Mechanism of Ac-SDKP on regulating CREB signal and Smad signal in order to restrain silicotic fibrosis
10.3969/j.issn.1006-5725.2017.21.010
- VernacularTitle:Ac-SDKP调节CREB、Smad信号抑制矽肺纤维化的作用
- Author:
Yi ZHANG
1
;
Yan LIU
;
Ying LI
;
Liyan ZHU
;
Jianhui WANG
;
Xiuhong YANG
;
Hong XU
;
Fang YANG
Author Information
1. 华北理工大学基础医学院河北省慢性疾病重点实验室
- Keywords:
silicosis;
cyclic adenosine monophosphate;
cAMP-response element binding protein;
n-acetyl-seryl-aspartyl-lysyl-proline
- From:
The Journal of Practical Medicine
2017;33(21):3539-3542
- CountryChina
- Language:Chinese
-
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.
