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隐丹参酮减轻病理性心脏重构及实验研究。

Cryptotanshinone Attenuated Pathological Cardiac Remodeling and Experiments.

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Cardiovascular Research Institute of Wuhan University, Wuhan, China.

出版信息

Oxid Med Cell Longev. 2023 Jan 27;2023:4015199. doi: 10.1155/2023/4015199. eCollection 2023.

DOI:10.1155/2023/4015199
PMID:36743695
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9897919/
Abstract

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 and .

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 .

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-/SMAD3 signaling pathways. In vitro experiments, CTS treatment markedly inhibited AngII-induced cardiomyocyte hypertrophy and TGF--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.

摘要

目的

心脏重构已被证明是各种类型心肌病的早期和常见途径，但尚未提出具体的治疗方法来预防其发展和进展。本研究旨在评估 Cryptotanshinone (CTS) 治疗是否能有效减轻心脏重构。

方法

采用主动脉缩窄 (AB) 手术建立压力超负荷诱导的小鼠心脏重构模型。通过超声心动图和压力-容积证明来检测小鼠心脏功能。采用苏木精和伊红 (HE) 和苦味酸-天狼猩红 (PSR) 染色来评估体内心脏重构。分别收集小鼠心脏以分析信号通路和心脏重构标志物。此外，分离新生大鼠心肌细胞 (NRCMs) 和心脏成纤维细胞 (CF)，以研究 CTS 治疗的作用和机制。

结果

CTS 给药显著减轻压力超负荷诱导的小鼠心脏功能障碍，抑制心肌肥厚，减少心脏纤维化。机制上，CTS 治疗显著抑制 STAT3 和 TGF-/SMAD3 信号通路。在体外实验中，CTS 治疗通过抑制 STAT3 磷酸化及其核易位，显著抑制 AngII 诱导的心肌细胞肥大和 TGF--诱导的肌成纤维细胞激活。最后，在小鼠心脏中过表达腺相关病毒 (AAV)9-STAT3 后，CTS 治疗不能保护小鼠免受压力超负荷诱导的心脏重构。

结论

CTS 治疗可能通过抑制 STAT3 依赖性途径减轻病理性心脏重构。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/faeb05244b77/OMCL2023-4015199.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/425f0e9f7766/OMCL2023-4015199.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/faeb05244b77/OMCL2023-4015199.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/425f0e9f7766/OMCL2023-4015199.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/4179a628d9a0/OMCL2023-4015199.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/683d120a59a7/OMCL2023-4015199.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce0/9897919/faeb05244b77/OMCL2023-4015199.007.jpg

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