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目的:探讨动脉粥样硬化中钾通道Kvl.3阻断剂抗hKvl.3E314抗体对巨噬细胞分化的影响。方法:培养THP-1单核细胞，给予佛波酷l00 μg/L诱导72 h使其分化为巨噬细胞。将巨噬细胞洗涤后重新接种在6孔板中，分为A组、B组和C组:A组加入LPS 10 ng/L和IFN-γ 20 μg/L诱导24 h使其分化；B组给予E314抗体(300 nmol/L)在37℃孵育2 h后加入LPS 10 ng/L和IFN-γ 20 μg/L诱导24 h使其分化；C组细胞不做任何处理。倒置相差显微镜下观察细胞形态学变化；流式细胞术鉴定巨噬细胞分型；ELLISA检测细胞上清液中IL-10、1L-12表达水平。结果:流式细胞术鉴定A组细胞iNOS抗体强阳性，为M1型，B组细胞CD206抗体强阳性，为M2型，C组流式结果为阴性ELLISA结果显示A组IL-12表达水平高于B组(P＜0.05)，A组IL-10表达水平低于B组(P＜0.05)。结论:体外诱导巨噬细胞分化，炎性因子促使其向M1型分化，具有促进炎症作用;加人Kvl.3通道阻断剂后，炎性因子同样诱导分化的巨噬细胞会向M2型抗炎方向发展。通过阻断巨噬细胞上的Kvl.3通道可以促进巨噬细胞向着具有抗炎作用的M2型巨噬细胞分化。
Objective: To investigate the effect of anti-hKvl.3E314 antibody against potassium channel Kvl.3 blocker on macrophage differentiation in atherosclerosis. Methods: THP-1 monocytes were cultured in vitro and induced to differentiate into macrophages by inducing with propofol l00 μg / L for 72 hours. The macrophages were washed and re-seeded into 6-well plates and divided into groups A, B and C: Group A was induced to differentiate by adding LPS 10 ng / L and IFN-γ 20 μg / L for 24 h; Group B The E314 antibody (300 nmol / L) was incubated for 2 h at 37 ℃, and then differentiated by adding LPS 10 ng / L and IFN-γ 20 μg / L for 24 h. Cells in group C were treated without any treatment. The morphological changes of cells were observed under inverted phase contrast microscope. The type of macrophages was identified by flow cytometry. The expression of IL-10 and IL-12 in supernatant was detected by ELLISA. Results: Flow cytometry showed that the iNOS antibody in group A was strongly positive, which was type M1. The CD206 antibody in group B was strongly positive for type M2. The flow cytometry was negative in group C. The results of ELLISA showed that the expression of IL-12 in group A was higher than B group (P <0.05). The expression of IL-10 in group A was lower than that in group B (P <0.05). CONCLUSION: Macrophage differentiation is induced in vitro. Inflammatory cytokines promote the differentiation of M1 macrophages and promote inflammation. After adding Kv1.3 channel blocker, the macrophages induced by inflammatory cytokines also induce M2-type The direction of inflammation. By blocking Kvl.3 channels on macrophages, macrophages can be promoted to differentiate toward anti-inflammatory M2 macrophages.