摘要
Objective To investigate the protective effect of apo lipoprotein (apo) AⅠ, AⅡ, CⅠ and CⅡ, the main proteins in high density lipoprotein (HDL), on the morphology and function of human umbilical vein endothelial cells injured with low density lipoprotein (LDL) in vitro. Methods Cultured human endothelial cells derived from umbilical veins were exposed to LDL, HDL, and apoAⅠ, AⅡ, CⅠ and CⅡ. The morphology of endothelial cells was examined with phase contrast and transmission electron microscope. The released amount of lactate dehydrogenase (LDH) and 6 keto prostaglandin F1α (PGF1α) was also measured. Results Endothelial cells after being injured by LDL showed cell contraction, increased release of LDH and decreased secrection of prostacyclin (PGI2). However, the addition of HDL, and apoAⅠ, AⅡ, CⅠ and CⅡ before incubation with LDL inhibited the cellular injury induced by LDL as demonstrated by lowered LDH release, increased level of PGF1α and prevention of morphological changes. Conclusion The results indicate that apoAⅠ, AⅡ, CⅠ and CⅡ, as well as HDL, may play an important role in combating atherogenesis by protecting endothelial cells from damages induced by LDL.
Objective To investigate the protective effect of apo lipoprotein (apo) AⅠ, AⅡ, CⅠ and CⅡ, the main proteins in high density lipoprotein (HDL), on the morphology and function of human umbilical vein endothelial cells injured with low density lipoprotein (LDL) in vitro. Methods Cultured human endothelial cells derived from umbilical veins were exposed to LDL, HDL, and apoAⅠ, AⅡ, CⅠ and CⅡ. The morphology of endothelial cells was examined with phase contrast and transmission electron microscope. The released amount of lactate dehydrogenase (LDH) and 6 keto prostaglandin F1α (PGF1α) was also measured. Results Endothelial cells after being injured by LDL showed cell contraction, increased release of LDH and decreased secrection of prostacyclin (PGI2). However, the addition of HDL, and apoAⅠ, AⅡ, CⅠ and CⅡ before incubation with LDL inhibited the cellular injury induced by LDL as demonstrated by lowered LDH release, increased level of PGF1α and prevention of morphological changes. Conclusion The results indicate that apoAⅠ, AⅡ, CⅠ and CⅡ, as well as HDL, may play an important role in combating atherogenesis by protecting endothelial cells from damages induced by LDL.
