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目的考察缺氧对心肌细胞摄取脂质体的影响,并对其机制进行探讨。方法利用心肌细胞原代培养技术分离培养乳鼠心肌细胞,将膜荧光标记的脂质体与心肌细胞分别在常氧与缺氧条件共同培养不同时间,用荧光分光光度计测定细胞摄取的荧光脂质体的量,对缺氧对心肌细胞摄取脂质体的影响进行考察。结果与常氧状态相比较,缺氧1h心肌细胞对脂质体的摄取增加了20%,而缺氧2h心肌细胞对脂质体的摄取减少了18%。结论脂质体可以保护心肌细胞,减低缺氧带来的损伤,在短时间内处于缺氧状态的心肌细胞对脂质体的摄取显著增加,而继续缺氧导致的心肌细胞膜的损伤使心肌细胞对脂质体的摄取减少。
Objective To investigate the effect of hypoxia on cardiomyocyte uptake of liposomes, and to explore its mechanism. Methods Primary cultured cardiomyocytes were used to culture cardiomyocytes isolated from neonatal rat cardiomyocytes. Fluorescent labeled liposomes and cardiomyocytes were incubated with normoxia and hypoxia for different time. Fluorescence spectrophotometer The amount of plastids investigated the effect of hypoxia on uptake of liposomes by cardiomyocytes. Results Compared with normoxia state, the uptake of liposomes increased by 20% in hypoxia 1h and up to 18% in hypoxia 2h cardiomyocytes. Conclusion Liposomes can protect cardiomyocytes and reduce the damage caused by hypoxia. The uptake of liposomes by hypoxic cardiomyocytes in hypoxia state increased significantly in a short time, while the myocardial cell membrane damage caused by hypoxia continued to make myocardial cells Reduced liposome uptake.