Sanguinarine protects against pressure overload‑induced cardiac remodeling via inhibition of nuclear factor-κB activation

Deng,Wei; Fang,Yi; Liu,Yuan; Zhou,Heng; Cheng,Zhihong; Zhang,Yang; Sun,Di; He,Mengying; Lin,Yafen; Zhang,Rui; Zhang,Jieyu; Li,Wei; Tang,Qizhu

doi:10.3892/mmr.2014.2206

Sanguinarine protects against pressure overload‑induced cardiac remodeling via inhibition of nuclear factor-κB activation

Authors:
- Wei Deng
- Yi Fang
- Yuan Liu
- Heng Zhou
- Zhihong Cheng
- Yang Zhang
- Di Sun
- Mengying He
- Yafen Lin
- Rui Zhang
- Jieyu Zhang
- Wei Li
- Qizhu Tang
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Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, National Pharmaceutical Engineering Research Center, Shanghai 201203, P.R. China
Published online on: May 2, 2014 https://doi.org/10.3892/mmr.2014.2206
Pages: 211-216

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Abstract

Cardiac remodeling is a major determinant of heart failure characterized by cardiac hypertrophy and fibrosis. Sanguinarine exerts widespread pharmacological effects, including antitumor and anti‑inflammatory responses. In the present study, the effect of sanguinarine on cardiac hypertrophy, fibrosis and heart function was determined using the model induced by aortic banding (AB) in mice. AB surgery and sham surgery were performed on male wild‑type C57 mice, aged 8‑10 weeks, with or without administration of sanguinarine from one week after surgery for an additional seven weeks. Sanguinarine protected against the cardiac hypertrophy, fibrosis and dysfunction induced by AB, as assessed by the heart weight/body weight, lung weight/body weight and heart weight/tibia length ratios, echocardiographic and hemodynamic parameters, histological analysis, and the gene expression levels of hypertrophic and fibrotic markers. The inhibitory effect of sanguinarine on cardiac remodeling was mediated by inhibiting nuclear factor (NF)‑κB signaling pathway activation. The findings indicated that sanguinarine protected against cardiac hypertrophy and fibrosis via inhibiting NF‑κB activation. These findings may be used to develop a potential therapeutic drug for treating cardiac remodeling and heart failure.

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