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目的:研究玉郎伞黄酮(FYLS)对大鼠离体心肌缺血再灌注损伤(I/R)心肌组织Na+-K+-ATP酶、Ca2+-ATP酶和凋亡蛋白的影响。方法:离体大鼠心脏采用Langendorff法灌流,停灌30 min再灌30 min造成I/R模型。测定心肌组织Na+-K+-ATP酶、Ca2+-ATP酶活性。同时观察药物对缺血再灌注后心肌组织病理形态、凋亡相关蛋白Bcl-2,Bax表达的影响。结果:FYLS高剂量(8×10-3g·L-1)可显著改善缺血-再灌注所致的心功能损伤,增加Na+-K+-ATP酶、Ca2+-ATP酶的活性;与模型组比较,FYLS高剂量组病理结果显示心肌组织受损程度明显减轻(P<0.05),且明显降低心肌Bax蛋白表达(P<0.01),对Bcl-2蛋白表达无明显影响,但能显著增加Bcl-2/Bax的比率(P<0.05)。结论:FYLS对I/R具有保护作用,其机制可能与减轻钙超载、下调Bax蛋白表达、增加Bcl-2/Bax的比率有关。
Objective: To investigate the effects of FYLS on Na + -K + -ATPase, Ca2 + -ATPase and apoptosis protein in isolated rat myocardial ischemia-reperfusion (I / R) myocardium. Methods: The isolated rat heart was perfused with Langendorff method and the I / R model was induced by 30 min reperfusion and 30 min reperfusion. The activity of Na + -K + -ATPase and Ca2 + -ATPase in myocardium was measured. At the same time, the effects of drugs on myocardial histopathology, expression of Bcl-2 and Bax in ischemia-reperfusion myocardium were observed. Results: FYLS high dose (8 × 10-3g · L-1) could significantly improve the cardiac function induced by ischemia-reperfusion and increase the activity of Na + -K + -ATPase and Ca2 + -ATPase. Compared with the model group (P <0.05), and significantly decreased the expression of Bcl-2 protein (P <0.01), but had no significant effect on the expression of Bcl-2 protein but significantly increased the expression of Bcl- 2 / Bax ratio (P <0.05). CONCLUSION: FYLS has a protective effect on I / R, and its mechanism may be related to the reduction of calcium overload, the down-regulation of Bax protein expression and the increase of Bcl-2 / Bax ratio.