MFHAS1促进诱导M2型巨噬细胞极化减轻马兜铃酸诱导急性肾损伤的研究  

MFHAS1 Promoted the Polarization of M2 Macrophage to Alleviate Acute Renal Injury Induced by Aristolochic Acid

作　　者：张黎[1] 孙婧 邓秋芳 甘金城 叶茂 ZHANG Li;SUN Jing;DENG Qiufang;GAN Jincheng;YE Mao(Nanxishan Hospital of Guangxi Zhuang Autonomous Region,Guilin 541002,China)

机构地区：[1]广西壮族自治区南溪山医院,广西桂林541002

出　　处：《中国医学创新》2020年第4期6-11,共6页Medical Innovation of China

基　　金：广西壮族自治区卫生和计划生育委员会科研项目(Z20180561)。

摘　　要：目的:研究MFHAS1对M2型巨噬细胞极化的影响以及M2型巨噬细胞对马兜铃酸诱导的肾上皮细胞HK-2急性损伤的影响。方法:Real-time PCR检测MFHAS1 mRNA的表达,MTT法检测细胞存活率,流式细胞术检测细胞凋亡和M2型巨噬细胞表面胞膜分子CD86和CD206的表达,Western blot检测MFHAS1及M2型巨噬细胞中Arg1和MRC1蛋白的表达,ELISA检测巨噬细胞培养上清中IL-10的含量。结果:THP-1细胞中过表达MFHAS1可使M2型巨噬细胞的Arg1、IL-10和MRC1表达量均显著上升(P<0.05),同时M2型巨噬细胞表面胞膜分子CD206表达量显著上升(P<0.05),CD86的表达显著下降(P<0.05),即THP-1细胞中过表达MFHAS1可促进IL-13诱导巨噬细胞向M2型极化;M2型巨噬细胞能抑制马兜铃酸对HK-2细胞的凋亡诱导作用,提升细胞存活率。结论:过表达MFHAS1可促进IL-13诱导巨噬细胞向M2型极化,M2型巨噬细胞可抑制马兜铃酸对肾上皮HK-2细胞的凋亡诱导作用,提升细胞存活率,减轻细胞损伤。Objective:To investigate the effect of MFHAS1 on polarization of M2 macrophages and the effect of M2 macrophages on acute kidney injury of renal epithelial HK-2 cells induced by aristolochic acid.Method:Real-time PCR was carried out to detect the expression levels of MFHAS1 mRNA.MTT assay was applied to detect cell viability.Flow cytometry was used to detect apoptosis and the expression levels of CD86 and CD206 on the surface of M2 macrophages.Western blot was used to detect the protein expression levels of MFHAS1,Arg1 and MRC1.ELISA was applied to detect the content of IL-10 in the supernatant of macrophage culture.Result:Overexpression of MFHAS1 in THP-1 cells significantly increased the expression of Arg1,IL-10 and MRC1 of M2 macrophages (P<0.05),while the expression of CD206 on the surface of M2 macrophages significantly increased (P<0.05),and the expression of CD86 significantly decreased (P<0.05).In other words,the overexpression of MFHAS1 in THP-1 cells promoted the induction of IL-13 on polarization of M2 macrophages.M2-type macrophages inhibited the apoptosis induction effect of aristolosic acid on HK-2 cells and elevated the cell survival rate.Conclusion:Overexpression of MFHAS1 promotes the induction of IL-13 on polarization of M2 macrophages.M2 macrophages inhibits the apoptosis induction effect of aristolosic acid on renal epithelial HK-2 cells,improve cell survival rate and alleviates cell injury.

关 键 词：急性肾损伤 THP-1 HK-2 MFHAS1 马兜铃酸 M2型巨噬细胞 存活率 凋亡率 

分 类 号：R692[医药卫生—泌尿科学]