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首页> 外文期刊>The Journal of Thoracic and Cardiovascular Surgery >Lipopolysaccharide pretreatment attenuates myocardial infarct size: A possible mechanism involving heat shock protein 70-inhibitory kappaBalpha complex and attenuation of nuclear factor kappaB.
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Lipopolysaccharide pretreatment attenuates myocardial infarct size: A possible mechanism involving heat shock protein 70-inhibitory kappaBalpha complex and attenuation of nuclear factor kappaB.

机译：脂多糖预处理可减轻心肌梗死面积：一种可能的机制涉及热休克蛋白70抑制性kappaBalpha复合物和核因子kappaB的减弱。

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OBJECTIVE: Lipopolysaccharide pretreatment is known to reduce myocardial infarct size, but the mechanism has not been elucidated. We hypothesized that heat shock protein 70, induced by lipopolysaccharide pretreatment, formed complexes with inhibitory kappaBalpha, thereby inhibiting degradation and attenuating activation of nuclear factor kappaB and cellular injury in rat myocardium. METHODS: Fifteen Sprague-Dawley rats were given saline solution (control group) or lipopolysaccharide. After 48 hours, 5 hearts in each group were excised without ischemia for examination of heat shock protein 70 and inhibitory kappaBalpha levels and detection of heat shock protein 70-inhibitory kappaBalpha complexes. Myocardium from the remaining 10 rats in each group was exposed to 30 minutes of ischemia and 30 minutes of reperfusion (n = 5) to evaluate nuclear factor kappaB activity or to 24 hours of reperfusion (n = 5) to evaluate infarct size. RESULTS: Infarct size was reduced in the lipopolysaccharide group (P <.05). Nuclear factor kappaB was activated in the control ischemia group and attenuated in the lipopolysaccharide group (P <.05). Heat shock protein 70 levels were increased in the lipopolysaccharide group (P <.05), but inhibitory kappaBalpha levels were similar in both groups. Heat shock protein 70-inhibitory kappaBalpha complexes were detected only in the lipopolysaccharide group. Colocalization of the 2 proteins was observed in the lipopolysaccharide group. CONCLUSIONS: Heat shock protein 70, induced by lipopolysaccharide pretreatment, forms complexes with inhibitory kappaBalpha and attenuates activation of nuclear factor kappaB and myocardial infarct size. Our results suggest that attenuation of nuclear factor kappaB through a mechanism forming heat shock protein 70-inhibitory kappaBalpha complexes might protect the myocardium from ischemia-reperfusion injury.
机译：目的：已知脂多糖预处理可减少心肌梗塞的大小，但其作用机理尚未阐明。我们假设通过脂多糖预处理诱导的热休克蛋白70与抑制性kappaBalpha形成复合物，从而抑制降解并减弱大鼠心肌中核因子kappaB的活化和细胞损伤。方法：15只Sprague-Dawley大鼠被给予盐溶液（对照组）或脂多糖。 48小时后，切下每组5个无缺血的心脏，以检查热休克蛋白70和抑制性κBα水平，并检测热休克蛋白70抑制性κBα复合物。每组其余10只大鼠的心肌暴露于缺血30分钟和再灌注30分钟（n = 5）以评估核因子κB活性或再灌注24小时（n = 5）以评估梗塞面积。结果：脂多糖组梗死面积减少（P <.05）。对照缺血组中核因子κB被激活，而脂多糖组中核因子κB被减弱（P <.05）。脂多糖组的热休克蛋白70水平升高（P <.05），但两组的抑制性kappaBalpha水平相似。仅在脂多糖组中检测到热休克蛋白70抑制性kappaBalpha复合物。在脂多糖组中观察到这两种蛋白质的共定位。结论：脂多糖预处理诱导的热休克蛋白70与抑制性kappaBalpha形成复合物，并减弱核因子kappaB的激活和心肌梗死面积。我们的结果表明，通过形成热休克蛋白70抑制性kappaBalpha复合物的机制减弱核因子kappaB可能会保护心肌免受缺血再灌注损伤。

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