Sodium Ferulate Prevents Daunorubicin - Induced Apoptosis in H9c2 Cells via Inhibition of the ERKs Pathway

Wu, Zhiyong; Yu, Jing; Fang, Qiujuan; Wang, Ruixing; Lian, Jiabian; He, Rui-Lan; Jiao, Haixia; Lin, Mo‐Jun

doi:10.1159/000430179

Cited by 9 publications

(9 citation statements)

References 46 publications

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“…Under normal conditions, the anti-apoptotic protein Bcl-2 binds to and sequesters the pro-apoptotic protein Bax. Thus, the ratio of Bax/Bcl-2 plays an important role in determining cell apoptosis or survival [44]. Western blotting of caspase 9, Bcl-2 and Bax, and flow cytometry analysis showed that expression of H7N9/ NS1 activates caspase 9 (Fig.…”

Section: Discussionmentioning

confidence: 98%

The Novel H7N9 Influenza A Virus NS1 Induces p53-Mediated Apoptosis of A549 Cells

Yan

Wang

et al. 2016

Cell Physiol Biochem

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Background: H7N9, emerged as an avian influenza virus outbreak in Eastern China in early 2013, and represented another major threat to global health. Roles of its NS1 protein, an essential viral factor, in regulating apoptosis remain unknown. Methods: Apoptotic effect and features of H7N9/NS1 in the human A549 alveolar basal epithelial cell line were examined by caspase 3/7 activity assay and western blotting of apoptotic associated proteins. Effects of H7N9/NS1on mitochondrial membrane potential were investigated by flow cytometry. Results: The expression of H7N9/NS1 in A549 cells activated caspase 3/7 and increased the protein levels of cleaved caspase 7 and cleaved poly (ADP-ribose) polymerase (PARP). H7N9/NS1-expressing A549 cells displayed a decrease in mitochondrial membrane potential. In addition, H7N9/NS1 increased the protein levels of total p53, p53 phosphorylated at Ser46 and Ser37, activated caspase 9, and the Bax/Bcl-2 ratio. Conclusion: Our results suggest that H7N9/NS1 protein causes the accumulation of p53 by increasing phosphorylation levels of p53 and the induction of mitochondrial dysfunction, which may contribute to H7N9/NS1-induced apoptosis in A549 cells.

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Section: Discussionmentioning

confidence: 98%

The Novel H7N9 Influenza A Virus NS1 Induces p53-Mediated Apoptosis of A549 Cells

Yan

Wang

et al. 2016

Cell Physiol Biochem

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“…Although several paradigms, including activation of PKC and ERK [29], inhibition of p38, inhibition of ER stress, decreased apoptosis, necrosis and autophagy, and altered gene expression [25][26][27] have been proposed as putative underlying mechanisms, to date none there has not been a unifying explanation to account for the cellular defects. Furthermore, additional pathways may also play a role in the mediation of the protective effects of FGF-2.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies suggest that the protective effects of FGF-2 are mediated by PKC and MAPK activation [27]. Moreover, the PI3K/AKT pathway, which is independent of the PKC, PKA, and MAPK signaling pathways [28,29], is activated by FGF-2 and prevents ROS-induced apoptosis in H9c2 cells through the Forkhead box O3 (FoxO3a) transcription factor [30]. The FoxO3a transcription factor is one of the most important downstream targets of PI3K/Akt signaling and a crucial regulator of apoptosis [18,[31][32][33].…”

