丹参多酚酸盐对高糖诱导的人脐静脉内皮细胞损伤的保护作用

目的探讨丹参多酚酸盐对体外高糖诱导人脐静脉内皮细胞损伤的保护作用及机制。方法将人脐静脉内皮细胞株分别培养在含5.5mmol/L葡萄糖(正常对照组)、30mmol/L葡萄糖(高糖损伤组)、30mmol/L葡萄糖±50mg/L丹参多酚酸盐(低剂量丹参多酚酸盐组)和30mmol/L葡萄糖±100mg/L丹参多酚酸盐(中剂量丹参多酚酸盐组)、30mmol/L葡萄糖 200mg/L丹参多酚酸盐(高剂量丹参多酚酸盐组)的培养基中培养48h,倒置相差显微镜观察细胞形态,并分别进行细胞活力、细胞培养上清液丙二醛含量、谷胱甘肽-过氧化物酶活力、一氧化氮和内皮素1分泌量的测定。结果高糖损伤组及低、中、高剂量丹参多酚酸盐组的细胞活力、丙二醛含量、谷胱甘肽-过氧化物酶活力、一氧化氮及内皮素1的分泌量与正常对照组比差异均有统计学意义(P<0.01);低、中、高剂量丹参多酚酸盐组的细胞活力、丙二醛含量、谷胱甘肽-过氧化物酶活力、一氧化氮及内皮素1的分泌量与高糖损伤组比差异均有统计学意义(P<0.01)。结论丹参多酚酸盐对体外高糖诱导的内皮细胞损伤具有保护作用,其作用机制可能通过保护细胞线粒体、清除活性氧、提高内皮细胞抗氧化酶体系的活力和抑制内皮素1的分泌而实现的。

Protective Effect of Salvianolate on Human Umbilical Vein Endothelial Cells Induced by High Glucose

Aim To investigate the protective effect of Salvianolate on the injury of human umbilical vein endothelial cells (HUVEC) induced by high glucose in vitro, and to explore its underlying mechanism. Method HUVEC were respectively cultured with 5.5 mmol/L glucose(Glu)(control group), 30 mmol/L Glu (high glucose injury group), 30 mmol/L Glu 50 mg/L Salvianolate (low dose Salvianolate group), 30 mmol/L Glu 100 mg/L Salvianolate (medium dose Salvianolate group), 30 mmol/L Glu 200 mg/L Salvianolate (high dose Salvianolate group) for 48 h. The morphous of cell was observed by inverted phase contrast microscope, and the cell viability as well as the activity of glutathione peroxidase (GSH-Px), malondialdehyde (MDA) content, the secretary content of nitric oxide(NO)and endothelin-1(ET-1), in supernatant were measured. Results In high glucose injury group, low dose Salvianolate group, medium dose Salvianolate group and high dose Salvianolate group, the cell viability, activity of GSH-Px and MDA content, secrete of ET-1 and NO were significantly different compared with those in control group(P<0.01); In low dose Salvianolate group, medium dose Salvianolate group and high dose Salvianolate group, the cell viability, activity of GSH-Px and MDA content, secrete of ET-1 and NO were significantly different compared with those in high glucose injury group(P<0.01). Conclusion The Salvianolate can protect HUVEC induced by high glucose in vitro, and the mechanism may be associated with scavenging reactive oxygen radicals, reducing lipid peroxidation, and increasing the activities of intracellular antioxidase, inhibiting the secrete of ET-1.