Data/hora: 27/07/2024 02:03:34

Provedor de dados: 	56	
País: 	Brazil	
Título: 	TNF-α inhibits SCF, ghrelin, and substance P expressions through the NF-κB pathway activation in interstitial cells of Cajal	
Autores: 	Ren,Keyu; Yong,Chunming; Yuan,Hao; Cao,Bin; Zhao,Kun; Wang,Jin.	
Data: 	2018-01-01	
Ano: 	2018	
Palavras-chave: 	TNF-α; SCF; Ghrelin; Substance P; NF-κB; Interstitial cells of Cajal.	
Resumo: 	Ulcerative colitis is a chronic inflammatory disease of the colon where intestinal motility is disturbed. Interstitial cells of Cajal (ICC) are required to maintain normal intestinal motility. In the present study, we assessed the effect of tumor necrosis factor-alpha (TNF-α) on viability and apoptosis of ICC, as well as on the expression of stem cell factor (SCF), ghrelin, and substance P. ICC were derived from the small intestines of Swiss albino mice. Cell viability and apoptosis were measured using CCK-8 assay and flow cytometry, respectively. ELISA was used to measure the concentrations of IL-1β, IL-6, ghrelin, substance P, and endothelin-1. Quantitative RT-PCR was used to measure the expression of SCF. Western blotting was used to measure the expression of apoptosis-related proteins, interleukins, SCF, and NF-κB signaling pathway proteins. TNF-α induced inflammatory injury in ICC by decreasing cell viability and increasing apoptosis and levels of IL-1β and IL-6. TNF-α decreased the levels of SCF, ghrelin, and substance P, but had no effect on endothelin-1. TNF-α down-regulated expressions of SCF, ghrelin, and substance P by activating the NF-κB pathway in ICC. In conclusion, TNF-α down-regulated the expressions of SCF, ghrelin, and substance P via the activation of the NF-κB pathway in ICC.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000600610	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20187065	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.51 n.6 2018	
Fonte: 	info:eu-repo/semantics/openAccess