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Publications (6)5.11 Total impact

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    ABSTRACT: This study assessed changes in myocardial ALDH2 expression in the diabetic rat, in particular the diabetic rat pretreated with ALDH2 activator ethanol (EtOH). The rats were divided into 6 groups: control, EtOH control, diabetic rat at fourth week (DM4W), eighth week (DM8W), twelfth week (DM12W) and EtOH+DM8W groups. Compared with control group, fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) levels were increased in DM groups. HbA1c level in DM12W group was higher than in DM4W group, HbA1c level in EtOH+DM8W group was lower than in DM8W group. Compared with control group, there were no changes of LVDP, HR and ±dp/dtmax in DM4W group, but there were decreased in DM8W and DM12W groups, and increased in the EtOH+DM8W group. In DM groups, SOD activity, ALDH2 mRNA and protein levels were reduced, MDA content was increased compared with control group; which decreased further as diabetes progressed. Compared with DM8W group, SOD and ALDH2 in EtOH+DM8W group was increased, MDA was decreased. Our results indicated with the development of diabetes, myocardial ALDH2 expression was further decreased accompanying decreased ventricular function. However, activation of ALDH2 can decrease diabetes induced myocardial injury. ALDH2 may be one key endogenous cardiac protective factor in diabetic individuals.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 03/2013; · 2.99 Impact Factor
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    ABSTRACT: The present study was designed to investigate the roles of Ca activated K channel (K) and protein kinase C (PKC) in the protective mechanisms of remote ischemic post conditioning (RPostC) when rat heart was subjected to ischemia/reperfusion (I/R) injury in vivo. Rat heart was subjected to regional ischemia for 45 min and reperfusion for 180 min in vivo to mimic I/R injury. RPostC was induced by 5 min right femoral artery occlusion followed by 5 min reperfusion for 3 cycles (totally 30 min) after 15 min of cardiac ischemia. Delayed remote ischemic post conditioning (delayed RPostC) was induced after 10 min of cardiac reperfusion. The hemodynamic parameters including mean arterial blood pressure and heart rate (HR) were recorded, and lactate dehydrogenase (LDH) release in plasma and infarct size were determined, and arrhythmia scores were calculated. In contrast to I/R, RPostC reduced infarct size and LDH release during reperfusion, the occurrence of arrhythmia was decreased, but no changes in delayed RPostC. The specific inhibitor of K iberiotoxin and PKC inhibitor chelerythrine both attenuated the role of RPostC. The findings indicated that RPostC had a protective effect on myocardial ischemia/reperfusion injury. Opening of K and activating of PKC may be involved in the mechanisms of RPostC.
    Pakistan journal of pharmaceutical sciences 03/2013; 26(2):285-90. · 0.95 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the role of mitofusin-2 (Mfn2) in different stages of diabetes in rats and to analyze the related mechanism(s). A diabetic model in SD rats was induced by a single intraperitoneal injection of 55 mg/kg streptozoticin (STZ). The hearts were isolated from diabetes mellitus (DM) rats at the fourth week (DM4W), eighth week (DM8W) and twelfth week (DM12W) and fasting blood glucose (FBG) levels and the ratio of heart weight to body weight (HW/BW) were measured. Malondialdehyde (MDA) content, superoxide dismutase (SOD) and caspase 3 activities were measured. The expression of Mfn2 of the left anterior myocardium at the mRNA level was detected using RT‑PCR. In contrast to the normal group, in the DM4W, DM8W and DM12W groups, there was a significant increase in the FBG levels, but no difference among the DM4W, DM8W and DM12W groups. The HW/BW ratio as well as the MDA content were increased, while SOD activity was reduced. Caspase‑3 activity was increased, while the expression of Mfn-2 mRNA levels was reduced. In addition, with the development of diabetic cardiomyopathy, the contents of MDA and caspase 3 were increased, whereas SOD activity and Mfn-2 mRNA levels were further reduced. In conclusion, our results indicated that with the development of diabetes, the expression of cardiac Mfn2 has showed a decrease, which may be associated with the decrease of antioxidant ability and progression of apoptosis.
