%0 Journal Article
%T 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<br>Effect of Baicalin and Geniposide Combination on Polarization and Inflammation of THP-1-Derived Macrophages
%A 韦亚琼
%A 胡雨蝶
%A 田维毅
%J Advances in Clinical Medicine
%P 6692-6698
%@ 2161-8720
%D 2023
%I Hans Publishing
%R 10.12677/ACM.2023.134936
%X 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 &lt; 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 &lt; 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 &lt; 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 &lt; 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。<br />
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 &lt; 0.05). Compared with the LPS group, iNOS protein expression was decreased in both the baicalin and geniposide combination groups (P &lt; 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 &lt; 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 &lt; 0.05). Conclusion: Baicalin and geniposide combination may improve the inflamma-tory response by inhibiting its polarization toward M1 type.
%K 黄芩苷，京尼平苷，巨噬细胞极化，炎症反应<br>Baicalin
%K Geniposide
%K Macrophage Polarization
%K Inflammatory Response
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=64738