Resveratrol prevents Ang II-induced cardiac hypertrophy by inhibition of NF-KB signaling

被引:13
|
作者
Ma, En [1 ]
Wu, Celiang [2 ]
Chen, Jinxiao [3 ]
Wo, Da [2 ,3 ]
Ren, Dan-ni [3 ]
Yan, Hongwei [1 ]
Peng, Luying [1 ,4 ]
Zhu, Weidong [2 ,3 ,5 ]
机构
[1] Tongji Univ, Shanghai East Hosp, Sch Med, Res Inst Heart Failure,Clin & Translat Res Ctr,Key, Shanghai, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Innovat & Transformat Ctr, Fuzhou, Fujian, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Fujian Key Lab Integrat Med Geriatr, Fuzhou, Fujian, Peoples R China
[4] Tongji Univ, Sch Med, 1239 Siping Rd, Shanghai 200092, Peoples R China
[5] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Innovat & Transformat Ctr, 1 Qiuyang Rd, Fuzhou 350122, Fujian, Peoples R China
关键词
Resveratrol; Cardiac hypertrophy; Ang II; AT1R; NF-KB signaling; KAPPA-B ACTIVATION; ANGIOTENSIN-II; HEART-FAILURE; RECEPTOR; HYPERTENSION; EXPRESSION; STRESS;
D O I
10.1016/j.biopha.2023.115275
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Pathological cardiac hypertrophy is a hallmark of various cardiovascular diseases (CVD) including chronic heart failure (HF) and an important target for the treatment of these diseases. Aberrant activation of Angiotensin II (Ang II)/AT1R signaling pathway is one of the main triggers of cardiac hypertrophy, which further gives rise to excessive inflammation that is mediated by the key transcription factor NF -KB. Resveratrol (REV) is a natural polyphenol with multiple anti-inflammatory and anti-oxidative effects, however the ability of REV in preventing Ang II-induced cardiac hypertrophy in combination with NF -KB signaling activation remains unclear. Methods: Murine models of cardiac hypertrophy was conducted via implantation of Ang II osmotic pumps. Pri-mary neonatal rat cardiomyocyte and heart tissues were examined to determine the effect and underlying mechanism of REV in preventing Ang II-induced cardiac hypertrophy. Results: Administrations of REV significantly prevented Ang II-induced cardiac hypertrophy, as well as robustly attenuated Ang II-induced cardiac fibrosis, and cardiac dysfunction. Furthermore, REV not only directly pre-vented Ang II/AT1R signal transductions, but also prevented Ang II-induced expressions of pro-inflammatory cytokines and activation of NF -KB signaling pathway. Conclusions: Our study provides important new mechanistic insight into the cardioprotective effects of REV in preventing Ang II-induced cardiac hypertrophy via inhibiting adverse NF -KB signaling activation. Our findings further suggest the therapeutic potential of REV as a promising drug for the treatment of cardiac hypertrophy and heart failure.
引用
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页数:9
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