“凉血潜阳法”通过ABCF1调控巨噬细胞向M2型极化治疗银屑病血热证机制研究

银屑病迁延难愈，寻找有效治疗手段是临床研究热点。前期研究明确，“凉血潜阳法”代表方“凉血潜阳方”通过促进银屑病中巨噬细胞由发挥促炎作用M1型向发挥抑炎作用M2型极化治疗银屑病血热证疗效确切，但机制不明，可能与调控M1、M2型巨噬细胞间相互转化的关键因子有关。ABCF1可以同时调控MyD88依赖型（M1型极化）和非依赖型（M2型极化）信号通路调节巨噬细胞极化。预实验结果显示，银屑病巨噬细胞低表达ABCF1，凉血潜阳方能提高ABCF1表达。因此，我们提出假说：凉血潜阳方可能通过升高ABCF1，分别正、负向调控MyD88非依赖型和依赖型信号通路，促进巨噬细胞向M2型极化，减轻银屑病炎症。课题组拟通过体内外实验，采用流式分选、慢病毒转染、RT-qPCR、Western Blot、ELISA等技术进一步阐明凉血潜阳方促进巨噬细胞向M2型极化调控机制。为“凉血潜阳法”治疗银屑病血热证提供科学依据。

To discover an effective therapy for protracted psoriasis is a clinical research focus. Previous studies have shown that the representative prescription of “Cooling Blood and Restrain Yang method”, “Liangxue Qianyang Decoction” had proved effect on treatment of psoriasis with blood heat syndrome through modulating macrophages polarization from pro-inflammatory M1 phenotype to anti-inflammatory M2 phenotype, but the underline mechanism remains unknown. It may relate to regulation of the key molecule that modulating mutual transformation of macrophages between M1 and M2 state. ABCF1 regulates both MyD88-dependent (polarization to M1 phenotype) and independent (polarization to M2 phenotype) signaling pathways to regulate the polarization of macrophages. The preliminary experiment found that ABCF1 decreased in psoriatic macrophages, and “Liangxue Qianyang Decoction” increased the expression of ABCF1. Therefore, the applicant proposed a hypothesis that “Liangxue Qianyang Decoction” may promote macrophages polarization to M2 phenotype by increasing ABCF1, further positively and negatively regulating the independent and dependent signaling pathways of MyD88, and alleviating inflammation of psoriasis. Flow sorting, lentivirus transfection, RT-qPCR, Western Blot, ELISA technologies will be used to further clarify the regulation mechanism of “Liangxue Qianyang Decoction” promoting macrophages polarization to M2 phenotype in vivo and vitro experiments. The results will provide scientific basis for the treatment of psoriasis with blood heat syndrome by “Liangxue Qianyang Decoction”.