| 引用本文:张鹏1，郭洁梅1，肖艳2，陈鹏1，张英杰1，刘俊1，陈雨1，邱梦婷2，苏友新1，2.壮骨健膝方对巨噬细胞极化的影响及作用机制研究[J].世界中医药,2024,(13):. |
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| 壮骨健膝方对巨噬细胞极化的影响及作用机制研究 |
| Effect and Mechanism of Zhuanggu Jianxi Formula on Macrophage Polarization |
| 投稿时间：2023-03-07 |
| DOI：10.3969/j.issn.1673-7202.2024.13.013 |
| 中文关键词: 壮骨健膝方 含药血清 膝骨关节炎 巨噬细胞极化 M1/M2型巨噬细胞 滑膜炎 THP-1源巨噬细胞 |
| English Keywords:Zhuanggu Jianxi Formula Drug-containing serum Knee osteoarthritis Macrophage polarization M1/M2 type macrophage Synovitis THP-1-derived macrophages |
| 基金项目:国家自然科学基金面上项目(81774347) |
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| 中文摘要: |
| 目的:探讨壮骨健膝方对巨噬细胞经典活化型(M1)/替代活化型(M2)极化的影响及作用机制。方法:佛波酯诱导人单核白血病细胞分化为非活化巨噬细胞(M0),脂多糖刺激M0复制M1极化模型,将细胞分为空白组(M0+空白血清)、模型组(M1+空白血清)、抑制剂组(M1+NF-κB抑制剂+空白血清)、壮骨健膝方组(M1+含药血清)。干预24 h后,检测各组M1标志分子诱导型一氧化氮合酶(iNOS)、主要组织相容性复合体Ⅱ(MHC-Ⅱ)、单核细胞趋化蛋白1(MCP-1),M2标志分子分化簇206、163、209(CD206、163、209)mRNA表达,炎症介质白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α),抗炎因子IL-4、IL-10水平及mRNA表达,核因子κB(NF-κB)信号通路中节点蛋白核内NF-κBp65、NF-κBp50及NF-κB抑制蛋白α(IκBα)表达。结果:模型组M1标志分子、炎症介质及NF-κBp65、NF-κBp50蛋白均高于空白组(P<0.05),CD206、IL-4 mRNA及IκBα蛋白,IL-4水平均低于空白组(P<0.05);抑制剂及壮骨健膝方组M1标志分子、炎症介质及NF-κBp65、NF-κBp50蛋白均低于模型组(P<0.05),M2标志分子、抗炎因子及IκBα蛋白均高于模型组(P<0.05);壮骨健膝方组MHC-Ⅱ、MCP-1 mRNA及炎症介质均低于抑制剂组(P<0.05),CD206、CD209、IL-10 mRNA及IL-4、IL-10水平均高于抑制剂组(P<0.05)。结论:壮骨健膝方可抑制脂多糖诱导的巨噬细胞M1极化,促进M2极化,其机制可能与降低细胞中NF-κB信号通路活性有关。 |
| English Summary: |
| To investigate the effect and mechanism of Zhuanggu Jianxi Formula(ZGJXF) on the polarization of macrophages into classical activation(M1) and alternative activation(M2) types.Methods:Phorbol 12-myristate 13-acetate was used to induce differentiation of human monocytic leukemia cells into non-activated macrophages(M0).Lipopolysaccharide was used to stimulate M0 to replicate the M1 polarization model.Cells were divided into a blank group(M0+blank serum)，a model group(M1+blank serum)，an inhibitor group(M1+NF-κB inhibitor+blank serum)，and a ZGJXF group(M1+medicated serum).After 24 hours of intervention，various indicators were measured，including M1 markers inducible nitric oxide synthase(iNOS)，major histocompatibility complex Ⅱ(MHC-Ⅱ)，monocyte chemotactic protein 1(MCP-1)，M2 markers CD206，CD163，CD209 mRNA expression，pro-inflammatory factors interleukin-1β(IL-1β)，tumor necrosis factor-α(TNF-α)，anti-inflammatory factors IL-4，IL-10 levels and mRNA expression，and key proteins in the NF-κB signaling pathway，such as nuclear NF-κBp65，NF-κBp50，and NF-κB inhibitor α(IκBα).Results:In the model group，M1 markers，pro-inflammatory factors，and NF-κBp65，NF-κBp50 proteins were significantly higher than those in the blank group(P<0.05)，while CD206，IL-4 mRNA，IκBα protein，and IL-4 levels were lower than those in the blank group(P<0.05).In the inhibitor and ZGJXF groups，M1 markers，pro-inflammatory factors，and NF-κBp65，NF-κBp50 proteins were lower than those in the model group(P<0.05)，while M2 markers，anti-inflammatory factors，and IκBα protein were higher than those in the model group(P<0.05).The ZGJXF group had lower levels of MHC-Ⅱ，MCP-1 mRNA，and pro-inflammatory factors than the inhibitor group(P<0.05)，and higher levels of CD206，CD209，IL-10 mRNA，IL-4，and IL-10(P<0.05).Conclusion:ZGJXF can inhibit lipopolysaccharide-induced M1 polarization of macrophages and promote M2 polarization.The mechanism may be related to the reduction of the activity of the NF-κB signaling pathway in cells. |
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