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目的观察硒与丹参酮ⅡA磺酸钠合用对家兔心肌缺血再灌注损伤心肌组织脂质过氧化的影响。方法将26只家兔随机分成4组,即假手术组、缺血再灌注组、丹参酮ⅡA磺酸钠组(DS-201)和硒+DS-201组。分别检测血浆CK、LDH含量和心肌组织的SOD、GSH-Px活力、MDA含量。结果DS-201组、硒+DS-201组血浆中CK、LDH含量和心肌组织MDA含量与缺血再灌注组相比均显著降低(P<0.01);硒+DS-201组与DS-201组相比。血浆CK、LDH含量和心肌组织MDA含量显著降低(P<0.01)。DS-201组、硒+DS-201组心肌组织匀浆中T-SOD活力与缺血再灌注组相比均显著升高(P<0.05),但硒+DS-201组与DS-201组相比,心肌组织匀浆中T-SOD活力没有显著性差异。DS-201组与缺血再灌注组相比心肌组织中GSH-Px活力无显著性差异。但硒+DS-201组心肌组织中GSH-Px活力与缺血再灌注组(P<0.01)、DS-201组(P<0.01)及假手术组(P<0.05)相比,均显著升高。结论硒与丹参酮ⅡA磺酸钠合用对家兔心肌缺血再灌注损伤具有明显的保护作用,并且优于丹参酮ⅡA磺酸钠。其作用机制与提高SOD、GSH-Px活性,清除自由基,抑制脂质过氧化反应有关。
Objective To observe the effect of selenium combined with sodium tanshinone Ⅱ A sulfonate on myocardial lipid peroxidation in rabbits with myocardial ischemia reperfusion injury. Methods Twenty-six rabbits were randomly divided into 4 groups: sham operation group, ischemia-reperfusion group, sodium tanshinone Ⅱ A sulfonate group (DS-201) and selenium + DS-201 group. Plasma CK and LDH contents, SOD, GSH-Px activities and MDA contents in myocardium were measured respectively. Results The contents of CK, LDH and MDA in DS-201 group and selenium + DS-201 group were significantly lower than those in ischemia-reperfusion group (P <0.01) Group compared. Plasma CK, LDH levels and myocardial MDA content decreased significantly (P <0.01). The activities of T-SOD in myocardial tissue of DS-201 group and selenium + DS-201 group were significantly increased compared with ischemia-reperfusion group (P <0.05) There was no significant difference in T-SOD activity in myocardial homogenate. There was no significant difference of GSH-Px activity in myocardium between DS-201 group and ischemia-reperfusion group. However, GSH-Px activity in myocardium of selenium + DS-201 group was significantly higher than that in ischemia-reperfusion group (P <0.01), DS-201 group (P <0.01) and sham operation group high. Conclusion Selenium combined with sodium tanshinone Ⅱ A sulfonate has obvious protective effect on myocardial ischemia-reperfusion injury in rabbits and is superior to tanshinone Ⅱ A sodium sulfonate. Its mechanism of action and increase SOD, GSH-Px activity, scavenging free radicals, inhibition of lipid peroxidation.