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本实验观察自由基发生系统(GSFR)对离体心脏和心肌细脂摄取~3H标记脂质体(DOPC/Chol/SA)的影响。结果发现GSFR使离体心脏脂质过氧化物MDA增加217.6％,同时,心脏摄取脂质俗的量增加55.9％,两者之间显著正相关(r=0.673,P<0.05)离体心肌细胞与GSFR孵育30分钟,细胞MDA含量增加4倍,而脂质体的摄取也增加48.9％。抗氧化剂维生索E能抑制GSFR的怍用,细胞MDA的含量和细胞摄取脂质体的量也明显减少。结果表明膜质脂过氧化促进心肌对脂质体的摄取,提示,膜脂质过氧化是缺氧、缺血及再灌法损伤时心肌摄取脂质体增加的可能机制之一。
In this study, we observed the effects of free radical generating system (GSFR) on uptake of ~ 3H labeled liposomes (DOPC / Chol / SA) in isolated heart and myocardial cells. The results showed that GSFR increased isolated heart lipid peroxidation MDA by 217.6%, meanwhile, the amount of lipid peroxidation in heart increased by 55.9%. There was a significant positive correlation between GSFR (r = 0.673, P <0.05) and isolated cardiomyocytes Incubation with GSFR for 30 minutes resulted in a 4-fold increase in cellular MDA content and uptake of liposomes by 48.9%. Antioxidant vitamin E can inhibit the use of GSFR, cell MDA content and the amount of liposome uptake was also significantly reduced. The results showed that membrane lipid peroxidation promoted myocardial uptake of liposomes, suggesting that membrane lipid peroxidation is one of the possible mechanisms of myocardial uptake of liposomes during hypoxia, ischemia and reperfusion injury.