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A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Cryptotanshinone Attenuated Pathological Cardiac Remodeling In Vivo and In Vitro Experiments
Wen-Jing Li1,2,3, Han Yan3,4, Zi-Ying Zhou1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Objective:
Cardiac remodeling has been demonstrated to be the early stage and common pathway for various types of cardiomyopathy, but no specific treatment has been suggested to prevent its development and progress. This study was aimed at assessing whether Cryptotanshinone (CTS) treatment could effectively attenuate cardiac remodeling in vivo and in vitro.
Methods:
Aortic banding (AB) surgery was performed to establish a pressure-overload-induced mouse cardiac remodeling model. Echocardiography and pressure-volume proof were used to examine mouse cardiac function. Hematoxylin and eosin (HE) and Picro-Sirius Red (PSR) staining were used to assess cardiac remodeling in vivo. Mouse hearts were collected to analysis signaling pathway and cardiac remodeling markers, respectively. Furthermore, neonatal rat cardiomyocyte (NRCMs) and cardiac fibroblast (CF) were isolated to investigate the roles and mechanisms of CTS treatment in vitro.
Results:
CTS administration significantly alleviated pressure-overload-induced mouse cardiac dysfunction, inhibited cardiac hypertrophy, and reduced cardiac fibrosis. Mechanically, CTS treatment significantly inhibited the STAT3 and TGF-β/SMAD3 signaling pathways. In vitro experiments, CTS treatment markedly inhibited AngII-induced cardiomyocyte hypertrophy and TGF-β-induced myofibroblast activation via inhibiting STAT3 phosphorylation and its nuclear translocation. Finally, CTS treatment could not protect against pressure overload-induced mouse cardiac remodeling after adenovirus-associated virus (AAV)9-mediated STAT3 overexpression in mouse heart.
Conclusion:
CTS treatment might attenuate pathological cardiac remodeling via inhibiting STAT3-dependent pathway.
Insights
Cryptotanshinone (CTS) treatment attenuates cardiac remodeling and dysfunction in mice by inhibiting the STAT3 signaling pathway. This study demonstrates CTS
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Molecular Medicine
Background:
- Cardiac remodeling is a precursor to various cardiomyopathies, lacking targeted preventative treatments.
- Understanding the molecular mechanisms underlying cardiac remodeling is crucial for developing effective therapies.
Purpose of the Study:
- To evaluate the efficacy of Cryptotanshinone (CTS) in preventing and treating cardiac remodeling.
- To elucidate the underlying molecular mechanisms of CTS action in cardiac remodeling.
Main Methods:
- A pressure-overload mouse model was established using aortic banding (AB) surgery.
- Cardiac function was assessed via echocardiography and pressure-volume loops.
- Histological analysis (HE, PSR) and molecular pathway analysis were performed on heart tissues.
- In vitro studies utilized neonatal rat cardiomyocytes (NRCMs) and cardiac fibroblasts (CFs).
Main Results:
- CTS treatment improved cardiac function and reduced cardiac hypertrophy and fibrosis in the mouse model.
- CTS inhibited the STAT3 and TGF-β/SMAD3 signaling pathways.
- In vitro, CTS prevented AngII-induced cardiomyocyte hypertrophy and TGF-β-induced myofibroblast activation by inhibiting STAT3 phosphorylation.
- STAT3 overexpression via AAV9 negated the protective effects of CTS against pressure overload.
Conclusions:
- Cryptotanshinone (CTS) shows potential in attenuating pathological cardiac remodeling.
- The protective effects of CTS are mediated through the inhibition of the STAT3 signaling pathway.
- Targeting the STAT3 pathway presents a viable therapeutic strategy for cardiac remodeling.
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