Section: Introductionmentioning

confidence: 99%

FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells

Chen

Han

et al. 2016

Cell Physiol Biochem

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Background/Aims: Cardiovascular disease is a growing major global public health problem. Necrosis is one of the main forms of cardiomyocyte death in heart disease. Oxidative stress is regarded as one of the key regulators of cardiac necrosis, which eventually leads to cardiovascular disease. Many pharmacological and in vitro studies have suggested that FGF-2 can act directly on cardiomyocytes to maintain the integrity and function of the myocardium and prevent damage during oxidative stress. However, the mechanisms by which FGF-2 rescues the myocardium from oxidative stress damage in cardiovascular disease remain unclear. The present study explored the protective effects of FGF-2 in the H₂O₂-induced necrosis of H9C2 cardiomyocytes as well as the possible signaling pathways involved. Methods: Necrosis of H9c2 cardiomyocytes was induced by H₂O₂ and assessed using a Cell Counting Kit-8 (CCK8) assay and flow cytometry analysis. The cells were pretreated with the PI3K/Akt inhibitor Wortmannin to investigate the possible involvement of the PI3K/Akt pathway in the protection by FGF-2. The levels of Akt, p-Akt, FoxO3a, p-FoxO3a, and BNIP3L were detected by Western blot. Chromatin immuno-precipitation (ChIP) analysis was used to test whether FoxO3a binds directly to the BNIP3L promoter region. A luciferase assay was used to study the effects of FoxO3a on BNIP3L gene promoter activity. Mitochondrial ΔΨM was quantified using tetramethylrhodamine methyl ester perchlorate (TMRM). The mitochondrial oxygen consumption rate (OCR) was assessed with a Seahorse XF24 Analyzer. Results: Treatment with H₂O₂ decreased the phosphorylation of Akt and FoxO3a, and it induced the nuclear localization of FoxO3a and the necrosis of H9c2 cells. These effects of H₂O₂ were abrogated by pretreatment with FGF-2. Furthermore, the protective effects of FGF-2 were abolished by the PI3K/Akt inhibitor Wortmannin. ChIP analyses indicated that FoxO3a binds directly to the BNIP3L promoter region. Using a luciferase assay, we further observed that FoxO3a increased BNIP3L gene promoter activity. As expected, overexpression of BNIP3L in H9C2 cardiomyoblast cells reduced the cardioprotection of FGF-2 in H₂O₂-induced necrosis and mitochondrial dysfunction. Conclusions: The present data suggest that FGF-2 protects against H₂O₂-induced necrosis of H9C2 cardiomyocytes via the activation of the PI3K/Akt/FoxO3a pathway. Moreover, the present results demonstrate that FoxO3a is an important transcription factor that acts by binding to the promoter and promoting the transcription of BNIP3L, and it contributes to the necrosis and mitochondrial dysfunction induced by H₂O₂ in H9c2 cardiomyoblast cells.

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“…Ferulic acid is present in Chinese medicinal herbs and exhibit pharmacological activities such antiinflammatory, platelet aggregation inhibitory, antihypertensive and anti-apoptotic effects [179,180]. In a daunorubicin-induced cardiotoxicity model in H9c2 cells, it was observed cellular protection by this compound from the induced apoptosis through a mechanism that involves the interruption of the ERKs signalling pathway [181]. In a scenario of anoxia/reoxygenation injury, where induced intracellular Ca 2+ overload is an important pathophysiological factor, it was observed that sodium ferulate attenuates this increase and improves cell survival in cultured cardiomyocytes through nitric oxide/cGMP-dependent protein kinase (cGMP/PKG) signal pathway [182].…”

Section: Phenolic Acidsmentioning

confidence: 99%

Pure Polyphenols Applications for Cardiac Health and Disease

Santos

Gomes

Oudot

et al. 2018

CPD

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Polyphenols are natural compounds present in fruits and vegetables that can exert beneficial effects on human health and notably, on the cardiovascular system. Some of these compounds showed significant protective activities toward atherosclerosis, hypertension, myocardial infarction, anthracyclin-induced cardiomyopathy, angiogenesis as well as heart failure. Polyphenols can act through systemic effects as well as through modulation of signaling pathways such as redox signaling, inflammation, autophagy and cell death in the heart and vessels. These effects can be mediated by changes in expression level and by post-translational modifications of proteins (e.g. Stat1, CaMKII, Sirtuins, BCL-2 family members, PDEs, TRF2, eNOS and SOD). This non-comprehensive short review aims to summarize recent knowledge on the main pharmacological effects and mechanisms of cardioprotection of pure polyphenols, using different approaches such as cell culture, animal models and human studies.

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Sodium Ferulate Prevents Daunorubicin - Induced Apoptosis in H9c2 Cells via Inhibition of the ERKs Pathway

Cited by 9 publications

References 46 publications

The Novel H7N9 Influenza A Virus NS1 Induces p53-Mediated Apoptosis of A549 Cells

The Novel H7N9 Influenza A Virus NS1 Induces p53-Mediated Apoptosis of A549 Cells

FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells

Pure Polyphenols Applications for Cardiac Health and Disease

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