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电压门控钾通道Kv1.3和钙激活钾通道KCa3.1是单核/巨噬细胞上的两种钾通道。本文旨在研究阻断Kv1.3和KCa3.1钾通道对于单核/巨噬细胞增殖和趋化功能的影响。用趋化实验检测单核/巨噬细胞对Ly-6Chi单核细胞(炎症型单核细胞)的趋化作用,用CCK8试剂盒检测单核/巨噬细胞的增殖情况,用ELISA法检测趋化因子CCL7的浓度变化,用趋化实验检测趋化因子CCL2和CCL7对炎症型单核细胞的趋化作用。结果显示,结果显示,分别用KCa3.1特异性阻断剂TRAM-34和Kv1.3强效阻断剂Sh K阻断这两种钾离子通道后,单核/巨噬细胞对Ly-6Chi单核细胞的趋化能力降低;Sh K使单核/巨噬细胞增殖受到显著抑制。用TRAM-34和Sh K孵育过的Ly-6Chi单核细胞对CCL2的敏感性下降。以上结果提示,Kv1.3和KCa3.1钾通道在单核/巨噬细胞活化、增殖和趋化过程起重要作用,这两种钾通道有望成为自身免疫性疾病和急性心肌梗死后心肌重塑调节的靶点。
Voltage-gated potassium channel Kv1.3 and calcium-activated potassium channel KCa3.1 are two potassium channels on monocytes / macrophages. This article aims to investigate the effects of blocking Kv1.3 and KCa3.1 potassium channels on monocyte / macrophage proliferation and chemotaxis. The chemotaxis of monocytes / macrophages to Ly-6Chi monocytes (inflammatory monocytes) was detected by chemotaxis assay. The proliferation of monocytes / macrophages was detected by CCK8 kit, The chemotactic effects of chemokines CCL2 and CCL7 on inflammatory monocytes were detected by chemotaxis assay. The results showed that monocytes / macrophages were significantly inhibited by Ly-6Chi, a KCa3.1-specific inhibitor of TRAM-34 and Kv1.3 potent blocker ShK, respectively Monocyte chemotactic ability decreased; Sh K monocyte / macrophage proliferation was significantly inhibited. Ly-6Chi monocytes incubated with TRAM-34 and Sh K had a decreased sensitivity to CCL2. The above results suggest that Kv1.3 and KCa3.1 potassium channels play an important role in the activation, proliferation and chemotaxis of monocytes / macrophages, both of which are expected to become autoimmune diseases and myocardial remodeling after acute myocardial infarction Regulated target.