摘要
[目的]探讨硫化氢预处理对大鼠心肌缺血再灌注损伤的保护机制。[方法]健康成年S-D雄性大鼠30只,随机分成三组,每组10只。假手术组(S组)仅开胸并分离冠状动脉左前降支,但不阻断血流;缺血再灌注组(IR组)行冠状动脉左前降支阻断30min,再灌注120min;硫化氢组(H组)予以静脉注射硫氢化钠0.05mg/kg,给药后24h同IR组处理。再灌注结束后检测血清IL-6和IL-10水平,免疫印迹法检测心肌过氧化物酶体增殖物激活受体γ(PPAR-γ)水平并比较。[结果]与s组比较,IR组和H组在缺血再灌注后血清IL-6和IL-10水平升高(P〈0.05);但与IR组比较,H组IL-10水平升高,IL-6水平下降(P〈0.05);与S组比较,IR组和H组PPAR-γ表达下降(P〈0.05);但与IR组比较,H组PPAR7表达升高(P〈0.05)。[结论]硫化氢预处理抑制大鼠心肌损伤的保护作用,可能与促进心肌PPAR-γ表达有关。
[Objective]To investigate the mechanism of hydrogen sulfide delayed preconditioning on myocardial ischemia reperfusion injury in rats. [Methods]Three groups ( n = 10 animals/group) of Sprague Dawley male rats were studied: group S consisted of control rats that received no treatment, Group IR consisted of rats treated with NS (1.0 ml/kg iv) 24 h before ischemia, and Group H consisted of rats treated with NariS (0.05 mg/kg) 24 h be- fore ischemia. Group IR and H were subjected to ischemia by 30 rnin of coronary artery occlusion followed by 2 h of reperfusion. At the end of reperfusion, the plasma concentration of IL-6 and IL-10 were measured. The peroxi some proliferator-activated receptor γ (PPAR-γ) was measured by Western blotting. [ResultslCompared with Group S, Group H and Group IR had higher levels of IL-6 and IL-10 ( P 〈0.05). Compared with Group IR, Group H had lower levels of IL-6 and higher levels of IL-10 ( P 〈0.05). Compared with Group S, Group H and Group IR had lower PPAR-γ protein expression in myocardium ( P〈0.05).Compared with Group IR, Group H had higher levels of PPAR-γ protein expression ( P〈0.05).[Conclusion]The hydrogen sulfide delayed precondi- tioning attenuates myocardial IR injury possibly through up-regulating PPAR-γ expression in rats.
出处
《医学临床研究》
CAS
2016年第8期1484-1485,1488,共3页
Journal of Clinical Research
基金
湖南省岳阳市科技局2012年第四批科技计划项目,湖南省科技厅项目(2013FJ4082)