVAD.fmk)可明显抑制Iso和缺氧/复氧所致细胞凋亡。结论:β-肾上腺素能受体激动剂可促使缺氧/复氧所诱导心肌细胞凋亡,其诱导凋亡的作用主要通过β1-受体介导,β1-受体拮抗剂可抑制二者共同作用所诱导心肌细胞凋亡。
AIM： To investigate the influence of beta - adrenergic stimulation and hypoxia- reoxygenation （H/R） on cardiomyocyte （CM） apoptosis in isolated mouse hearts. METHODS： The rates of cardiomyocyte apoptosis were measured in isolated retrograde perfusing hearts of mouse, which were disposed with different doses of isoproterenol （Iso） and with varied periods of hypoxia before reoxygenation. The influence of β1 - adrenergic receptor blocker, caspase inhibitor and Bcl - 2 on CM apoptotic rate was investigated. The rates of CM apoptosis were quantified hislotogically using the terminal transferase VTP nick and labeling （TUNEL） assay. RESULTS： Although Iso did not change the apoptotic rate of CM after normal perfusion, it increased the apoptotic rate induced by H/R. Metoprolol （β1 -adrenergic receptor blocker）, zVAD. fmk （caspase inhibitor） and Bcl- 2 overexpression inhibited dramatically the apoptotic rate induced by Iso and H/R. CONCLUSION： β1 - adrenergic receptor agonist increases the CM apoptotic induced by H/R. This effect is mediated by β1 - adrenergic receptor. β1 - adrenergic receptor blocker attenuate the CM apoptosis of mouse hearts induced by β1 - adrenergic receptor agonist and H/R.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第2期270-273,共4页
Chinese Journal of Pathophysiology
