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LPS刺激巨噬细胞产生IFN-β在抵御外来病原微生物的免疫反应中发挥重要作用。本研究探讨新抗生素S632A3促进LPS诱导巨噬细胞产生IFN-β及其分子机制。采用实时定量PCR检测mRNA含量,ELISA检测细胞因子含量,激酶分析检测GSK-3β活性,Western blotting检测蛋白磷酸化水平。结果表明:S632A3可显著促进LPS诱导的巨噬细胞产生IFN-β,其分子机制是抑制细胞内GSK-3β活性,降低转录因子c-Jun苏氨酸239位点的磷酸化并增加c-Jun稳定性。结果提示,S632A3是一个新的抗炎先导化合物,通过抑制GSK-3β活性促进LPS诱导巨噬细胞产生IFN-β。
LPS stimulates macrophages to produce IFN-β, which plays an important role in the immune response against foreign pathogenic microorganisms. This study investigated the new antibiotic S632A3 to promote LPS-induced macrophage IFN-β production and its molecular mechanisms. The content of mRNA was detected by real-time quantitative PCR, the content of cytokines was detected by ELISA, the activity of GSK-3β was detected by kinase analysis, and the protein phosphorylation was detected by Western blotting. The results showed that S632A3 could significantly enhance the production of IFN-β by LPS-induced macrophages, and its molecular mechanism was inhibition of intracellular GSK-3β activity, phosphorylation of threonine 239 site of transcription factor c-Jun and increase of c-Jun stability. The results suggest that S632A3 is a new anti-inflammatory lead compound that promotes LPS-induced production of IFN-β by macrophages by inhibiting GSK-3β activity.