Si-Miao-Yong-An decoction attenuates cardiac fibrosis via suppressing TGF-β1 pathway and interfering with MMP-TIMPs expression

心室重构 转化生长因子 心脏纤维化 压力过载 SMAD公司 CTGF公司 心力衰竭 纤维化 心肌纤维化 心室 心功能曲线 医学 内分泌学 药理学 射血分数 内科学 生长因子 受体 心肌肥大
作者
Congping Su,Qing Wang,Hui Luo,Wenchao Jiao,Jiayang Tang,Lin Li,Lei Tian,Xiangyang Chen,Bin Liu,Xue Yu,Sen Li,Shuzhen Guo,Wei Wang
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:127: 110132-110132 被引量:19
标识
DOI:10.1016/j.biopha.2020.110132
摘要

Myocardial fibrosis is an important pathological feature of pressure overload cardiac remodeling. Si-Miao-Yong-An decoction (SMYAD), a traditional Chinese formula, is now clinically used in the treatment of cardiovascular diseases in China. However, its mechanisms in the prevention of heart failure are not fully revealed. To determine whether treatment with SMYAD for 4 weeks would lead to changes in collagen metabolism and ventricular remodeling in a mice model of heart failure. Mice were subjected to transverse aorta constriction to generate pressure overload induced cardiac remodeling and then were administered SMYAD (14.85 g/kg/day) or captopril (16.5 mg/kg/day) intragastrically for 4 weeks after surgery. Echocardiography and immunohistochemical examination were used to evaluate the effects of SMYAD. The mRNA of collagen metabolism biomarkers were detected. Protein expression of TGF-β1/Smad and TGF-β1/TAK1/p38 pathway were assessed by Western blot. SMYAD significantly improved cardiac function, increased left ventricle ejection fraction, and decreased fibrosis area and αSMA expression. Moreover, SMYAD reduced proteins expression related to collagen metabolism, including Col1, Col3, TIMP2 and CTGF. The increased levels of TGF-β1, Smad2, and Smad3 phosphorylation were attenuated in SMYAD group. In addition, SMYAD reduced the levels of TGF-β1, p-TAK1 and p-p38 compared with TAC group. SMYAD improved cardiac fibrosis and heart failure by inhibition of TGF-β1/Smad and TGF-β1/TAK1/p38 pathway. SMYAD protected against cardiac fibrosis and maintained collagen metabolism balance by regulating MMP-TIMP expression. Taken together, these results indicate that SMYAD might be a promising therapeutic agent against cardiac fibrosis.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
好好学习完成签到,获得积分10
1秒前
学渣路过完成签到,获得积分10
2秒前
2秒前
now发布了新的文献求助10
5秒前
5秒前
Ava应助朴素碧琴采纳,获得10
5秒前
六六完成签到,获得积分10
6秒前
我又不乱来完成签到,获得积分10
7秒前
7秒前
开朗的戎完成签到,获得积分10
7秒前
7秒前
8秒前
Singularity应助九品芝麻官采纳,获得10
8秒前
CodeCraft应助ljs采纳,获得10
8秒前
裘凛发布了新的文献求助50
9秒前
9秒前
9秒前
9秒前
活力尔竹发布了新的文献求助10
9秒前
咖啡味椰果完成签到,获得积分10
10秒前
恋恋青葡萄完成签到,获得积分10
10秒前
青呀青呀乔完成签到,获得积分10
11秒前
无奈芮发布了新的文献求助10
12秒前
怕孤独的山灵完成签到,获得积分10
12秒前
茵茵完成签到,获得积分10
13秒前
研友_599Y85发布了新的文献求助10
13秒前
tianzml0应助Llllllxxxxxxx采纳,获得10
14秒前
Murray应助Llllllxxxxxxx采纳,获得10
14秒前
14秒前
14秒前
卢佳丰发布了新的文献求助10
14秒前
小马甲应助caicailang84采纳,获得10
14秒前
16秒前
英俊的铭应助小七采纳,获得10
16秒前
格拉希尔完成签到,获得积分10
16秒前
小橘发布了新的文献求助10
16秒前
朴素碧琴完成签到,获得积分10
18秒前
18秒前
kkuma完成签到,获得积分10
19秒前
高分求助中
Tracking and Data Fusion: A Handbook of Algorithms 1000
Models of Teaching(The 10th Edition,第10版!)《教学模式》(第10版!) 800
La décision juridictionnelle 800
Rechtsphilosophie und Rechtstheorie 800
Academic entitlement: Adapting the equity preference questionnaire for a university setting 500
Full waveform acoustic data processing 400
Bounded Meaning 400
热门求助领域 (近24小时)
化学 医学 材料科学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 物理化学 催化作用 免疫学 细胞生物学 电极
热门帖子
关注 科研通微信公众号,转发送积分 2878114
求助须知:如何正确求助?哪些是违规求助? 2491708
关于积分的说明 6745165
捐赠科研通 2172980
什么是DOI,文献DOI怎么找? 1154746
版权声明 586099
科研通“疑难数据库(出版商)”最低求助积分说明 566839