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ABSTRACT: BACKGROUND: It has been reported that the induction of heme oxygenase-1 (HO-1) mediated by β1-adrenergic receptor inhibits high mobility group box 1 protein (HMGB1) release and increases the survival rate in cecal ligation and puncture-induced septic mice. The present study aimed to investigate whether dobutamine, a selective β1-adrenergic receptor agonist, could inhibit HMGB1 release via β1-adrenergic receptor-mediated HO-1 induction and attenuate myocardial ischemia/reperfusion (I/R) injury in rats. MATERIALS AND METHODS: Anesthetized male rats were pretreated with dobutamine (5 or 10 μg. Kg-1. min-1, intravenous) before ischemia in the absence and/or presence of LY294002 (0.3 mg/Kg), a phosphatidylinositol 3-kinase (PI3K)< inhibitor; SB203580 (1 mg/Kg), a p38 mitogen-activated-protein kinase (P38 mitogen-activated-protein kinase [p38 MAPK]) inhibitor, and zinc protoporphyrin IX ([ZnPPIX], 10 mg/Kg), a HO-1 inhibitor, respectively, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. The myocardial I/R injury and oxidative stress were assessed. Likewise, the expressions of HO-1 protein, nuclear factor kappa B (NF-κB) p65, and HMGB1 were measured by Western blot analysis. RESULTS: Dobutamine significantly and dose-dependently attenuated myocardial I/R injury, reduced oxidative stress, and caused the induction of HO-1, the reduction of NF-κB activation and HMGB1 over expression. However, all the effects caused by dobutamine were significantly reversed by the presence of LY294002, SB203580, and ZnPPIX, respectively. CONCLUSIONS: The present study demonstrated that dobutamine mediated the induction of HO-1 by selectively stimulating β1-adrenergic receptor via PI3K and p38 MAPK, which inhibited HMGB1 release and attenuated rat myocardial I/R injury in vivo.
Journal of Surgical Research 03/2013; · 2.25 Impact Factor
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ABSTRACT: Exogenous high-mobility group box 1 protein (HMGB1) injection could prevent left ventricular remodeling and enhance left ventricular function during myocardial infarction (MI). However, the mechanism remains unclear. This paper was to investigate in the mechanism of cardioprotection of HMGB1 during MI in rats. Anesthetized male rats were treated once with HMGB1 (200 ng) 4 h after MI and then executed after 7 and 28 days, respectively. Cardiac function, collagen deposition, and dishevelled-1 and β-catenin protein expression were measured. After MI 7 days or 28 days, the left ventricular ejection fraction (LVEF) was significantly decreased compared to that of sham-operated control group (P < 0.05). However, the LVEF HMGB1-treated groups were significantly higher compared to those of the MI group in both 7 days and 28 days (P < 0.05). The collagen volume fraction was significantly reduced in the HMGB1-treated group in infarcted border zone. HMGB1 could activate the expression of dishevelled-1 and β-catenin proteins (P < 0.05). Our study suggested that exogenous high-mobility group box 1 protein injection improves cardiac function after MI, which may be involved in Wnt/β-catenin signaling activation.
Journal of Biomedicine and Biotechnology 01/2012; 2012:743879. · 2.44 Impact Factor
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International journal of cardiology 05/2011; 150(2):222-3. · 7.08 Impact Factor
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ABSTRACT: High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Ethyl pyruvate (EP), a potent reactive oxygen species scavenger, has been reported to inhibit myocardial apoptosis and reduce myocardial I/R injury. The aim of this study was to investigate the mechanism by which EP reduces myocardial I/R injury in rats. Anesthetized male rats were once treated with EP (50 mg/kg, i.p.) before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that pretreatment of EP (50 mg/kg) could significantly reduce the infarct size and the levels of LDH and CK after 4 h reperfusion (all P<0.05). EP could also significantly inhibit the increase of the MDA level, the decrease of the SOD level (both P<0.05). Meanwhile, EP could significantly inhibit the expression of HMGB1 induced by I/R. The present study suggested that ethyl pyruvate could attenuate myocardial I/R injury by inhibiting HMGB1 expression.
