Dobutamine-mediated heme oxygenase-1 induction via PI3K and p38 MAPK inhibits high mobility group box 1 protein release and attenuates rat myocardial ischemia/reperfusion injury in vivo

Wang, Jichun; Yang, Hongxin; Hu, Xiaorong; Fu, Wenwen; Xie, Jing; Zhou, Xin; Wang, Xu; Jiang, Hong

doi:10.1016/j.jss.2013.02.051

Cited by 41 publications

(32 citation statements)

References 30 publications

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“…Meanwhile, HO-1 has been reported to depend on PI3K/p38MAPK signaling pathway in many cells [9,[23][24][25]. Otherwise, HO-1 has been further demonstrated to be induced by dobutamine and inhibit HMGB1 release during myocardial I/R injury [11]. Importantly, cultured neonatal cardiomyocytes may present with a very stable phenotype and the contractile profile of cultured neonatal cardiomyocytes during H/R has been proved to be comparable with that of in situ adult hearts during I/R [26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

“…Otherwise, Salie et al [10] revealed that PI3K activation may be associated with the cardioprotective effects of pre-ischemic β1-ARs stimulation during myocardial I/R injury. Furthermore, Wang et al [11] demonstrated that DOB mediated the induction of HO-1 by stimulating β1-adrenergic receptors via PI3K and p38 MAPK pathway and inhibited HMGB1 release for attenuating rat myocardial I/R injury in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

Wang

Xie

et al. 2015

Cell Physiol Biochem

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This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Key WordsNuclear factor erythroid 2-related factor 2 • Heme oxygenase-1 • High mobility group box 1 protein Abstract Backgroud/Aims: The aim of the study was to evaluate the effects of beta1-adrenergic receptors (β1-ARs) -mediated nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 (HO-1)-high mobility group box 1 protein (HMGB1) axis regulation in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes. Methods: The neonatal cultured cardiomyocytes were concentration-dependently pretreated by dobutamine (DOB), a selective β1-adrenergic receptor agonist, in the absence and/or presence of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), SB203580 (a p38mitogen-activated-protein kinase (p38MAPK) inhibitor), Nrf2siRNA and HO-1siRNA, respectively, and then treated by H/R. The effects and mechanisms by which H/R-induced cardiomyocytes injury were evaluated. Results: Significant increase of HO-1 was found in neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Significant change for Nrf2 translocation was also revealed in neonatal cultured cardiomyocytes treated with DOB. Insignificant decreases of NFkappaB p65 activation and HMGB1 release were observed in H/R-induced neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Importantly, DOB treatment significantly increased the cell viability and decreased the levels of LDH and MDA in H/R-induced cardiomyocytes injury. However, DOB failed to increase HO-1, inhibit NF-kappaB p65 activation, prevent HMGB1 release and attenuate H/R-induced cardiomyocytes injury when the cultured cardiomyocytes were pretreated by Nrf2siRNA, HO-1siRNA, PI3K inhibitor (LY294002) and p38MAPK inhibitor (SB203580), respectively. Conclusions: β1-ARs-mediated Nrf2-HO-1-HMGB1 axis regulation plays a critical protective role in H/R-induced neonatal rat cardiomyocytes injury in vitro via PI3K/p38MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

Wang

Xie

et al. 2015

Cell Physiol Biochem

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“…Activation of Akt, which is downstream of PI3K, of the protective mechanism of ischemic preconditioning that inhibits myocardial I/R injury abolish the cardioprotective effects of simvastatin on I/R injury. Wang et al [23] reported that the PI3K pathway may be associated with the inhibition of HMGB1 expression in a rat pathway may mediate the protective effects of hesperidin in neural crest cell survival. Hence, we hypothesize that hesperidin-induced HMGB1 expression inhibition depends on the PI3K/Akt pathway.…”

Section: Introductionmentioning

confidence: 99%

Short-Term Hesperidin Pretreatment Attenuates Rat Myocardial Ischemia/Reperfusion Injury by Inhibiting High Mobility Group Box 1 Protein Expression via the PI3K/Akt Pathway

Wang

et al. 2016

Cell Physiol Biochem

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Background/Aims: Hesperidin pretreatment has been shown to protect against myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism is poorly understood. This study aimed to investigate the cardioprotective effects of a 3-day hesperidin pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the PI3K/Akt pathway. Methods: In a fixed-dose study, hematoxylin and eosin staining and myocardial enzyme measurements were used to determine the optimal dose of hesperidin that elicited the best cardioprotective effects against I/R injury. Furthermore, rats were pretreated with 200 mg/kg hesperidin, and infarct size and the levels of myocardial enzymes, apoptosis, inflammatory and oxidative indices, and HMGB1 and p-Akt expression were measured. Results: Our results indicated that while different 3-day hesperidin pretreatment doses promoted histopathological changes and reduced myocardial enzymes induced by I/R the optimal dose was 200 mg/kg. Moreover, the 200 mg/kg hesperidin pretreatment not only significantly decreased the infarct size as well as myocardial enzyme levels but also inhibited myocardial apoptosis, the inflammatory response and oxidative stress. Additionally, hesperidin downregulated HMGB1 expression and upregulated p-Akt expression in the myocardium. LY294002, a specific PI3K inhibitor, partially reversed the decreased HMGB1 expression, increased p-Akt expression induced by hesperidin and abolished the anti-apoptotic, anti-inflammatory and anti-oxidative effects of hesperidin. Conclusion: These findings suggest that short-term pretreatment with hesperidin protects against myocardial I/R injury by suppressing myocardial apoptosis, the inflammatory response and oxidative stress via PI3K/Akt pathway activation and HMGB1 inhibition.

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“…Therefore, the role of HO-1 may also play an important role in myocardial I/R injury-induced cardiac remodeling. In conclusion, since Nrf-2 translocation-mediated HO-1 induction has demonstrated to suppress high mobility group box 1 protein (HMGB1) release for attenuating rat myocardial I/R injury [11,12], these suggested that the Nrf-2/ARE-HO-1 axis may exist in myocardial I/R injury and play a potential therapeutic approach for attenuating myocardial I/R injuryinduced cardiac remodeling.…”

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confidence: 99%

The Nrf-2/ARE–HO-1 axis: An important therapeutic approach for attenuating myocardial ischemia and reperfusion injury-induced cardiac remodeling

Wang¹,

Hu²,

Jiang³

2015

International Journal of Cardiology

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Dobutamine-mediated heme oxygenase-1 induction via PI3K and p38 MAPK inhibits high mobility group box 1 protein release and attenuates rat myocardial ischemia/reperfusion injury in vivo

Cited by 41 publications

References 30 publications

Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

Short-Term Hesperidin Pretreatment Attenuates Rat Myocardial Ischemia/Reperfusion Injury by Inhibiting High Mobility Group Box 1 Protein Expression via the PI3K/Akt Pathway

The Nrf-2/ARE–HO-1 axis: An important therapeutic approach for attenuating myocardial ischemia and reperfusion injury-induced cardiac remodeling

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