黄芩苷和京尼平苷联用对THP-1来源巨噬细胞极化和炎症的影响
Effect of Baicalin and Geniposide Combination on Polarization and Inflammation of THP-1-Derived Macrophages
DOI: 10.12677/ACM.2023.134936, PDF,    国家自然科学基金支持
作者: 韦亚琼, 胡雨蝶, 田维毅*:贵州中医药大学基础医学院,贵州 贵阳
关键词: 黄芩苷京尼平苷巨噬细胞极化炎症反应Baicalin Geniposide Macrophage Polarization Inflammatory Response
摘要: 目的:观察黄芩苷和京尼平苷联用对脂多糖(LPS)诱导人髓系白血病单核细胞(THP-1)来源巨噬细胞极化方向以及炎症反应的影响。方法:采用LPS诱导THP-1来源巨噬细胞极化与炎症,通过免疫荧光法检测M1型特征分子一氧化氮合酶(iNOS)的表达,ELISA法检测细胞上清白介素6 (IL-6)、肿瘤坏死因子α (TNF-α)水平。结果:与对照组比较,LPS组M1型巨噬细胞标志物一氧化氮合成酶(iNOS)均升高(P < 0.05);与LPS组比较,黄芩苷和京尼平苷联用组细胞iNOS蛋白表达均降低(P < 0.05)。与对照组比较,LPS组细胞上清炎症相关因子IL-6、TNF-α水平表达均升高(P < 0.05);与LPS组比较,黄芩苷和京尼平苷联用组细胞炎症相关因子IL-6、TNF-α水平均降低(P < 0.05)。结论:黄芩苷和京尼平苷联用可能通过抑制脂多糖(LPS)诱导THP-1来源巨噬细胞向M1型极化,改善炎症反应。
Abstract: Objective: To observe the effects of baicalin and geniposide combination on LPS-induced polariza-tion direction of THP-1-derived macrophages and inflammatory response. Methods: LPS was used to induce polarization and inflammation in THP-1-derived macrophages, and the expression of M1-type polarization marker Inducible Nitric Oxide Synthase (iNOS) was detected by immunofluo-rescence, and the levels of IL-6 and TNF-α in cell supernatants were measured by ELISA. Results: Compared with the control group, iNOS, a molecular marker of M1-type macrophages, was increased in the LPS group (P < 0.05). Compared with the LPS group, iNOS protein expression was decreased in both the baicalin and geniposide combination groups (P < 0.05). Compared with the control group, the expression of cellular supernatant inflammation-related factors IL-6 and TNF-α levels were increased in the LPS group (P < 0.05); compared with the LPS group, the levels of cellular in-flammation-related factors IL-6 and TNF-α were decreased in the baicalin and geniposide combina-tion group (P < 0.05). Conclusion: Baicalin and geniposide combination may improve the inflamma-tory response by inhibiting its polarization toward M1 type.
文章引用:韦亚琼, 胡雨蝶, 田维毅. 黄芩苷和京尼平苷联用对THP-1来源巨噬细胞极化和炎症的影响[J]. 临床医学进展, 2023, 13(4): 6692-6698. https://doi.org/10.12677/ACM.2023.134936

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