Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

被引：23

作者：

Lu, Guangping ^{[1
]}

Liu, Qingbo ^{[1
]}

Gao, Ting ^{[1
]}

Li, Jiahao ^{[1
]}

Zhang, Jingjing ^{[2
]}

Chen, Ou ^{[1
]}

Cao, Cong ^{[1
]}

Mao, Min ^{[1
]}

Xiao, Mengjie ^{[1
]}

Zhang, Xiaohui ^{[1
]}

Wang, Jie ^{[1
]}

Guo, Yuanfang ^{[1
]}

Tang, Yufeng ^{[3
]}

Gu, Junlian ^{[1
]}

机构：

[1] Shandong Univ, Cheeloo Coll Med, Sch Nursing & Rehabil, Jinan 250012, Peoples R China

[2] China Med Univ, Hosp 1, Dept Cardiol, Shenyang 110016, Peoples R China

[3] Shandong First Med Univ, Affiliated Hosp 1, Dept Orthoped Surg, Jinan 250014, Peoples R China

来源：

NUTRIENTS | 2022年 / 14卷 / 19期

基金：

中国国家自然科学基金;

关键词：

doxorubicin; cardiotoxicity; SIRT1; NRF2; oxidative stress; DIABETIC CARDIOMYOPATHY; OXIDATIVE STRESS; CELL-CYCLE; APOPTOSIS; PROLIFERATION; ANTIOXIDANT; DYSFUNCTION; MCF-7; NRF2;

D O I：

10.3390/nu14194017

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

Doxorubicin (DOX) has received attention due to dose-dependent cardiotoxicity through abnormal redox cycling. Native fibroblast growth factor 1 (FGF1) is known for its anti-oxidative benefits in cardiovascular diseases, but possesses a potential tumorigenic risk. Coincidentally, the anti-proliferative properties of resveratrol (RES) have attracted attention as alternatives or auxiliary therapy when combined with other chemotherapeutic drugs. Therefore, the purpose of this study is to explore the therapeutic potential and underlying mechanisms of co-treatment of RES and FGF1 in a DOX-treated model. Here, various cancer cells were applied to determine whether RES could antagonize the oncogenesis effect of FGF1. In addition, C57BL/6J mice and H9c2 cells were used to testify the therapeutic potential of a co-treatment of RES and FGF1 against DOX-induced cardiotoxicity. We found RES could reduce the growth-promoting activity of FGF1. Additionally, the co-treatment of RES and FGF1 exhibits a more powerful cardio-antioxidative capacity in a DOX-treated model. The inhibition of SIRT1/NRF2 abolished RES in combination with FGF1 on cardioprotective action. Further mechanism analysis demonstrated that SIRT1 and NRF2 might form a positive feedback loop to perform the protective effect on DOX-induced cardiotoxicity. These favorable anti-oxidative activities and reduced proliferative properties of the co-treatment of RES and FGF1 provided a promising therapy for anthracycline cardiotoxicity during chemotherapy.

引用

页数：16

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