    Molecular Medicine Reports 07/2012; 6(4):811-4. · 1.17 Impact Factor
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    ABSTRACT: To evaluate the anti-apoptotic effect of aldehyde dehydrogenase 2 (ALDH2) on myocardial ischemia/reperfusion (I/R) injury in diabetic rats. Normal male SD rats were divided into normal, diabetes and ethanol (the agonist of ALDH2) + diabetes groups. In the latter two groups, diabetes was induced by an intraperitoneal injection of 55 mg/kg STZ. Four weeks after the modeling, myocardial I/R was mimicked ex vivo, and lactate dehydrogenase (LDH) content in the coronary flow was determined. The activities of caspase-3 and ALDH2 were evaluated, and the expressions of Bcl-2 and Bax mRNA in the left anterior myocardium were detected using RT-PCR. In diabetic group, LDH release and caspase-3 activity were increased, while ALDH2 activity and Bcl-2/Bax mRNA expression were decreased as compared to those in normal control group. Compared with the diabetic group, ALDH2 agonist ethanol significantly reduced LDH release and caspase-3 activity, increased ALDH2 activity and Bcl-2/Bax mRNA expression. In diabetic rats, enhanced ALDH2 expression can offer mycardial protection possibly in relation to suppress cell apoptosis.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 03/2012; 32(3):345-8.
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    ABSTRACT: To observe the role of activation of aldehyde dehydrogenase 2 (ALDH2) on myocardial ischemia/reperfusion (I/ R) injury in diabetic rats. Diabetic rat model was simulated by intraperitoneal injection 55 mg/kg streptozotocin (STZ) and divided into diabetes and ethanol + diabetes groups (n = 8). After 8 weeks, myocardial ischemia/reperfusion model was mimicked in vitro. The ventricular dynamical parameters and lactate dehydrogenase (LDH) content in coronary flow were determined. The fasting blood glucose and glycosylated hemoglobin (HbA1c) level were determined by automatic biochemistry analyzer. The ALDH2 mRNA and protein expressions of left anterior myocardium were evaluated by RT-PCR and Western blot. In contrast to I/R in normal rat, in diabetic rat, left ventricular development pressure (LVDP), maximal rise/fall rate of left ventricular pressure (+/- dp/dtmax) and left ventricular work (RPP) were decreased, left ventricular end diastolic pressure (LVEDP) and LDH release were increased, and ALDH2 mRNA and protein expressions were decreased; compared with I/R in diabetic rat, ALDH2 agonist ethanol significantly promoted the recovery of LVDP, +/- dp/dtmax, RPP, reduced HbA1c level, LVEDP and LDH released, ALDH2 mRNA and protein expressions were increased. In diabetic rat, the expression of ALDH2 was decreased when heart was subjected to I/R. Enhanced mitochondrial ALDH2 expression in diabetic rat could play cardiac protective role.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 03/2012; 28(2):133-7.
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    ABSTRACT: To investigate whether the release of nitric oxide (NO) was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts. Hearts isolated from male SD rats were subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min (at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min). The rats were divided into five groups: normal, ischemia and reperfusion, ethanol postconditioning, ethanol postconditioning + L-nitro-arginine-methylester (L-NAME) and ethanol postconditioning + atractyloside. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis. In contrast to ischemia and reperfusion, ethanol postconditioning improved left ventricular developed pressure, rate pressure product during reperfusion, reduced LDH release and infarct size. NO content was decreased. The ratio of Bcl-2/Bax was increased. Administration of nitric o-xide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning, which inhibited the recovery of hemodynamic parameters, the decreases of LDH and infarct size. NO content was decreased furtherly. The ratio of Bcl-2/Bax was decreased. The cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release, inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.
    Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 01/2012; 28(1):9-13.