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Variations of Hsp60 and HSF-1 in Primary Myocardial Cells of Rats Under Various Durations of in vitro Heat Stress

机译:体外热应激持续时间下大鼠原代心肌细胞Hsp60和HSF-1的变化

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The relationship between the heat stress induced variations of protective Hsp60 and its regulating factor HSF-1 expression in the heat-stressed primary myocardial cells of neonatal rats in in vitro was studied by using enzyme detections.immunoblotting and qPCR.The enzymes elevations displayed injuries of myocardial cells after heat exposure at 42℃.The enzymes elevated at 42℃ heat exposure and displayed injuries of myocardial cells.Hsp60 expression level was fluctuated during heat stress and decreased significantly after 20 min,then elevated at 120 min and reduced at 360 min of heat stress.The damages of myocardial cells characterized by enzyme elevations and over consumption of Hsp60 concerned to the functional disorder of myocardial cells at early stage of heat stress.However the significant induction results of hsp60 mRNA levels (P<0.01 )from the beginning up t0 240 min of heat stress were not consistent with the classic regulatory mechanisms.hsf-1 mRNA level was significantly increased from 10 min of heat stress,but HSF-1 protein was not simultaneously increased,indicating that HSF-1 is not the sole regulator of Hsp60 expression.
机译:通过酶检测,免疫印迹和qPCR研究了热应激诱导的新生大鼠热应激原代心肌细胞中保护性Hsp60变异与其调节因子HSF-1表达的关系。在42℃高温下暴露的心肌细胞。在42℃高温下酶升高并表现出心肌细胞损伤。热应激中Hsp60表达水平波动,20min后明显下降,120min时升高,360min时降低。热应激早期以心肌酶功能升高和Hsp60过量消耗为特征的心肌细胞损伤对心肌细胞功能障碍的影响。然而,从一开始,hsp60 mRNA水平的显着诱导结果(P <0.01)。 t0 240分钟的热应激与经典的调控机制不一致.hsf-1 mRNA水平显着升高从热应激10分钟开始,但是HSF-1蛋白没有同时增加,表明HSF-1不是Hsp60表达的唯一调节剂。

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