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中国临床药理学与治疗学 ›› 2020, Vol. 25 ›› Issue (7): 728-733.doi: 10.12092/j.issn.1009-2501.2020.07.002

• 基础研究 • 上一篇    下一篇

芝麻酚调控巨噬细胞极化改善肥胖小鼠脂肪组织炎症及胰岛素抵抗

孔祥1,2,华强1,姚新明1,孟祥健1,钟民2,郭莉群3   

  1. 1皖南医学院第一附属医院 弋矶山医院内分泌科,芜湖 241001,安徽; 2皖南医学院第一附属医院 弋矶山医院中心实验室,芜湖 241001,安徽; 3皖南医学院药学院药理学教研室,芜湖 241002,安徽
  • 收稿日期:2020-04-03 修回日期:2020-06-24 出版日期:2020-07-26 发布日期:2020-07-31
  • 通讯作者: 郭莉群,通信作者,女,硕士,副教授,研究方向:心血管及内分泌药理。 Tel: 0553-3932464 E-mail: wy_glq@163.com
  • 作者简介:孔祥,男,博士,副教授,副主任医师,研究方向:糖尿病及其并发症的发病机理及防治。 Tel: 0553-5739856 E-mail: wnmcyaolikx@sina.com
  • 基金资助:
    国家自然科学基金(81970699);弋矶山医院引进人才科研基金项目(YR202014);弋矶山医院“高峰”培育计划项目(GF2019J04)

Sesamol improves inflammation and insulin resistance in adipose tissue of obese mice by regulating macrophage polarization

KONG Xiang 1,2, HUA Qiang 1, YAO Xinming 1, MENG Xiangjian 1, ZHONG Min 2, GUO Liqun 3   

  1. 1 Department of Endocrinology, Yijishan Hospital, the First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui, China; 2 Department of Central Laboratory, Yijishan Hospital, the First Affiliated Hospital of Wannan Medical College, Wuhu 241001, Anhui, China; 3 Department of Pharmacology, School of Pharmacy, Wannan Medical College, Wuhu 241002, Anhui, China
  • Received:2020-04-03 Revised:2020-06-24 Online:2020-07-26 Published:2020-07-31

摘要: 目的:探讨芝麻酚能否通过调控巨噬细胞极化改善肥胖小鼠脂肪组织炎症及胰岛素抵抗。方法:建立高脂饲料喂饲的肥胖小鼠模型,灌服芝麻酚(100 mg/kg)8周,行腹腔糖耐量及胰岛素耐量试验后处死小鼠,测血脂和胰岛素水平。免疫印迹检测附睾脂肪组织P-AKT和P-JNK蛋白表达。脂肪组织切片行F4/80及Cd11c免疫组化及免疫荧光染色。实时荧光定量PCR测脂肪组织细胞因子及趋化因子mRNA表达。结果: 芝麻酚治疗后降低肥胖小鼠体质量及血脂水平,改善糖耐量损伤及胰岛素抵抗。芝麻酚治疗组小鼠脂肪组织巨噬细胞浸润减少,P-AKT表达恢复,P-JNK表达降低,M1型巨噬细胞标志物(Cd11c、iNOS、TNF-α和IL-6)mRNA表达减少,M2型标志物(Chi3l3、Arg1和Mgl1)mRNA表达增加。结论:芝麻酚减轻肥胖小鼠脂肪组织炎症和胰岛素抵抗,其作用与芝麻酚抑制脂肪组织JNK信号通路,改善巨噬细胞极化失衡状态有关。

关键词: 芝麻酚, 肥胖小鼠, 巨噬细胞极化

Abstract: AIM: To investigate whether sesamol could improve inflammation and insulin resistance in adipose tissue of obese mice by regulating macrophage polarization. METHODS: An obese animal model was established in mice by inducing obesity with high-fat diet. The obese mice were administrated with sesamol (100 mg/kg) for 8 weeks. The mice were sacrificed after the intraperitoneal glucose tolerance test and insulin tolerance test, and the plasma lipid and insulin levels were measured. The expression of p-Akt and p-JNK in adipose tissue of epididymis was detected by Western blotting. F4/80 and Cd11c immunohistochemistry and immunofluorescence staining were performed on the adipose tissue sections. The mRNA expression of cytokines and chemokines in adipose tissue was measured by Real-time fluorescence quantitative PCR. RESULTS: Sesamol treatment reduced body weight and lipid level of obese mice, improved glucose tolerance and insulin resistance. In sesamol treated group, macrophage infiltration in adipose tissue was decreased, p-Akt expression was enhanced, p-JNK expression was reduced, mRNA expression of M1 type of macrophage markers (Cd11c, iNOS, TNF-α and IL-6) was down-regulated, mRNA expression of M2 type markers (chi3l3, Arg1 and Mgl1) was up-regulated. CONCLUSIONS: sesamol could alleviate inflammation and insulin resistance in adipose tissue of obese mice. These effects maybe associated with inhibition of JNK signal pathway and improvement of polarization imbalance of macrophages in adipose tissue.

Key words: sesamol, obese mice, macrophage polarization

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