The purpose of this study was to explore the role and mechanism of transient receptor potential M(2) (TRPM(2)) in antigen-induced arthritis (AIA) mice. Twelve C57BL/6 mice and 12 TRPM(2) knockout mice were divided into 4 groups, includingwild type control group, wild type AIA group, TRPM(2) knockout control group and TRPM(2) knockout AIA group, with 6 mice in each group. Methylated bovine serum albumin (mBSA) was used to establish AIA mouse model. The degree of joint swelling and inflammatory cell infiltration were recorded, as well as synovial hyperplasia of the knee joints. Real-time quantitative polymerase chain reaction (PCR) was used to detect the expression of interleukin (IL)-6, IL-8, chemokine ligand 6 (CXCL-6) and tumor necrosis factor alpha (TNFα) mRNA in synovial cells of knee joints. The results showed that compared with the wild-type AIA group, the TRPM(2) knockout AIA group had more significant synovial proliferation and inflammatory cell infiltration in the synovial tissue.The neutrophil and macrophage counts rather than monocytes in the knee joints of TRPM(2) knockout AIA group were higher than those in wild-type AIA mice. The expression of IL-6, IL-8 and CXCL-6 mRNA were significantly increased in the knock out mice. In summary, TRPM(2) may inhibit inflammatory cytokines such as IL-6 and IL-8 in knee joints of AIA mice by reducing the infiltration of neutrophils and macrophages, the refore alleviates the manifestations of knee arthritis.
本研究初步探索瞬时受体电位M(2)（TRPM(2)）在抗原诱导关节炎（AIA）小鼠中的作用及机制。取C57BL/6小鼠12只，TRPM(2)基因敲除小鼠12只，分为野生型对照组、野生型AIA组、TRPM(2)基因敲除对照组、TRPM(2)基因敲除AIA组，每组6只。采用甲基化牛血清白蛋白（mBSA）建立野生型小鼠和TRPM(2)基因敲除小鼠AIA模型，进行小鼠膝关节肿胀程度、炎性细胞浸润、滑膜增生评分：实时荧光定量聚合酶链反应检测膝关节滑膜细胞白细胞介素（IL）-6、IL-8、趋化因子配体6（CXCL-6）、肿瘤坏死因子α（TNFα）mRNA表达。结果显示，与野生型AIA组小鼠比，TRPM(2)基因敲除AIA组小鼠膝关节肿胀更明显；膝关节滑膜细胞增生，滑膜组织炎性细胞浸润明显增加，膝关节中中性粒细胞、巨噬细胞计数升高，单核细胞无明显差异；IL-6、IL-8、CXCL-6 mRNA表达水平明显增加，TNFα mRNA表达无明显变化。TRPM(2)可通过减少AIA小鼠膝关节中性粒细胞和巨噬细胞的浸润，抑制小鼠膝关节IL-6、IL-8等炎性细胞因子表达，减轻AIA小鼠膝关节炎症状。.
Keywords: Antigen-induced arthritis; Arthritis, rheumatoid; Innate immunecells; Transient receptor potential M(2).