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目的观察热应激诱导心肌热休克蛋白70(heat shock protein 70,HSP70)表达上调对兔快速心房起搏心肌Ca_v1.2,α1c的影响。方法 24只新西兰大白兔随机分为热应激起搏组、起搏组和假手术组,每组各8只。热应激起搏组先给予热应激,再以600次/min行右心房起搏6h,起搏组以600次/min行右心房起搏6h,假手术组仅植入电极不起搏。采用反转录-PCR检测各组心肌HSP70mRNA、Ca_v1.2,α1cmRNA表达水平,采用免疫组织化学法检测各组心肌HSP70和Ca_v1.2,α1c蛋白表达水平。结果热应激起搏组左心房、右心房、左心耳、右心耳HSP70 mRNA(1.37±0.26、1.35±0.30、1.28±0.21、1.31±0.24)和HSP70蛋白(69.75±3.45、69.00±2.93、68.63±3.23、68.75±2.82)表达水平较起搏组(HSP70mRNA为0.63±0.08、0.64±0.06、0.61±0.09、0.62±0.07,HSP70蛋白为39.75±2.82、37.00±3.85、39.00±3.89、38.38±2.92)和假手术组(HSP70mRNA为0.59±0.10、0.54±0.09、0.57±0.10、0.54±0.13,HSP70蛋白为39.00±3.21、38.38±3.74、37.75±3.28、39.00±4.00)明显增高(P<0.01),起搏组与假手术组比较差异无统计学意义(P>0.05);起搏组左心房、右心房、左心耳、右心耳Ca_v1.2,α1cmRNA(0.51±0.15、0.50±0.09、0.53±0.09、0.53±0.10)和Ca_v1.2,α1c蛋白(21.88±2.36、21.75±2.49、21.50±2.45、21.38±2.33)表达水平较热应激起搏组(Ca_v1.2,α1cmRNA为0.66±0.06、0.68±0.05、0.68±0.05、0.64±0.38,Ca_v1.2,α1c蛋白为26.00±2.73、25.25±1.83、25.13±2.03、25.38±2.00)和假手术组(Ca_v1.2,α1cmRNA为0.64±0.10、0.66±0.10、0.67±0.04、0.63±0.03,Ca_v1.2,α1c蛋白为26.75±3.37、26.63±1.85、26.50±3.07、26.13±3.91)明显降低(P<0.01),热应激起搏组与假手术组比较差异无统计学意义(P>0.05)。结论心肌HSP70表达上调后可抑制快速心房起搏心肌Ca_v1.2,α1c的重构。
Objective To investigate the effect of heat stress-induced up-regulation of heat shock protein 70 (HSP70) on Ca_v1.2 and α1c in rapid atrial pacing in rabbits. Methods Twenty-four New Zealand white rabbits were randomly divided into heat stress group, pacemaker group and sham operation group, with 8 rats in each group. The thermal stress group was given heat stress first, then the right atrial pacing was performed 600 times / min for 6 hours, the right atrial pacing was performed for 600 times / min in the pacing group for 6 hours, and the sham-operated group was implanted only with the electrode without pacing . The expressions of HSP70mRNA, Ca_v1.2 and α1cmRNA in each group were detected by RT-PCR. The expression of HSP70, Ca_v1.2 and α1c in myocardium were detected by immunohistochemistry. Results HSP70 mRNA (1.37 ± 0.26,1.35 ± 0.30,1.28 ± 0.21,1.31 ± 0.24) and HSP70 protein (69.75 ± 3.45,69.00 ± 2.93,68.63, P <0.01) in the left atrium, right atrium, ± 3.23, 68.75 ± 2.82) were significantly higher than that of pacing group (HSP70 mRNA was 0.63 ± 0.08,0.64 ± 0.06,0.61 ± 0.09,0.62 ± 0.07, HSP70 protein was 39.75 ± 2.82,37.00 ± 3.85,39.00 ± 3.89,38.38 ± 2.92 (P <0.01) and sham operation group (HSP70mRNA was 0.59 ± 0.10,0.54 ± 0.09,0.57 ± 0.10,0.54 ± 0.13, HSP70 protein was 39.00 ± 3.21,38.38 ± 3.74,37.75 ± 3.28,39.00 ± 4.00) , There was no significant difference between pacing group and sham operation group (P> 0.05). In the pacing group, Ca_v1.2, α1cmRNA (0.51 ± 0.15,0.50 ± 0.09,0.53 ± 0.09,0.53 ± 0.10) and Ca_v1.2, α1c protein (21.88 ± 2.36,21.75 ± 2.49,21.50 ± 2.45,21.38 ± 2.33) were significantly higher than those in heat stress group (Ca_v1.2, α1cmRNA was 0.66 ± 0.06, 0.68 ± 0.05,0.68 ± 0.05,0.64 ± 0.38, Ca_v1.2, α1c protein was 26.00 ± 2.73,25.25 ± 1.83,25.13 ± 2.03,25.38 ± 2.00) and sham operation group (Ca_v1.2, α1cmRNA was 0.64 ± 0.10, 0.66 ± 0.10, 0.67 ± 0.04, 0.63 ± 0.03, Ca_v1.2, α1c proteins were 26.75 ± 3.37,26.63 ± 1.85,26.50 ± 3.07,26.13 ± 3.91, P <0.01) There was no significant difference between group and sham operation group (P> 0.05). Conclusion The up-regulation of HSP70 can inhibit the remodeling of Ca1v1.2 and α1c in the atrial myocardium.