| 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） |
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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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