Effect of astaxanthin on expression of type Ⅰ and type Ⅲ collagen in cardiac fibroblasts and its mechanism based on TGF-β1/Smad3 signaling pathway
10.3969/j.issn.1001-1978.2018.06.020
- VernacularTitle:基于TGF-β1/Smad3信号通路探讨虾青素对心肌成纤维细胞Ⅰ、Ⅲ型胶原表达的影响
- Author:
Zhe MENG
1
;
Hai-Yu LI
;
Hai-Long TAO
Author Information
1. 郑州大学第一附属医院心血管内科
- Keywords:
astaxanthin;
transforming growth factorβ1;
cardiac fibroblasts;
fibrosis;
ROS;
Smad3
- From:
Chinese Pharmacological Bulletin
2018;34(6):841-845
- CountryChina
- Language:Chinese
-
Abstract:
Aim To observe the effects of astaxanthin ( ASTX) on the expression of collegeⅠ( ColⅠ) and type Ⅲcollagen ( Col Ⅲ) of cardiac fibroblasts( CFs) which caused by transforming growth factor β1 ( TGF-β1) and to explore its mechanism of action. Methods CFs were induced by TGF-β1 , and then pretreated with different concentrations of ASTX ( 0 , 5 , 10 , 20 , 40, 80, 160 μmol·L-1) for 24 h. MTT assay was used to determine the activity of CFs. The activation of ROS in CFs cells was detected by DCFH-DA kit. Smad3 gene was silenced by siRNA technique, and re-al-time PCR was used to detect the expression of ColⅠ, Col Ⅲ mRNA before and after Smad3 silencing. Western blot was used to detect the expression of ColⅠ, Col Ⅲ and Smad3 protein levels before and after Smad3 silencing. Results ASTX had no obvious cyto-toxicity in the range of 0 ~20 μmol · L-1 , and could significantly reduce ROS production induced by TGF-β1 in CFs (P<0.05). In addition, ASTX significant-ly inhibited the expression of ColⅠand ColⅢmRNA and protein ( P<0.01 ) of TGF-β1-induced CFs in a concentration-dependent manner. Also, ASTX could significantly down-regulate phosphorylation of Smad3 in TGF-β1-induced CFs ( P <0.01 ) . The expression of Col Ⅰ and Col Ⅲ mRNA and protein was also signifi-cantly down-regulated by Smad3 gene silencing ( P <0.01 ) . Conclusions ASTX can effectively inhibit the expression of Col Ⅰ, Col Ⅲ mRNA and protein of TGF-β1-induced CFs, and the possible mechanism may involve the down-regulation of Smad3 phosphoryla-tion.