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白术乙醇提取物调节PPAR-γ信号通路促进小胶质细胞摄取及降解Aβ的作用机制研究
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| 篇名： | 白术乙醇提取物调节PPAR-γ信号通路促进小胶质细胞摄取及降解Aβ的作用机制研究 |
| TITLE： | Study on the promotion effect mechanism of ethanol extract from Atractylodes macrocephala on microglia phagocytosis and degradation of Aβ based on regulating PPAR-γ signaling pathway |
| 摘要： | 目的 基于过氧化物酶体增殖物激活受体γ（PPAR-γ）信号通路研究白术乙醇提取物（EEAM）促进小胶质细胞摄取及降解β淀粉样蛋白（Aβ）的作用机制。方法以小鼠神经小胶质细胞BV2为研究对象，采用激光共聚焦荧光显微镜观察EEAM（低、中、高剂量分别为0.3、0.4、0.5mg/mL，下同）对细胞摄取和降解Aβ的影响；利用人胚胎肾细胞HEK293考察EEAM对PPAR-γ萤光素酶转录活性的影响；采用免疫荧光法考察EEAM对PPAR-γ核移位的影响；以Aβ1-42诱导阿尔茨海默病BV2细胞模型，并采用定量聚合酶链式反应法考察EEAM对PPAR-γ下游靶基因（Lxra、Lxrb、Abca1、Abcg1、Cd36、Sra和Apoe）mRNA表达的影响。结果Aβ摄取实验结果显示，经中、高剂量EEAM干预后，BV2细胞中Aβ荧光强度均显著升高（P＜0.05）；Aβ降解实验结果显示，经中、高剂量EEAM干预后，BV2细胞中Aβ荧光强度均显著降低（P＜0.05）。经各剂量EEAM干预后，HEK293细胞中PPAR-γ萤光素酶转录活性均显著升高（P＜0.05），BV2细胞中和细胞核中PPAR-γ蛋白的荧光强度（低剂量组除外）均显著升高（P＜0.05），BV2细胞中Lxra、Lxrb、Abca1、Abcg1、Cd36、Sra、ApoemRNA的表达水平均显著升高（P＜0.05）。结论EEAM可通过激活PPAR-γ信号通路，促进小胶质细胞对Aβ的摄取与降解作用，进而改善阿尔茨海默病。 |
| ABSTRACT： | OBJECTIVE To explore the effect mechanism of ethanol extract from Atractylodes macrocephala （EEAM） on microglial phagocytosis and degradation of amyloid β （Aβ） based on peroxisome proliferator-activated receptor γ （PPAR- γ） signaling pathway. METHODS Taking neuromicroglial cell BV2 as subjects， confocal microscopy was used to observe the effects of EEAM （0.3， 0.4， 0.5 mg/mL， similarly hereinafter） on phagocytosis and degradation of Aβ in microglia. Human embryonic kidney cell HEK293 was used to investigate the effects of EEAM on luciferase transcriptional activity of PPAR-γ. The effect of EEAM on nuclear translocation of PPAR-γ was investigated by immunofluorescence. Alzheimer’s disease BV2 cell model was induced by Aβ1-42， and quantitative polymerase chain reaction was used to investigate the effects of EEAM on mRNA expressions of PPAR-γ downstream target genes （Lxra， Lxrb， Abca1， Abcg1， Cd36， Sra and Apoe）. RESULTS The results of Aβ uptake experiment showed that after the intervention of medium and high doses of EEAM， fluorescence intensity of Aβ in BV2 cells increased significantly （P＜0.05）. The degradation experiment of Aβ showed that after the intervention of medium and high doses of EEAM， fluorescence intensity of Aβ in BV2 cells decreased significantly （P＜0.05）. After the intervention of different doses of EEAM， luciferase transcriptional activity of PPAR-γ in HEK293 cells increased significantly （P＜0.05）； fluorescence intensity of PPAR-γ in BV2 cells and nuclei （except for low-dose group） increased significantly （P＜0.05）. mRNA expressions of Lxra， Lxrb， Abca1， Abcg1， Cd36， Sra and Apoe in BV2 cells were increased significantly （P＜0.05）. CONCLUSIONS EEAM can promote the uptake and degradation of Aβ in microglia by activating PPAR-γ signaling pathway， thus improving Alzheimer’s disease. |
| 期刊： | 2023年第34卷第01期 |
| 作者： | 初双；吴延娆；吴丽敏；崔正浩；王潘；孙意冉；谢治深；张振强 |
| AUTHORS： | CHU Shuang，WU Yanrao，WU Limin，CUI Zhenghao，WANG Pan，SUN Yiran，XIE Zhishen，ZHANG Zhenqiang |
| 关键字： | 白术乙醇提取物；过氧化物酶体增殖物激活受体 γ；小胶质细胞；β淀粉样蛋白；阿尔茨海默病 |
| KEYWORDS： | ethanol extract from Atractylodes macrocephala； |
| 阅读数： | 202 次 |
| 本月下载数： | 12 次 |
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