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机构地区:[1]苏州大学附属第一医院护理部,江苏苏州215006 [2]山东大学教育部和卫生部心血管重构与功能研究重点实验室,山东济南250012 [3]山东大学护理学院,山东济南250012
出 处:《苏州大学学报(医学版)》2010年第1期50-53,共4页Suzhou University Journal of Medical Science
基 金:山东大学青年基金资助项目(21330051310061)
摘 要:目的研究短期运动对大鼠心肌缺血再灌注损伤的保护作用及与蛋白激酶C(PKC)和锰超氧化物歧化酶(MnSOD)的关系。方法72只Wistar大鼠随机分为4组:对照组(CON组)、运动组(EXE组)、运动+PKC抑制剂CHE组(E+C组)和PKC抑制剂组(CHE组)。以上4组大鼠每组再随机分成2组:(1)I/R组:应用Langendorff离体心脏缺血/再灌注模型,观察各组大鼠再灌注期间心功能指标恢复率及心肌梗死范围;(2)假处理组:取左心室心肌组织进行MnSOD活性测定。结果EXE组大鼠左心室发展压(LVDP)和心率压力乘积(RPP)的恢复率明显高于CON组和E+C组(P<0.05或<0.01),心肌梗死范围显著低于CON组和E+C组(均P<0.01);CON组和CHE组上述指标无明显差异(P>0.05)。EXE组大鼠心肌组织MnSOD活性高于CON组和E+C组(P<0.05),CHE组和CON组MnSOD活性无明显差异(P>0.05)。结论短期运动通过激活PKC、升高MnSOD活性,发挥对心肌缺血/再灌注损伤的保护作用;PKC是MnSOD活性升高的中间信号分子。Objective To investigate the protective effect of short-term exercise on ischemic/reperfused myocardium and its correlation with PKC and MnSOD.Methods Seventy-two Wistar rats were randomly divided into 4 groups:the control group(CON group),exercise group(EXE group),exercise + PKC inhibitor group(E+C group)and PKC inhibitor group(CHE group).Each of the above 4 groups were divided into 2 groups randomly:(1)I/R group:the recovery of cardiac function and infarct size were observed by using the Langendorff-ischemia/reperfusion model in isolated rat heart in vitro;(2)the sham treated group:ischemia/reperfusion model was not made,but the activity of MnSOD in left ventricle was measured.Results Recovery rate of LVDP and RPP of EXE group were higher than those in the CON and E + C groups(P0.05 or0.01),infarct size in the EXE group was dramatically lower than that in the CON and E + C groups(P0.01);The above parameters between CHE and CON groups were not statistically different(P0.05).The activity of MnSOD in the EXE group was higher than that in the CON and E + C groups(P0.05);The activity of MnSOD between CHE and CON groups was of no difference(P0.05).Conclusion Short-term exercise improves the tolerance of rat heart to ischemia/reperfusion injury via the activation of PKC and MnSOD;The activation of PKC during exercise is a signaling intermediate for the expression of MnSOD.
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