Changes in phosphorylation of tau protein and COX-2 expression in colon submucosal neurons of IBD model rats induced by TNBS
10.3969/j.issn.1000-4718.2015.06.028
- VernacularTitle:TNBS 诱导炎症性肠病大鼠结肠神经元 tau 蛋白磷酸化以及 COX－2表达的变化
- Author:
Tingkun ZHAO
;
Zhidong WANG
;
Fengjiao LIU
;
Meihua QU
;
Zhiqin GAO
- Publication Type:Journal Article
- Keywords:
Inflammatory bowel diseases;
Tau protein;
Cyclooxygenase 2;
Enteric nervous system
- From:
Chinese Journal of Pathophysiology
2015;(6):1125-1129
- CountryChina
- Language:Chinese
-
Abstract:
[ ABSTRACT] AIM:To investigate the change of phosphorylation of tau protein and expression of cyclooxygenase 2 ( COX-2) in colon submucosal neurons of enteric nerve system in inflammatory bowel disease ( IBD) rats induced by tri-nitrobenzene sulfonic acid (TNBS).METHODS:Male rats (n=30) were randomly assigned to 3 groups (n=10 each):control group, IBD group and TNBS group.The IBD rats were induced by TNBS+ethanol enema for 14 d.The control and TNBS rats were given an equal volume of saline and TNBS, respectively.The general situation and the histopathologic change of the rat colon were observed.Immunofluorescence was used to check the change of phosphalated tau protein and COX-2 expression in the submucosal neurons of the colon.The expression of COX-2 and phosphorylated tau231 and tau262 in the rat colon submucosal neurons was observed by double immunofluorescence staining.RESULTS:Compared with con-trol group, the number of neurons in the colon of IBD rats decreased obviously and the expression of phospholated tau231 and tau262 was significantly increased.The number of neurons in the colon of TNBS rats showed no significant difference compared with control rats.The rat neurons in control group and TNBS group did not express COX-2.COX-2 expression was observed in the nucleus and cytoplasm of colonic neurons in IBD rats, which showed significantly different from control and TNBS rats.CONCLUSION:The decreased neurons in the enteric nerve system of IBD rats might be associated with the phosphorylation of tau protein and the expression of inducible COX-2.
