| 唐玥，陈曼，初云惠，庞晓伟，秦川，田代实.共轭亚油酸通过PPARγ通路调控小胶质细胞的炎症表型[J].神经损伤功能重建,2022,17(10):563-566 |
| 共轭亚油酸通过PPARγ通路调控小胶质细胞的炎症表型 |
| Conjugated Linoleic Acid Regulates the Inflammatory Phenotype of Microglia via PPARγ Path⁃way |
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| DOI： |
| 中文关键词: 小胶质细胞 共轭亚油酸 PPARγ通路 炎症表型 |
| 英文关键词: microglia conjugated linoleic acid PPARγ pathway inflammatory phenotype |
| 基金项目:国家自然科学基金
（No. 82071380） |
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| 摘要点击次数: 1274 |
| 全文下载次数: 2006 |
| 中文摘要: |
| 目的：探究共轭亚油酸（CLA）对脂多糖（LPS）刺激的小胶质细胞炎症表型转化的作用及机制。方法：
①体外构建LPS刺激的小胶质细胞炎症模型，给予CLA处理24 h。②PPARγ抑制剂GW9662处理小胶质细
胞炎症模型，同时给予CLA处理。采用实时荧光定量PCR，免疫荧光的方法探究小胶质细胞的炎症表型转
化。结果：①与对照组相比，LPS刺激小胶质细胞后，促炎分子IL-6、iNOS、IL-1β和TNF-α转录水平较对照
组显著上调（均 P＜0.05）；小胶质细胞内促炎标志物 CD16/32 蛋白水平明显升高（P＜0.05），抗炎标志物
CD206水平明显降低（P＜0.05）。②与单纯LPS刺激相比，给予CLA处理后，小胶质细胞促炎基因被下调
（均P＜0.05），而抗炎基因上调（均P＜0.05）。③给与PPARγ抑制剂处理后，与CLA处理组相比，小胶质细胞
的促炎基因表达明显上调（均 P＜0.05），抗炎基因表达明显下调（均 P＜0.05）。结论：CLA 可能通过激活
PPARγ通路调控小胶质细胞由促炎表型向抗炎表型转化。 |
| 英文摘要: |
| To investigate the effect and mechanism of conjugated linoleic acid (CLA) on lipopolysaccharide (LPS)-stimulated microglia inflammatory phenotype transformation. Methods: (1) LPS-stimulated
primary microglia cells cultured in vitro were treated with CLA for 24 hours. (2) The PPARγ pathway was inhibited by selective antagonist GW9662, and cells were treated with CLA. The microglia inflammatory phenotype
transformation was observed by RT-qPCR and immunofluorescence. Results: (1) The mRNA transcription of
IL-6, iNOS, IL-1β, and TNF-α in LPS-stimulated microglia cells was markedly upregulated compared to that of
the control group (all P<0.05). Likewise, the protein level of CD16/32 was significantly increased (P<0.05) and
that of CD206 was significantly decreased (P<0.05) in the LPS group. (2) Compared to cells with only LPS stimulation, microglia cells with additional CLA treatment dramatically downregulated pro-inflammatory genes (all
P<0.05) but upregulated anti-inflammatory genes (all P<0.05). (3) The mRNA transcription and protein expression levels of pro-inflammatory markers in the LPS+CLA+GW9662 group were significantly higher than that of
the LPS+CLA group (all P<0.05), while the mRNA transcription and protein expression level of anti-inflammatory markers were significantly lower (all P<0.05). Conclusion: CLA may promote the transformation of
LPS-stimulated microglia from the pro-inflammatory to anti-inflammatory phenotype via the PPARγ pathway. |
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