Effects of intestinal flora metabolite trimethylamine oxide on glomerular mesangial cells and renal tubular epithelial cells via NF-κB/MAPK signaling pathway
10.13200/j.cnki.cjb.004274
- VernacularTitle:肠道菌群代谢产物氧化三甲胺对肾小球系膜细胞和肾小管上皮细胞NF-κB/MAPK信号通路的影响
- Author:
SONG Yuejuan
- Publication Type:Journal Article
- Keywords:
Trimethylamine oxide(TMAO);
Renal injury;
Signaling pathway;
Human glomerular mesangial cells;
Human renal tubular epithelial cells
- From:
Chinese Journal of Biologicals
2024;37(8):932-937
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of trimethylamine oxide(TMAO),a metabolite of intestinal flora,on the nuclear factor-kappa B(NF-κB)/mitogen activated protein kinase(MAPK)signaling pathway in human glomerular mesangial cells HMC and renal tubular epithelial cells HK-2.MethodsHMC and HK-2 cells were treated with TMAO and the control group was treated with TMAO for 0 h. The mRNA transcription levels of MCP-1,IL-6,TNF-α and IL-1β were detected by Real-time PCR,while the expression of NF-κB and MAPK signaling pathway-related proteins by Western blot. HMC and HK-2 cells were treated with NF-κB inhibitor BAY11-7082 to verify the pro-inflammatory effects of TMAO.ResultsCompared with the control group,the expression levels of inflammatory factors MCP-1,IL-6,TNF-α and IL-1βmRNA significantly increased in the TMAO-treated group(t = 33. 349,P = 0. 001),indicating that TMAO had a significant pro-inflammatory effect on glomerular mesangial cells and renal tubular epithelial cells. TMAO activated NF-κB and MAPK signaling pathway in HMC and HK-2 cells,causing inflammatory response and damage to the kidney.ConclusionThe increase of TMAO level can activate the NF-κB/MAPK signaling pathway in HMC and HK-2 cells,stimulate the release of inflammatory cytokines from the both kinds of cells,which leads to the occurrence and development of renal injury.