Molecular Biology Reports 05/2011; 39(1):227-31. · 2.93 Impact Factor
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ABSTRACT: High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been reported that it could inhibit HMGB1 expression. This study investigated the effect of sodium butyrate on myocardial I/R injury in rats. Anesthetized male rats were once treated with sodium butyrate (100 or 300mg/kg, i.p.) 30min before ischemia, and then subjected to ischemia for 30min followed by reperfusion for 4h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. After 4h reperfusion, pretreatment of sodium butyrate (300mg/kg) could significantly inhibit the infarct size and the levels of LDH and CK (all P<0.05). Sodium butyrate (300mg/kg) could also inhibit significantly the increase of the MDA level and the decrease of the SOD level (both p<0.05). Sodium butyrate (300mg/kg) could also inhibit significantly the expression of HMGB1 induced by I/R. The present study suggested that pretreatment of sodium butyrate could protect against myocardial I/R injury by inhibiting HMGB1 expression.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 09/2010; · 2.24 Impact Factor
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ABSTRACT: Minocycline has been shown to protect against myocardial ischemia and reperfusion injury. However, the mechanism remains unclear. This study was to investigate the role of high mobility group box 1 protein (HMGB1) in the cardioprotection of minocycline during myocardial ischemia and reperfusion in rats. Anesthetized male rats were once treated with minocycline (45 mg/kg, i.p.) 1h before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4h. The lactate dehydrogenase (LDH), creatine kinase (CK) and infarct size were measured and the myocardial tissue apoptosis was assessed by TUNNEL assay. Neonatal rat ventricular myocytes were prepared and then cultured with recombinant HMGB1. Cell apoptosis was measured using an annexin V-FITC apoptosis detection kit. HMGB1 expression was assessed by immunoblotting. After 4h of reperfusion, minocycline could significantly decrease the infarct size, myocardium apoptosis and the levels of LDH and CK (all P<0.05). Meanwhile, minocycline could also significantly inhibit the HMGB1 expression during myocardial ischemia and reperfusion compared to that in ischemia and reperfusion group (P<0.05). In vitro, HMGB1 could significantly decrease the cell viability and promote the apoptosis of neonatal myocytes in a dose-dependent manner. The present study suggested that minocycline could protect against myocardial ischemia and reperfusion injury by inhibiting HMGB1 expression.
European journal of pharmacology 07/2010; 638(1-3):84-9. · 2.59 Impact Factor
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ABSTRACT: Sex hormones and gender differences have been reported to be associated with the occurrences of ventricular arrhythmias. This study investigated the relationship between sex hormones and idiopathic outflow tract ventricular arrhythmias (IOTVA) in adult male patients. Serum sex hormonal levels, which include testosterone, estradiol, and progestogen, were measured by using commercially prepared immunoassay kits. The average count of premature ventricular contractions (PVCs) (number/24h) was assessed by 72h electrocardiographic monitoring. No differences were found in the levels of testosterone and progestogen between the IOTVA male patients and the control males (both P>0.05). However, the level of estradiol in the IOTVA male patients was significantly lower than that in the control males (P<0.05). A significant negative correlation was observed between the number of PVCs and the level of estradiol in the IOTVA male patients (r=0.702, P<0.05). The current study suggested that IOTVA might be associated with the reduction of estradiol level in adult male patients.
Translational Research 11/2009; 154(5):265-8. · 2.99 Impact Factor
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ABSTRACT: High mobility group box 1 (HMGB1) protein has been identified as a novel pro-inflammatory cytokine in coronary artery disease (CAD). We investigated the relationship between serum HMGB1 level and the severity of coronary artery stenosis.
Serum HMGB1 concentration in patients was measured by ELISA. All patients underwent coronary angiography and were assigned into groups according to the quartile of HMGB1 level.
HMGB1 level in USAP group was higher than that in control and SAP group. HMGB1 level in SAP group was higher than that in control group (p<0.05). Gensini scores in the highest quartile group (group IV), group III and group II were all significantly higher than that in the lowest quartile group (group I). There was significant correlation between angiographic Gensini score and serum level of HMGB1 (r=0.710, p<0.05). However, in subgroup analysis, we found that serum HMGB1 level was only correlated with angiographic Gensini score in SAP patients (r=0.786, p<0.05), but not USAP patients.
Serum HMGB1 level was markedly increased with the severity of coronary artery stenosis in patients with SAP and USAP, especially in SAP patients, which suggested that increased serum HMGB1 may involve in the pathogenesis of atherosclerotic CAD.
Clinica chimica acta; international journal of clinical chemistry 06/2009; 406(1-2):139-42. · 2.54 Impact Factor
