摘要
目的评价内脂素对小鼠树突状细胞(DC)系DC2.4细胞的活化作用,探讨内脂素在动脉粥样硬化发病机制中的作用机理。方法将DC2.4细胞分4组:正常对照组、脂多糖组(LPS,1 mg/L)、低剂量内脂素组(100μg/L)、高剂量内脂素组(200μg/L)。流式细胞仪检测各组DC2.4细胞表面MHC-II类分子、CD86和CD80的表达,酶联免疫法检测各组细胞培养上清液肿瘤坏死因子α(TNF-α)与白细胞介素12(IL-12)水平的变化,通过混合淋巴细胞反应检测内脂素对同种异体T淋巴细胞的刺激能力。结果与对照组比较,低剂量内脂素组、高剂量内脂素组、脂多糖组细胞突触增多增粗,细胞体积增大,呈现成熟DC2.4细胞形态。细胞表面MHC-Ⅱ类分子、CD80和CD86分子表达水平增高,上清液的TNF-α、IL-12水平明显升高,差异有统计学意义(P<0.05)。与对照组比较,刺激细胞∶效应细胞的比例为1∶10和1∶25时,低剂量内脂素组、高剂量内脂素组和LPS组刺激指数明显升高(P均<0.05)。结论内脂素可能通过激活T淋巴细胞,启动免疫炎症反应,参与并促进动脉粥样硬化发生及发展。
Aim To study the effects of visfatin on the maturity of DC2.4 cells and the mechanism of visfatin in the pathogenesis of atherosclerosis. Methods The DC2. 4 cells were divided into four groups： normal control group,LPS group（ LPS,1 mg /L）,low-dose visfatin group（ 100 μg /L） and high-dose visfatin dose group（ 200 μg /L）. MHCII,CD86 and CD80 expression were detected by flow cytometry. Tumor necrosis factor-α（ TNF-α） and interleukin-12（ IL-12） levels in cell culture supernatant were measured by enzyme-linked immunosorbent assay. The ability of visfatin to stimulate allogeneic T lymphocytes was measured by mixed lymphocyte reaction assay. Results Compared with the control group,the synaptic of cells enlarged and cell volume increased in low-dose visfatin group,high dose visfatin group and LPS group. The levels of MHC-Ⅱ,CD80 and CD86 molecule expression increased,the supernatant TNF-α,IL-12 levels were significantly increased（ P〈0. 05）. Compared with the control group,when stimulating cell∶ effector cell ratio was 1∶ 10 and 1∶ 25,visfatin low dose group and high dose group and visfatin stimulation index LPS group was significantly higher（ P〈0. 05）. Conclusion The results suggested that visfatin could participate in the development of atherosclerosis by activating T lymphocytes and initiating the immune inflammation response.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2014年第8期795-798,共4页
Chinese Journal of Arteriosclerosis
基金
山东省卫生厅资助项目(2011HW094)
