Protection of intravenous HMGB1 on myocardial ischemia reperfusion injury

Zhang, Deyong; Zhang, Aixia; Zhou, Yanhong; Wang, Lanhua; Yao, Heng‐Chen

doi:10.1016/j.ijcard.2015.02.068

Cited by 8 publications

(8 citation statements)

References 11 publications

(11 reference statements)

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“…These are in accordance with some recent reported studies [5][6][7]. Recently, some studies have reported that exogenous HMGB1 protect heart against myocardial infarction [8] or myocardial ischemia reperfusion injury [9]. Thus HMGB1 may be a potential therapeutic target [10] both for basic myocardial ischemia and reperfusion injury research and clinical study in patients with ischemic heart disease.…”

supporting

confidence: 91%

Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure”

Gao

Zhou

Liu

et al. 2015

International Journal of Cardiology

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supporting

confidence: 91%

Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure”

Gao

Zhou

Liu

et al. 2015

International Journal of Cardiology

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“…P38MaPK can be activated by different extracellular stimuli and successfully converted to phosphorylated (p)-p38MAPK by specific serine or threonine phosphorylation and is subsequently transferred from the cytoplasm into the nucleus, where it activates the expression of transcription factors, regulates related genes and participates in numerous biological processes, such as tissue development, cell reproduction or apoptosis, inflammation and cancer metastasis (11)(12)(13)(14)(15). in previous studies of myocardial ischemia-reperfusion injury, asthma and intestinal injury, HMGB1 has been reported to be associated with the p38MaPK signalling pathway (16)(17)(18). However, it has not previously been reported whether HMGB1 participates in the pathogenesis of epilepsy by regulation of the p38MaPK signalling pathway.…”

Section: Introductionmentioning

confidence: 99%

Glycyrrhizin regulates the HMGB1/P38MAPK signalling pathway in status epilepticus

Luo

Zhang

et al. 2023

Mol Med Rep

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in recent decades, studies have reported that inflammation serves key roles in epilepsy and that high mobility group box protein-1 (HMGB1) may be involved in status epilepticus. However, it has not been reported whether HMGB1 participates in the pathogenesis of status epilepticus through the regulation of the p38 mitogen-activated protein kinase (p38MaPK) signalling pathway. in the present study, Sprague-dawley rats were randomly divided into four groups as follows: control, status epilepticus (Se), dimethyl sulfoxide treatment (dMSo + Se), and glycyrrhizin treatment (Gl + Se) groups. Behavioural changes were then evaluated using the racine score. in the hippocampus, the protein expression levels of HMGB1 were assessed using western blotting, the neuronal damage was evaluated using haematoxylin and eosin staining and transmission electron microscopy, and the activation of microglia was assessed using immunochemistry and immunofluorescence. The results demonstrated that, in the hippocampal region, HMGB1 existed in neurons and astrocytes and the protein expression levels of HMGB1, p38MaPK and phosphorylated-p38MAPK were significantly inhibited after treatment with Gl. Furthermore, Gl could alleviate neuronal injury in the ca1 region of the hippocampus and prevented HMGB1 translocation from the nucleus into the cytoplasm in these areas. These findings expand the understanding of how HMGB1 may participate in Se and lay a foundation for evaluation of HMGB1 as a drug target.

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“…Specifically, inhibition of myocardial expression of HMGB1 attenuates the extent of myocardial injury in rats following myocardial I/R (Yao et al, 2015). Additionally, administration of exogenous HMGB1 decreases IS and improves myocardial function; these effects are associated with suppressed myocardial inflammation (Abarbanell et al, 2011;Zhou et al, 2012;Zhang et al, 2015;Yao et al, 2016). However, whether exogenous HMGB1 affects the myocardial expression of VEGF remains unknown.…”

Section: Introductionmentioning

confidence: 99%

“…The PI3K/Akt signaling pathway is essential in the protection of the myocardium against I/R injury (Chen et al, 2014;Yu et al, 2014). Recently, our laboratory was the first to report that intravenously delivered HMGB1 protects the heart from I/R injury (Zhang et al, 2015) through the upregulation of hypoxia-inducible factor-1α (HIF-1α) in the myocardium. This effect can be mediated by the activation of the protein kinase B-dependent signaling pathway (Yao et al, 2016), or by the inhibition of the p38 MAPK pathway (Zhou Y.H.…”

Section: Introductionmentioning

confidence: 99%

HMGB1 Protects the Heart Against Ischemia–Reperfusion Injury via PI3K/AkT Pathway-Mediated Upregulation of VEGF Expression

et al. 2020

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Delivery of exogenous high mobility group box 1 (HMGB1) may exert a beneficial effect on myocardial ischemia-reperfusion (I/R) injury. Since the expression of vascular endothelial growth factor (VEGF) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) in the myocardium mediates the cardioprotective function of basic fibroblast growth factor, we hypothesized that VEGF and the PI3K/Akt signaling pathway also mediate the protective effects of intravenously delivered HMGB1. Thus, the objective of the present study was to analyze the impact of intravenous administration of HMGB1 on the myocardial expression of VEGF, myocardial fibrosis, and cardiac function in rats subjected to acute myocardial I/R. The ischemia was induced by ligation of the left anterior descending coronary artery for 30 min and was followed by 3 h of reperfusion. Myocardial malondialdehyde content, infarct size, and collagen volume fraction decreased, while the activity of superoxide dismutase was increased, the expression of VEGF and p-Akt was upregulated, and cardiac function was improved in the HMGB1-treated group when compared with rats subjected to I/R only (all P < 0.05). However, these effects of HMGB1 were abolished by LY294002. The obtained results demonstrate that the cardioprotective effects of intravenous administration of HMGB1 prior to I/R may be mediated by upregulation of myocardial expression of VEGF, which may activate the PI3K/Akt signaling pathway.

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Protection of intravenous HMGB1 on myocardial ischemia reperfusion injury

Cited by 8 publications

References 11 publications

Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure”

Response to letter regarding “Increased serum HMGB1 level may predict the fatal outcomes in patients with chronic heart failure”

Glycyrrhizin regulates the HMGB1/P38MAPK signalling pathway in status epilepticus

HMGB1 Protects the Heart Against Ischemia–Reperfusion Injury via PI3K/AkT Pathway-Mediated Upregulation of VEGF Expression

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