苯烯莫德对人外周血单个核细胞增殖、凋亡作用及对T细胞NF-κB的调节

Benvitimod Regulates Apoptosis of Human Peripheral Blood Mononuclear Cells and T Lymphocyte NF-κB Signaling

目的探讨苯烯莫德对人外周血单个核细胞(PBMC)增殖凋亡及T细胞核因子NF-κB的调节作用。方法提取健康志愿者外周血,密度梯度离心法分离单个核细胞,用CCK-8法测定苯烯莫德对人PBMC增殖的影响;用流式细胞法测定苯烯莫德对人PBMC凋亡的影响;用Western blot法检测活化的人T细胞核因子NF-κB p65,p-NF-κb p65,IKK,p-IKK,IκBα,p-IκBα蛋白表达的经时变化。结果苯烯莫德抑制人PBMC增殖的IC50为9.67μmol/L;苯烯莫德可诱导人PBMC的早期凋亡和晚期凋亡;苯烯莫德作用于活化的T细胞后,随着时间的延长,NF-κB通路中活化性因子p-NF-κB p65和p-IKK表达逐渐降低,而抑制性因子p-IκBα表达却逐渐升高,提示苯烯莫德对NF-κB通路为负向调节。结论苯烯莫德抑制人PBMC增殖,诱导其凋亡。苯烯莫德对T细胞NF-κB通路为负向调节。

Objective To study the effects of benvitimod on human peripheral blood mononuclear cell （PBMC） apopto- sis and I lymphocyte NF-KB signaling. Methods Human peripheral blood mononuclear cells were obtained from healthy volunteers through density gradient centrifuga/ion. PBMC proliferation was measured by cell counting Kit 8 （CCK8）. Cell apoptosis was detected by flow cytometry. NF-KB p65,p-NF-kB p65, IKK,p- IKK, IkBα,p-IKBα of the activated human T lymphocytes were measured by Western blot. Results Benviti- mod was indicated to inhibit PBMC proliferation with the IC50 being 9.67μmo1/L. Benvitimod could induce the early apoptosis and late apoptosis of human PBMC. Benvitimod down-regulated p-NF-KB p65 and p-IKK while up-regulated p-IkBα in human T lymphocytes. Conclusion Benvitimod could induce the apoptosis of human PBMC, and down-regulate T lymphocyte NF-kB signaling.