丹皮酚对ox-LDL诱导的大鼠血管内皮细胞黏附功能的抑制作用

目的:研究氧化型低密度脂蛋白(ox-LDL)对体外培养的大鼠单核细胞(MC)与大鼠主动脉内皮细胞(RAECs)黏附的影响及丹皮酚(Pae)含药血清对其的抑制作用.方法:制备Pae含药血清并用RP-HPLC测定血清中Pae含量;改良沉淀法分离大鼠血清低密度脂蛋白(LDL),Cu2 氧化制备ox-LDL;组织块预消化贴壁法培养RAECs;大鼠淋巴细胞分离液分离单核细胞;孟加拉玫瑰红活细胞染色法测定MC与RAECs的黏附功能.结果:ox-LDL在25～400 mg/L时呈剂量依赖性地诱导MC与RAECs的黏附,100 mg/L时促MC与RAECs黏附达最大值;ox-LDL与RAECs共育1 h即可明显促进黏附作用,3 h时达最大诱导效应.Pae含药血清在浓度为1.8～4.2 mg/L时,呈剂量依赖性地抑制ox-LDL诱导的黏附作用;4.2 mg/L孵育24 h时抑制作用最明显.结论:Pae对ox-LDL诱导的大鼠MC与RAECs黏附功能有抑制效应,Pae对ox-LDL介导的血管内皮细胞炎症环节的影响是其抗AS的作用机制之一.

Inhibitory Effect of Paeonal on ox-LDL Induced Adhesion Reaction of Rat Vascular Endothelial Cells

objective: To study the inhibitory effects of Paeonal(Pae) contained serum on oxidized low density lipoprotein(ox-LDL) induced adhesion reaction of monocytes(MC) with cultured rat aortic endothelial cells(RAECs) in vitro.Methods: Pae contained serum was prepared and its concentration was detected by reversed-phase high performance liquid chromatography(RP-HPLC).Serum LDL in healthy rat was separated by precipitate method and oxidized by Cu2 .Advanced digestion of explant primary cultured RAECs in vitro, MC was separated by rat lymphocyte separation medium.The adhesion reaction of MC with RAECs was detected using Rose Bengal stain.Results: With concentration from 25 to 400 mg/L,ox-LDL was shown to induce adhesion reaction of MC with RAECs in a dose-dependent manner.The effect of ox-LDL reached maximum at 100 mg/L.After 1 h incubation with RAECs,ox-LDL significantly induced the adhesion reaction of MC with RAECs,after 3 h incubation the effect reached maximum.With concentration from 1.8 to 4.2 mg/L,Pae contained serum was shown to inhibit adhesion reaction of MC with RAECs in a dose-dependent manner induced by ox-LDL for 3 h.The inhibition effect of Pae contained serum reached maximum at 4.2 mg/L,after 24 h incubation the effect reached maximum.Conclusion: Pae can inhibit the adhesion reaction of MC with RAECs induced by ox-LDL.Pae influenced component element of vascular endothelial cell inflammation mediated by ox-LDL,which is one of the mechanisms of action for antiatherosclerosis.