[1]雷豆豆,何浩强,商怡丰,等.芒果苷对骨关节炎的潜在治疗机制:通过抑制巨噬细胞NF-κB调节巨噬细胞M2极化[J].中华老年骨科与康复电子杂志,2023,(01):33-38.[doi:10.3877/cma.j.issn.2096-0263.2023.01.007]
 Lei Doudou,He Haoqiang,Shang Yifeng,et al.Potential therapeutic mechanism of mangiferin for osteoarthritis: regulation of macrophage M2 polarization by inhibiting macrophages NF-κB[J].Chin J Geriatr Orthop Rehabil(Electronic Edition),2023,(01):33-38.[doi:10.3877/cma.j.issn.2096-0263.2023.01.007]
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芒果苷对骨关节炎的潜在治疗机制:通过抑制巨噬细胞NF-κB调节巨噬细胞M2极化()
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中华老年骨科与康复电子杂志[ISSN:1674-3911/CN:11-9292/R]

卷:
期数:
2023年01期
页码:
33-38
栏目:
关节炎
出版日期:
2023-02-05

文章信息/Info

Title:
Potential therapeutic mechanism of mangiferin for osteoarthritis: regulation of macrophage M2 polarization by inhibiting macrophages NF-κB
作者:
雷豆豆12何浩强12商怡丰12郑立13高明13
530021 南宁,广西医科大学再生医学与医用生物资源开发应用协同创新中心1,广西医科大学广西组织器官修复医用生物材料工程技术研究中心2;530021 南宁,广西医科大学第一附属医院3
Author(s):
Lei Doudou12 He Haoqiang12 Shang Yifeng12 Zheng Li13 Gao Ming13
1Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application, Guangxi Medical University, Nanning 530021, China; 2Guangxi Engineering Center in Biomedical Materials for Tissue and Organ Regeneration, Guangxi Medical University, Nanning 530021, China; 3First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China
关键词:
芒果苷 巨噬细胞 NF-κB通路 细胞极化 骨关节炎
Keywords:
Mangiferin Macrophages NF-κB pathway Cell polarization Osteoarthritis
DOI:
10.3877/cma.j.issn.2096-0263.2023.01.007
文献标志码:
A
摘要:
目的 芒果苷通过抑制巨噬细胞 NF-κB调节巨噬细胞极化为M2,探索芒果苷治疗骨关节炎的潜在机制。方法 RAW264.7小鼠巨噬细胞系进行体外培养,IL-4诱导巨噬细胞M2极化,用芒果苷对巨噬细胞进行干预。实验分为空白组、对照组和实验组。CCK-8检测芒果苷的细胞毒性。钙黄绿素(Calcein-AM)和碘化丙啶(PI)双荧光染色法检测细胞活性,流式细胞仪检测细胞凋亡的情况。免疫荧光染色评估甘露糖受体(CD206抗体)在巨噬细胞的分泌情况,实时荧光定量 PCR(qRT-PCR)法检测NF- κB通路相关基因RelA(p65)及M2巨噬细胞相关基因CD206、IL-10的表达情况。结果 浓度为20 μM的芒果苷对巨噬细胞无明显毒性作用,芒果苷在该浓度下能显著下调RelA的表达和上调IL-10、CD206的表达,从而抑制NF-κB通路激活巨噬细胞M2极化。结论 芒果苷能够抑制巨噬细胞NF-κB调节巨噬细胞极化为M2,M2巨噬细胞具有抗炎功能,促进软骨修复功能,为芒果苷在骨关节炎的研究中提供可能的机制理论。
Abstract:
Objective To investigate the effect of mangiferin on the treatment of osteoarthritis by inhibiting the NF-κB pathway and regulating the polarization of macrophages to M2. Methods The RAW264.7 mouse macrophage cell line was cultured in vitro, IL-4 induced M2 polarization of macrophages, and the macrophages were intervened with mangiferin. The experiment was divided into blank group, control group and experimental group. CCK-8 detected the cytotoxicity of mangiferin. Calcein-AM (calcein) and PI (propidium iodide) double fluorescent staining was used to detect cell viability, and flow cytometry was used to detect cell apoptosis. Immunofluorescence staining was used to evaluate the secretion of mannose receptor (CD206 antibody) in macrophages, and real-time quantitative PCR (qRT-PCR) was used to detect the NF-κB pathway-related gene RelA (p65) and M2 macrophage-related genes CD206, IL-10 expression. Results Mangiferin at a concentration of 20 μM had no significant toxic effect on macrophages, and mangiferin could significantly down-regulate the expression of RelA and up-regulate the expression of 1L-10 and CD206 at this concentration, thereby inhibiting the activation of M2 macrophages by the NF-κB pathway and thus alleviating arthritis in mice. Conclusions Mangiferin can inhibit the NF-κB pathway and regulate the polarization of macrophages to M2. M2 macrophages have anti-inflammatory functions and promote cartilage repair, which may provide a theoretical basis for new treatment of osteoarthritis.

备注/Memo

备注/Memo:
基金项目:广西科技基地和人才专项(桂科AD19254003)
更新日期/Last Update: 2023-03-30