Department of Laboratory Medicine, The Fourth People's Hospital of Nanhai District of Foshan City, 528000, Foshan, Guangdong, China.
Department of Laboratory Medicine, Foshan Fourth People's Hospital, 528041, Foshan, Guangdong, China.
Mol Biol Rep. 2024 Jan 6;51(1):84. doi: 10.1007/s11033-023-09015-x.
Investigate the role of COX signaling in activating the PGE2-EP2 pathway.
Utilized a marine Mycobacterium infection model in zebrafish. Marine mycobacteria were stained with fluorescein isothiocyanate. The COX inhibitor indomethacin, EP2 receptor inhibitor AH6809, EP4 receptor inhibitor AH23848 and clodronate Liposomes were used to investigate the role of COX, EP2, EP4 and macrophage whether participating in combat marine mycobacterial infection. The expression level of the target gene was detected using real-time fluorescence quantitative PCR instrument.
The findings revealed that larvae exposed to the COX inhibitor indomethacin or the EP2 receptor inhibitor AH6809 demonstrated a significantly higher mortality rate due to marine mycobacterium infection than those in the control group. Administration of exogenous prostaglandin E2 (PGE2) rescued the survival of zebrafish infected with marine mycobacteria and treated with indomethacin. Additionally, a significant reduction in survival rate was noted in macrophage-depleted zebrafish infected with marine mycobacteria.
The host may combat marine mycobacterium infection via COX signaling, which activates the PGE2-EP2 pathway and mediates macrophage resistance.
研究 COX 信号在激活 PGE2-EP2 通路中的作用。
利用斑马鱼的海洋分枝杆菌感染模型。用异硫氰酸荧光素标记海洋分枝杆菌。用 COX 抑制剂吲哚美辛、EP2 受体抑制剂 AH6809、EP4 受体抑制剂 AH23848 和氯膦酸脂质体来研究 COX、EP2、EP4 和巨噬细胞是否参与对抗海洋分枝杆菌感染。用实时荧光定量 PCR 仪检测靶基因的表达水平。
研究结果表明，与对照组相比，暴露于 COX 抑制剂吲哚美辛或 EP2 受体抑制剂 AH6809 的幼虫因海洋分枝杆菌感染而导致的死亡率显著升高。外源性前列腺素 E2（PGE2）可挽救感染海洋分枝杆菌并用吲哚美辛处理的斑马鱼的存活。此外，海洋分枝杆菌感染的巨噬细胞耗竭的斑马鱼的存活率显著降低。
宿主可能通过 COX 信号来抵抗海洋分枝杆菌感染，该信号激活 PGE2-EP2 通路并介导巨噬细胞抵抗。
