丹皮酚通过抑制NF-κB信号通路下调高脂血清诱导的人脐静脉内皮细胞黏附分子的表达

Paeonol reduces expression of adhesion molecules in HUVECs induced by hyperlipidemic serum via inhibiting the pathway of NF-κB signaling

目的:观察丹皮酚对高脂损伤人脐静脉内皮细胞(HUVECs)核因子-κB(NF-κB)的活化及细胞黏附分子表达的影响,探讨丹皮酚抗动脉粥样硬化的分子机制。方法:以培养HUVECs作为靶细胞,用高脂血清制备损伤模型。采用MTT法检测细胞活性;RT-PCR法检测NF-κB p65 mRNA的表达;Western blotting法检测κB抑制蛋白α(IκB-α)、细胞间黏附分子-1(ICAM-1)和E-选择素的蛋白表达。结果:丹皮酚能使高脂损伤的HUVECs存活率增加,形态趋于正常;降低NF-κB p65 mRNA的表达,提高IκB-α的表达;下调ICAM-1和E-选择素的蛋白表达。结论:丹皮酚通过抑制血管内皮细胞NF-κB/IκB通路,下调ICAM-1和E-选择素的表达,减少炎症反应,这可能是丹皮酚抗动脉粥样硬化的机制之一。

AIM： To observe the anti - atherosclerosis effect of paeonal（Pae） on the activation of NF - κB and the expression of cell adhesion molecules in human umbilical vein endothelial ceils（HUVECs） induced by hyperlipidemic serum. METHODS： Cultured HUVECs were used as target cells. Hyperlipidemic serum was added to the culture medium to establish the injury mode of HUVECs. Methyl thiazolyl tetrazolium（MTT） method was used to examine the cell viability. The mRNA expression of NF - KB 1365 was determined by RT - PCR. The protein levels of IKB - α, intercellular cell adhesion molecule - 1 （ ICAM - 1 ） and E - selectin were detected by Western blotting. RESULTS ： After treated with Pae, the cell viability was increased and the morphological changes of HUVECs injured by hyperlipidemic serum trended to normal. The expression of IKB - α in HUVECs injured by hyperlipidemic serum increased, while the expression of NF - κB p65 mRNA, ICAM - 1 and E - selectin protein was decreased. CONCLUSION： The anti - atherosclerosis mechanism of poeonal may be related to the inhibitory effect of the natural compound on the pathway of NF - κB/IKB, thereby reducing the expression of ICAM -1 and E -selectin and attenuating the inflammatory reaction in vasceilum.