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热休克反应对缺血 |
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谭红梅 吴伟康 罗汉川 梁天文
摘要 目的：探讨热休克反应对大鼠缺血-再灌心肌保护作用的可能机制。方法：SD大鼠，随机分为对照组及热休克组，动物经热休克处理恢复2或24 h后复制缺血再灌模型并进行各项检测。结果：①热休克处理后心肌组织内SOD活性显著高于对照组，MDA含量则显著低于对照组。②热休克组心肌组织内乳酸及ATP含量均显著高于对照组，糖原含量则显著低于对照组。③热休克反应能诱导HSP70i的转录。结论：热休克反应对缺血-再灌心肌的保护作用与心肌能量代谢的改善、抗氧化能力的增强以及HSP70i的转录合成增强有关。
主题词 热；休克；再灌注损伤；能量代谢；自由基
Mechanisms responsible for the effect of heat-shock response
on ischemia and reperfusion myocardium
TAN Hong-Mei，WU Wei-Kang，LUO Han-Chuan，LIANG Tian-Wen
Department of Pathophysiology,Sun Yat-sen University of Medical Sciences,Guangzhou (510089)
Abstract AIM: To explore mechanism of heat-shock (HS) response could protect ischemia/reperfusion rat heart in vitro and in vivo.METHODS:SD rats,randomly allocated into heat shock group and control group.The following parameters were examined: ① SOD and MDA,② glycogen,lactic acid and ATP,③Northern dot blot of inducible heat shock protein (HSP70i).RESULTS: ①The SOD activity of HS group is significantly higher than that of control group,and the MDA concentration of HS group is significantly lower than that of control group.②The concentration of lactic acid and ATP of HS group are significantly higher than that of control group,and the concentration of glycogen of HS group is significantly lower than that of control group.③The results of HSP70i mRNA Northern dot blot suggested that HSP70i gene of left ventricular of HS group expressed obviously at 2 hours after heat shock.After 24 hours of recovery,no detectable expression could be seen in HS group; while the control group was negative after 2 or 24 hours of recovery.CONCLUSION: The protective mechanism of heat shock response on ischemia and reperfusion injury may be related to the improving of antioxidation and energy metabolism and the increased expression of HSP70i gene.
MeSH Heat; Shock; Reperfusion injury; Energy metabolism; Free radicals
关于热休克反应对缺血-再灌心肌的保护作用已得到了一定的承认［1］，但保护作用的机制尚未[1] [2] [3] 下一页
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