文章摘要
徐维佳,陈揭剑,严丽群,张 勇,王丽萍,庄永泽.黄芪甲苷对马兜铃酸诱导的巨噬细胞M1型极化的作用及机制研究[J].,2021,(6):1040-1045
黄芪甲苷对马兜铃酸诱导的巨噬细胞M1型极化的作用及机制研究
Effect of Astragaloside IV on Aristolochic Acid-induced M1-type Polarization of Macrophages and Its Mechanism Study
投稿时间:2020-08-28  修订日期:2020-09-22
DOI:10.13241/j.cnki.pmb.2021.06.009
中文关键词: 黄芪甲苷  马兜铃酸  巨噬细胞  M1型极化  p38 MAPK信号通路
英文关键词: Astragaloside IV  Aristolochic acid  Macrophages  M1-type polarization  p38 MAPK signaling pathway
基金项目:福建省自然科学基金面上项目(2017J01324);国家自然科学基金面上项目(81373837);福建省临床重点专科建设项目(闽卫医政函[2017]739号)
作者单位E-mail
徐维佳 中国人民解放军联勤保障部队第九〇〇医院肾脏病科 福建 福州 350025福建医科大学福总临床医学院 福建 福州 350004 xwj1707@163.com 
陈揭剑 中国人民解放军联勤保障部队第九〇〇医院肾脏病科 福建 福州 350025福建医科大学福总临床医学院 福建 福州 350004  
严丽群 福建医科大学福总临床医学院 福建 福州 350004  
张 勇 中国人民解放军联勤保障部队第九〇〇医院肾脏病科 福建 福州 350025福建医科大学福总临床医学院 福建 福州 350004  
王丽萍 中国人民解放军联勤保障部队第九〇〇医院肾脏病科 福建 福州 350025福建医科大学福总临床医学院 福建 福州 350004  
庄永泽 中国人民解放军联勤保障部队第九〇〇医院肾脏病科 福建 福州 350025福建医科大学福总临床医学院 福建 福州 350004  
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中文摘要:
      摘要 目的:探讨黄芪甲苷对马兜铃酸诱导的RAW264.7细胞向M1型极化的影响,并初步探索其可能的作用机制。方法:分别采用马兜铃酸和脂多糖(LPS)刺激RAW264.7细胞24 h,伴或不伴黄芪甲苷进行药物干预处理。采用细胞计数检测试剂盒-8(CCK 8)检测细胞活性变化,流式细胞仪检测巨噬细胞分型,酶联免疫吸附试验(ELISA) 检测细胞上清液中白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α) 的分泌量。反转录实时定量PCR(RT-qPCR)技术检测RAW264.7细胞IL-6、TNF-α mRNA表达。蛋白免疫印迹法(Western blot)检测RAW264.7细胞p-p38和p38 MAPK蛋白表达水平。结果:CCK8结果提示黄芪甲苷在5~50 μg/mL浓度范围对RAW264.7巨噬细胞无明显毒性,本研究选取10 μg/mL作为实验干预浓度。黄芪甲苷能够显著改善马兜铃酸诱导的巨噬细胞活性(P<0.05),同时减少IL-6和TNF-α的分泌水平和mRNA表达水平(均P<0.05),抑制马兜铃酸和LPS诱导的M1/M2巨噬细胞比例(P<0.05)。黄芪甲苷可部分抑制马兜铃酸诱导的巨噬细胞p38 MAPK磷酸化水平(P<0.05)。结论:黄芪甲苷可减少巨噬细胞M1型极化,降低炎症因子IL-6和TNF-α水平,减少巨噬细胞的活性,从而起到减缓马兜铃酸肾损害的作用,其作用机制可能与部分抑制p38 MAPK信号活性有关。
英文摘要:
      ABSTRACT Objective: To investigate the effect of astragaloside IV on the polarization of RAW264.7 cells induced by aristolochia acid to M1-type, and to explore its possible mechanism. Methods: Aristolocholic acid and Lipopolysaccharide (LPS) were used to stimulate RAW264.7 cells for 24 h successively, with or without astragaloside IV for drug intervention. Cell counting kit-8 (CCK-8) was used to detect the change of cell activity, flow cytometry was used to detect the type of macrophages, and enzyme-linked immunosorbent assay (ELISA) was used to detect the secretion of interleukin-6 (IL-6) and tumor necrosis factor - α (TNF-α) in cell supernatant. The expression of IL-6 and TNF-α mRNA in RAW264.7 cells were detected by real-time quantitative reverse transcription PCR (RT-qPCR). The protein expression levels of p-p38 and p38 MAPK in RAW264.7 cells were detected by Western blot. Results: The results of CCK8 indicated that astragaloside IV had no obvious toxicity to RAW264.7 macrophages in the concentration range of 5-50 μg/ mL, and 10 μg/ mL was selected as the experimental intervention concentration in this study. Astragaloside IV could significantly improve the increase of macrophage activity induced by aristolochic acid (P<0.05), and decreased the secretion and expression levels of IL-6, TNF-α and mRNA expression (all P<0.05), inhibit the increase of M1/M2 macrophage ratio induced by aristolochic acid and LPS (P<0.05). Astragaloside IV could partially inhibited the increased phosphorylation of p38 MAPK in macrophages induced by aristolochic acid (P<0.05). Conclusion: Astragaloside IV can reduce the M1-type polarization of macrophages, reduce the levels of inflammatory cytokines IL-6 and TNF-α, and reduce the activity of macrophages, thus playing a role in slowing the renal damage of aristolochian acid. The mechanism of action may be related to the partial inhibition of p38 MAPK signaling activity.
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