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The protective effect and mechanism of TLR2 on permeability of intestinal epithelial barrier / 国际儿科学杂志
International Journal of Pediatrics ; (6): 484-487,501, 2016.
Artigo em Chinês | WPRIM | ID: wpr-604629
ABSTRACT
Objective Intestinal epithelial barrier damage is closely related to a variety of gastrointestinal disease,how to maintain its function effectively is the key to treat all these diseases.This research attempts to explore the protective effect and its mechanism of toll-like receptor 2 (Toll-like receptor,TLR2)on permeability of intestinal epithelial barrier by experiments in vitro,to lay a foundation for new treatment methods.Methods We cultured non-transfected Caco-2 cells,TLR2-deficiency Caco-2 cells,TLR2-overexpressed Caco-2 cells in normal control group until the 21 st d,then tested transepithelial electrical resistance(TEER) which reacts the permeability of epithelial barrier.We cultured 3 types of cells in inflammation group until the 19th d treated with 10 ng/ml IL-1 beta for 48 h,then tested TEER values at the 21st d.We treated 3 types of cells in inhibition group with PI3K/Akt pathway inhibitor for 1h befor IL-1 beta,then tested TEER values at the 21st d.Results TEER value of TLR2-deficiency Caco-2 cell monolayer significantly reduced (P < 0.01),whereas TEER value of TLR2-overexpressed Caco-2 monolayer raised,but without statistically significant.TLR2 can prevent IL-1 beta caused TEER decreasing (P < 0.01),but the effect disappeared after given PI3K/Akt pathway inhibitor.Conclusion TLR2 can regulate the permeability of intestinal epithelial barrier.In addition,TLR2 can protect permeability increasing caused by inflammation,this effect mediated by PI3 K/Akt pathway.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: International Journal of Pediatrics Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: International Journal of Pediatrics Ano de publicação: 2016 Tipo de documento: Artigo