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过氧化物酶体增殖物激活受体γ在应激致小鼠心肌损伤中的作用
Effect of peroxisome proliferator-activated receptor γ on the myocardial injury caused by stress in mice
【摘要】 目的探讨应激致小鼠心肌损伤中过氧化物酶体增殖物激活受体γ(PPARγ)的变化特征及吡格列酮的防护作用。方法 50只KM小鼠,完全随机分为5组,每组10只:对照组、力竭游泳运动组、噪声组、复合刺激组、吡格列酮干预组(药物组)。造模成功后,分别取血清和心肌组织,HE染色法观察心肌形态变化;ELISA检测法测定血清皮质酮(CORT)、肌钙蛋白I(TnI)和超氧化物歧化酶(SOD)含量;Real-time PCR检测心肌组织PPARγmRNA表达,Western blot检测心肌组织PPARγ的蛋白表达。结果 HE染色结果显示,各组小鼠心肌形态变化不明显。与对照组相比,三组应激源作用组血清CORT和TnI升高明显(CORT:106.75±33.96,96.43±20.63,173.17±22.28;TnI:0.113±0.032,0.077±0.034,0.133±0.041;P<0.05),SOD则显著下降(103.36±10.43,124.93±8.47,97.16±17.30),心肌PPARγmRNA和蛋白水平明显降低(P<0.05)。药物干预组与三组应激源作用组比较,血清CORT和TnI显著降低(P<0.05),SOD则显著升高,心肌PPARγmRNA和蛋白水平明显升高(P<0.05)。结论应激可导致心肌微损伤;应激条件下,PPARγ在心肌的表达降低;吡格列酮干预可使应激导致的心肌微损伤得到有效防护。
【Abstract】 Objective To analyze the effect of peroxisome proliferator-activated receptorγ(PPARγ) on the myocardial injury caused by stress in mice and the preventive roles of pioghtazone.Methods Fifty mice were randomly assigned to control group, exhausted-swimming group,white noise group,exhausted-swimming plus white noise group,pioghtazone intervention group.The changes in myocardium structure were observed using HE staining.The serum levels of troponin I(TnI),corticosterone(CORT), superoxide dismutase(SOD) were determined by ELISA.The expression of PPARγmRNA and protein was detected by real-time fluorescence quantitative PCR and Western blot respectively.Results HE staining showed normal myocardial structure in all groups. The serum levels of CORT and TnI were raised after different stress attack(CORT:106.75±33.96,96.43±20.63,173.17±22.28;TnI: 0.113±0.032,0.077±0.034,0.133±0.041;P<0.05),while the level of SOD was reduced(103.36±10.43,124.93±8.47,97.16±17.30;P<0.05).The expressions of PPARγmRNA and protein were depressed in exhausted-swimming group,white noise group,and exhausted-swimming plus white noise group.In the pioghtazone group,the serum levels of TnI,CORT,and SOD and the expressions of PPARγmRNA and protein were resumed.Conclusion Stress results in the myocardial injury.The expression of PPARγin myocardial tissue was reduced under stress.Pioghtazone intervention can prevent myocardium against the injury caused by stress.
【Key words】 stress; peroxisome proliferator-activated receptorγ; superoxide dismutase; corticosterone; troponin I;
- 【文献出处】 中华老年多器官疾病杂志 ,Chinese Journal of Multiple Organ Diseases in the Elderly , 编辑部邮箱 ,2011年02期
- 【分类号】R541
- 【被引频次】1
- 【下载频次】73