Curcumin prevents experimental autoimmune encephalomyelitis by inhibiting proliferation and effector CD4+ T cell activation.

姜黄素 流式细胞术 MTT法 克隆形成试验 细胞凋亡 分子生物学 生物 实验性自身免疫性脑脊髓炎 活力测定 T细胞 细胞生长 癌症研究 化学 免疫学 药理学 免疫系统 生物化学
作者
Liu Jq,Yan Yq,Liu Jt,Wang Yr,Xuepeng Wang
出处
期刊:PubMed [National Institutes of Health]
卷期号:23 (20): 9108-9116 被引量:17
标识
DOI:10.26355/eurrev_201910_19314
摘要

OBJECTIVE: Multiple sclerosis (MS) has affected over 2 million people worldwide and it is thought to be initiated by the activated central nervous system (CNS). Reactive CD4+ T cells (TH1, TH17, and Treg phenotypes) are crucial to MS. The TH1 phenotype can promote major histocompatibility complex-II expression and TH17 can induce inflammatory gene expression. Curcumin, a yellow pigment, is found in turmeric rhizomes and has been reported to have various activities, such as anti-proliferative and anti-inflammatory activity. Curcumin has great potential in MS treatment. Little is known about the effect of curcumin on MS. Therefore, we investigated the effect of curcumin on MS, especially on CD4+ T cells. MATERIALS AND METHODS: CD4+ T cells (TH1, TH17, and Treg cells) were cultured in Iscove's Modified Dulbecco's Medium (IMDM) medium. Cell proliferation was evaluated by MTT assay. The ability of individual CD4+ T cells to aggregate into viable colony clusters was assessed by clonogenic survival assay. Apoptosis of CD4+ T cells was determined by flow cytometry. The expression of Bcl-2, Bax, and active caspase-3 was detected by Western blotting. The effect of curcumin on the activation molecule was also evaluated by flow cytometry. RESULTS: MTT assay showed that curcumin significantly inhibited CD4+ T cell viability. Furthermore, TH1, TH17, and Treg all showed a dose-dependent but not time-dependent. The results of clonogenic survival assay revealed that curcumin markedly decreased the colony formation ability of CD4+ T cells. Flow cytometry results indicated that curcumin-induced remarkable apoptosis in TH1, TH17, and Treg cells. After treatment with curcumin, the expression of Bcl-2 was decreased and that of Bax and active caspase-3 was increased. Western blotting results also showed that curcumin-induced apoptosis in CD4+ T cells. Hence, our results demonstrated that curcumin inhibited CD4+ T cell proliferation via inducing apoptosis in CD4+ T cells. Meanwhile, flow cytometry results also showed that curcumin directly inhibited CD4+ T cell activation. CONCLUSIONS: Curcumin could inhibit CD4+ T cell proliferation and effector cell activation.
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