Mechanism of Ac-SDKP on regulating CREB signal and Smad signal in order to restrain silicotic fibrosis / 实用医学杂志
The Journal of Practical Medicine
; (24): 3539-3542, 2017.
Article
em Zh
| WPRIM
| ID: wpr-663653
Biblioteca responsável:
WPRO
ABSTRACT
Objective To observe the function of Ac-SDKP on p-CREB,p-Smad2/3 signal and restraining silicotic fibrosis.Methods Wistar rats were randomly divided into:control group;silicosis group;Ac-SDKP post-treatment group;Ac-SDKP pre-treatment group.The morphology of lung tissue was observed by Van Gieson stain-ing.The expression of α-SMA,cAMP,PKA,p-CREB and p-Smad2/3 protein were assessed by Western blot.The colocalization of p-Smad2/3 and α-SMA were detected by immuno-fluorescence. Results In silicosis group,the deposition of collagen were visible in the fibrotic area,the expression of α-SMA and p-Smad2/3 increased signifi-cantly,and the expression of cAMP,PKA and p-CREB decreased significantly. After Ac-SDKP treatment,the expression of cAMP,PKA and p-CREB were significantly up-regulated,the expression of -SMA and p-Smad2/3 protein were significantly down-regulated,lung tissue damage and collagen deposition decreased. Conclusion By activating the signal of cAMP/PKA/p-CREB,Ac-SDKP was capable of restraining the expression of p-Smad2/3,so as to restrain silicotic fibrosis.
Texto completo:
1
Índice:
WPRIM
Idioma:
Zh
Revista:
The Journal of Practical Medicine
Ano de publicação:
2017
Tipo de documento:
Article