Lutein attenuates Propionibacterium acnes-induced inflammation by inhibiting pyroptosis of human keratinocyte cells via TLR4/NLRP3/Caspase-1 pathway.
Abstract Source:Int Immunopharmacol. 2023年4月; 117：109937。 EPUB 2023 3月8日。PMID： 37012890 Haojun Xiong, Jingyi Yuan, Yuting Zhang, Lin Yang, Guishu Zhong, Xiang Li, Tingting Zhu
Article Affiliation:Yan Chen
Abstract:BACKGROUND: Previous studies found Propionibacterium acnes (P. acnes) has a strong association痤疮炎症和细胞凋亡。由于当前痤疮药物的各种副作用，重要的是要探索具有抗炎活性的替代药物对痤疮疟原虫。我们探索了叶黄素对痤疮诱导的细胞凋亡的影响，并加速了REC。体外和体内痤疮炎症的无效。
方法： lutein用于暴露HACAT角化形成细胞热杀死的痤疮P.处理的HACAT细胞。接下来，将活的痤疮痤疮室内注射到ICR小鼠的右耳中，以诱导痤疮炎症的小鼠，并研究了叶黄素对活疟原虫诱导的炎症的作用。 Moreover, we explored the mechanism of Lutein on TLR4/NLRP3/Caspase-1 pathways by ELISA, immunofluorescence microscopy, and western blot assay.
RESULTS: Heat-killed P. acnes triggered remarkable cell pyroptosis, pyroptotic inflammatory factors and HACAT细胞中的分解代谢酶，包括上调白介素（IL）-1β，IL-18，TNF-α，MMP3，MMP13，ADAMTS4和ADAMTS5，TLR4，TLR4，NLRP3燃气D与裂解的气蛋白D之比，而这些作用被叶黄素抑制。另外，叶黄素有效改善了耳朵发红，肿胀和TLR4，IL-1β和TNF-αin体内的表达。 Finally, NLRP3 activator (nigericin) increased caspase-1, IL-1βand IL-18 level, while TLR4 inhibitor (TAK-242) significantly blocked this effect in heat-killed P. acnes-treated cells.
CONCLUSIONS: Lutein attenuated P. acnes-caused Hacats的凋亡和随后通过TLR4/NLRP3/CASPASE-1途径的痤疮炎症。