【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。(2)PPARγ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、i NOS、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。更多还原

【Abstract】 Objective: 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.更多还原