Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating Nrf2 signaling pathway

Jiang, Qianqian; Chen, Xu; Tian, Xiaoyi; Zhang, Jingmei; Xue, Song; Jiang, Yanyan; Liu, Tiantian; Wang, Xiaoping; Sun, Qianbin; Hong, Yiqin; Li, Chun; Guo, Dongqing; Wang, Yong; Wang, Qiyan

doi:10.1016/j.phymed.2022.154439

Cited by 53 publications

(24 citation statements)

References 37 publications

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“…The Nrf2-ARE is the most critical antioxidant signaling pathway in biological organisms ( Dai et al, 2022 ; Guo et al, 2022 ; Jiang et al, 2022 ; Qiu et al, 2022 ; Shen et al, 2022a ; Yan et al, 2022 ). So far, accumulating evidence has shown that a large amount of natural active substances activate Nrf2-mediated antioxidant signaling pathway and regulate the expression of cytoprotective enzymes, thus playing an important role in preventing antioxidant damage ( Eggler et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Characterization of tangeretin as an activator of nuclear factor erythroid 2-related factor 2/antioxidant response element pathway in HEK293T cells

Liang

et al. 2023

Current Research in Food Science

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Section: Introductionmentioning

confidence: 99%

Characterization of tangeretin as an activator of nuclear factor erythroid 2-related factor 2/antioxidant response element pathway in HEK293T cells

Liang

et al. 2023

Current Research in Food Science

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“…Nrf2 acts as the key regulator in anti‐oxidant defense system and interacts with downstream target HO‐1 to exert beneficial effect against oxidative stress (Ma, 2013). It is reported that Tanshinone I protects heart against DOX‐induced oxidative stress via activation of Nrf2/HO‐1 pathway (Guo et al, 2022; Jiang et al, 2022). Knockout of Nrf2 exaggerates oxidative insult in DOX‐induced cardiomyopathy (Li et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Galangin attenuates doxorubicin‐induced cardiotoxicity via activating nuclear factor erythroid 2‐related factor 2/heme oxygenase 1 signaling pathway to suppress oxidative stress and inflammation

Fang,

Li,

Yang

et al. 2023

Phytotherapy Research

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Doxorubicin (DOX) has aroused contradiction between its potent anti‐tumor capacity and severe cardiotoxicity. Galangin (Gal) possesses antioxidant, anti‐inflammatory, and antiapoptotic activities. We aimed to explore the role and underlying mechanisms of Gal on DOX‐induced cardiotoxicity. Mice were intraperitoneally injected with DOX (3 mg/kg, every 2 days for 2 weeks) to generate cardiotoxicity model and Gal (15 mg/kg, 2 weeks) was co‐administered via gavage daily. Nuclear factor erythroid 2‐related factor 2 (Nrf2) specific inhibitor, ML385, was employed to explore the underlying mechanisms. Compared to DOX‐insulted mice, Gal effectively improved cardiac dysfunction and ameliorated myocardial damage. DOX‐induced increase of reactive oxygen species, malondialdehyde, and NADPH oxidase activity and downregulation of superoxide dismutase (SOD) activity were blunted by Gal. Gal also markedly blocked increase of IL‐1β, IL‐6, and TNF‐α in DOX‐insulted heart. Mechanistically, Gal reversed DOX‐induced downregulation of Nrf2, HO‐1, and promoted nuclear translocation of Nrf2. ML385 markedly blunted the cardioprotective effects of Gal, as well as inhibitive effects on oxidative stress and inflammation. Gal ameliorates DOX‐induced cardiotoxicity by suppressing oxidative stress and inflammation via activating Nrf2/HO‐1 signaling pathway. Gal may serve as a promising cardioprotective agent for DOX‐induced cardiotoxicity.

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“…Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor in antioxidant stress response. Tanshinone I (Tan I) is an active ingredient extracted from the Chinese herb Danshen, and it has been shown to upregulate the phosphorylation of AKT and promote the Nrf2 shuttle into the nucleus, activate the expression of its downstream antioxidant enzymes, and then relieve oxidative stress and mitochondrial damage to improve cardiac function ( 82 ). On the one hand, the above studies indicate that TCM has a remarkable and beneficial effect in AMI treatment, and on the other hand, transcription factors and epigenetic regulatory factors can be used as key targets to treat diseases.…”

Section: Treatment Of Hf With Traditional Chinese Medicine Through Tr...mentioning

confidence: 99%

Transcriptional regulation of macrophages in heart failure

Wang

Sun

et al. 2023

Front. Cardiovasc. Med.

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Adverse cardiac remodeling after acute myocardial infarction is the most important pathological mechanism of heart failure and remains a major problem in clinical practice. Cardiac macrophages, derived from tissue resident macrophages and circulating monocyte, undergo significant phenotypic and functional changes following cardiac injury and play crucial roles in inflammatory response and tissue repair response. Currently, numerous studies indicate that epigenetic regulatory factors and transcription factors can regulate the transcription of inflammatory and reparative genes and timely conversion of inflammatory macrophages into reparative macrophages and then alleviate cardiac remodeling. Accordingly, targeting transcriptional regulation of macrophages may be a promising option for heart failure treatment. In this review, we not only summarize the origin and function of cardiac macrophages, but more importantly, describe the transcriptional regulation of macrophages in heart failure, aiming to provide a potential therapeutic target for heart failure.

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Tanshinone I inhibits doxorubicin-induced cardiotoxicity by regulating Nrf2 signaling pathway

Cited by 53 publications

References 37 publications

Characterization of tangeretin as an activator of nuclear factor erythroid 2-related factor 2/antioxidant response element pathway in HEK293T cells

Characterization of tangeretin as an activator of nuclear factor erythroid 2-related factor 2/antioxidant response element pathway in HEK293T cells

Galangin attenuates doxorubicin‐induced cardiotoxicity via activating nuclear factor erythroid 2‐related factor 2/heme oxygenase 1 signaling pathway to suppress oxidative stress and inflammation

Transcriptional regulation of macrophages in heart failure

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