首页|阿魏酸对M2型巨噬细胞极化的抗炎机制研究

阿魏酸对M2型巨噬细胞极化的抗炎机制研究

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目的 对阿魏酸进行体外抗炎活性及机制研究。方法 在适宜条件下构建M2型巨噬细胞体外炎症模型。采用CCK-8法测M2型巨噬细胞活性,采用流式细胞术测M2型巨噬细胞的极化程度,采用酶联免疫吸附法(ELISA)和实时荧光定量PCR法测M2型巨噬细胞分泌产物转化生长因子-β1(TGF-β1)、IL-10的蛋白和mRNA表达水平;采用蛋白质免疫印迹法(Western blot)测M2型巨噬细胞p38 MAPK、NF-κB p65蛋白的表达水平。结果 在阿魏酸的作用下,CD206+M2型巨噬细胞数量显著增多,M2型巨噬细胞TGF-β1、IL-10的蛋白和mRNA表达水平上升,M2型巨噬细胞中p-p38 MAPK和p-NF-κB p65的蛋白表达水平明显升高,上述作用均呈剂量依赖性。结论 阿魏酸促进M0型巨噬细胞向M2型极化,提高抗炎因子的表达,其抗炎机制与促进M2型巨噬细胞中p38 MAPK和NF-κB p65信号通路活化有关。
Anti-inflammatory Mechanism Research of Ferulic Acid on M2 Polarization of Macrophages
OBJECTIVE To study the in vitro anti-inflammatory activity and mechanism of ferulic acid.METHODS Establishing the in vitro M2 type macrophages inflammation model under the suitable condi-tion.CCK-8 method was used to detect the activity of M2 macrophages.Flow cytometry was used to detect the polari-zation of M2 macrophages.ELISA and real-time quantitative PCR were used to detect the mRNA and protein expres-sion of transforming growth factor-β1(TGF-β1)and interleukin-10(IL-10)by M2 type macrophages.Western blot was used to detect the expression of p38 MAPK and NF-κB p65.RESULTS Under ferulic acid treatment,the ex-pression of M2 type macrophage marker CD206+was significantly decreased,the expression of TGF-β1,IL-10,p-p38 MAPK and p-NF-κB p65 on M2 type macrophages were significantly promoted in a dose-dependent man-ner.CONCLUSION Ferulic acid can promote the polarization of M0 macrophages towards M2 type and promote the expression of anti-inflammatory factors,which is related to the promotion of p38 MAPK and NF-κB signaling pathway.

Ferulic acidMacrophagesp38 MAPKNF-κB p65Inflammation

张雯雯、韦子强、罗文汇、林少杰、李沐真、郭嘉亮、王春华、谢倩、刘正、曾煦欣

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佛山科学技术学院,广东佛山 528000

广东一方制药有限公司,广东佛山 528000

佛山市药学会,广东佛山 528000

阿魏酸 巨噬细胞 p38 MAPK NF-κB p65 炎症

2024

海峡药学
中国药学会福建分会

海峡药学

影响因子:0.643
ISSN:1006-3765
年,卷(期):2024.36(10)