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目的:观察高密度脂蛋白(HDL)对氧化低密度脂蛋白(ox-LDL)抑制内皮细胞一氧化氮(NO)生成的保护作用,并探讨其与二甲基精氨酸二甲胺水解酶(DDAH)/非对称性二甲基精氨酸(ADMA)通路的关系。方法:Ox-LDL(100μg/ml)孵育人脐静脉内皮细胞(HUVECs)24小时或不同浓度的HDL(10、50、100μg/ml)预处理HUVECs细胞1小时,再与ox-LDL(100μg/ml)共孵育细胞24小时,收集细胞培养上清液检测NO、ADMA的浓度,收集内皮细胞检测DDAH-Ⅱ的mRNA和蛋白表达以及DDAH的活性。结果:Ox-LDL(100μg/ml)孵育HUVECs24小时后,细胞培养上清液中NO的浓度显著降低,ADMA水平显著增高,细胞内DDAH-Ⅱ的mRNA和蛋白表达以及DDAH的活性均显著降低。HDL(10、50、100μg/ml)可以拮抗ox-LDL(100μg/ml)的上述作用。结论:HDL能显著抑制ox-LDL诱导的内皮细胞NO产生减少,其保护作用与其调节DDAH/ADMA通路有关。
OBJECTIVE: To observe the protective effect of high density lipoprotein (HDL) on the nitric oxide (NO) production induced by ox-LDL in endothelial cells and to explore its relationship with dimethylarginine dimethylamine hydrolase (DDAH) / asymmetric dimethylarginine (ADMA) pathway. Methods: HUVECs were pretreated with ox-LDL (100μg / ml) for 24 hours or different concentration of HDL (10,50,100μg / ml) for 1 hour in HUVECs. ml) for 24 hours. The cell culture supernatants were collected to detect the concentration of NO and ADMA. The mRNA and protein expression of DDAH-Ⅱ and the activity of DDAH in endothelial cells were collected. Results: The concentration of NO was significantly decreased, the level of ADMA was significantly increased, the mRNA and protein expression of DDAH-Ⅱ and the activity of DDAH in HUVECs incubated with Ox-LDL (100μg / ml) for 24 hours were significantly decreased. HDL (10, 50, 100 μg / ml) antagonized the above effects of ox-LDL (100 μg / ml). CONCLUSION: HDL can significantly inhibit the NO production induced by ox-LDL in endothelial cells, and its protective effect is related to its regulation of DDAH / ADMA pathway.