First Affiliated Hospital of Shihezi University, Shihezi, 832000, China.
College of pharmacy, Shihezi University, Shihezi, 832000, China.
Cell Biochem Biophys. 2024 Sep;82(3):2297-2319. doi: 10.1007/s12013-024-01341-6. Epub 2024 Aug 22.
This study established an LPS-induced RAW264.7 macrophage inflammatory injury model and an AS mouse vulnerable plaque model to observe the effect of JPHYP on macrophage inflammation, plaque formation, blood lipids, inflammation levels, intestinal flora and the influence of TLR4/MyD88/MAPK pathway, and explore the anti-AS effect and molecular mechanism of JPHYP, and detected 16S rRNA of mice intestinal microbes. The difference of intestinal flora in different groups of mice was compared to further explore the intervention effect of JPHYP and clarify the molecular biological mechanism of JPHYP in preventing and treating AS by regulating TLR4/MyD88/MAPK inflammatory signaling pathway and improving intestinal flora.
本研究建立了 LPS 诱导的 RAW264.7 巨噬细胞炎症损伤模型和 AS 小鼠易损斑块模型,观察 JPHYP 对巨噬细胞炎症、斑块形成、血脂、炎症水平、肠道菌群及 TLR4/MyD88/MAPK 通路的影响,探讨 JPHYP 的抗 AS 作用及分子机制,并检测小鼠肠道微生物 16S rRNA。比较不同组别小鼠肠道菌群的差异,进一步探讨 JPHYP 的干预作用,阐明 JPHYP 通过调控 TLR4/MyD88/MAPK 炎症信号通路、改善肠道菌群来防治 AS 的分子生物学机制。