地塞米松诱导热休克蛋白72减轻大鼠心肌缺血再灌注损伤

Heat Shock Protein 72 induced by Dexamethasone attenuates ischemia/reperfusion injury in rats heart

目的探讨地塞米松预处理诱导SD大鼠心肌热休克蛋白72(HSP72)表达对大鼠心肌缺血再灌注损伤的作用。方法将SD大鼠予地塞米松预处理,生理盐水预处理设为对照。预处理后构建缺血再灌注损伤动物模型。Westernblot法观察HSP72表达;动态观测缺血前及再灌注期间心功能、心律失常的变化;测定心肌梗塞面积及冠状动脉流出液肌酸激酶MB同工酶(CK-MB)的总量。结果与对照组相比,地塞米松预处理诱导大鼠心肌HSP72的表达显著增加(P<0.05);改善再灌注期间心功能(P<0.01);减少室性心律失常的积分(P<0.01);缩小心肌梗塞面积(P<0.01);降低冠状动脉流出液CK-MB的总量(P<0.05)。结论地塞米松作为新型HSP72诱导剂,上调HSP72表达,可减轻大鼠心肌缺血再灌注损伤。

[Objective] To explore the expression of the cardiac Heat Shock Protein 72 （HSP72） induced by Dexamethasone（DEX） pretreatment and its effects on ischemia/reperfusion injury in Spraque-Dawley rats heart. [Methods] The rats were pretreated with DEX before their hearts were separated for perfusion and for mimic isehemia/ reperfusion, sodium chloride served as control. HSP72 was examined by using western blotting. The left ventrieular functions and reperfusion arrhythmias were observed dynamically before ischemia and after 60 minute reperfusion following 30 minute isehemia. The hearts were perfused with TTC after 60 minute reperfusion. The myocardial infarct sizes were measured through Adobe Photoshop. The total amounts of CK-MB were analyzed by chemical methods. [Results] Compared with control group, the expression of HSP72 was significantly increased （P 〈0.05）, the left ventrieular functions （±dp/dtmax） were greatly improved （P 〈0.01）, the accumulated point of ventrieular arrhythmia was significantly reduced （P 〈0.01）, and the infarct size was significantly reduced （P 〈0.01）. Moreover, the total amount of CK-MB was significantly decreased （P〈0.05）. [Condusions] As a novel inducer of HSP72, DEX induces upregulation of HSP72, which functions to attenuate isehemia/reperfusion injury in rats heart.