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Publications (7)11.98 Total impact

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    ABSTRACT: Ischemia postconditioning (IpostC) is an effective way to alleviate ischemia and reperfusion injury; however, the protective effects seem to be impaired in candidates with diabetes mellitus. To gain deep insight into this phenomenon, we explored the role of DJ-1, a novel oncogene, that may exhibit powerful antioxidant capacity in postconditioning cardioprotection in a rat model of myocardial ischemia reperfusion injury. Compared with normal group, cardiac DJ-1 was downregulated in diabetes. Larger postischemic infarct size as well as exaggeration of oxidative stress was observed, while IpostC reversed the above changes in normal but not in diabetic rats. DJ-1 was increased after ischemia and postconditioning contributed to a further elevation; however, no alteration of DJ-1 was documented in all subgroups of diabetic rats. Alteration of the cardioprotective PI3K/Akt signaling proteins may be responsible for the ineffectiveness of postconditioning in diabetes. There is a positive correlation relationship between p-Akt and DJ-1 but a negative correlation between infarct size and DJ-1, which may partially explain the interaction of DJ-1 and IpostC cardioprotection. Our result indicates a beneficial role of DJ-1 in myocardial ischemia reperfusion. Downregulation of cardiac DJ-1 may be responsible for the compromised diabetic heart responsiveness to IpostC cardioprotection.
    Oxidative Medicine and Cellular Longevity 01/2013; 2013:564902.
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    ABSTRACT: To evaluate the efficacy and safety of dexmedetomidine for emergence agitation after tonsillectomy in children. 120 ASA physical status I and II children, aged 5-14 years, undergoing anesthesia for tonsillectomy, were randomly divided into 3 groups: Placebo group, the low dexmedetomidine concentration group and the high dexmedetomidine concentration group. Before the entrance of the operating room (OR), all of the children received intravenous injection 40 μg kg(-1) midazolam to reduce anxiety at first, and then dexmedetomidine was given intravenously at an initial loading dose of 0.5 μg kg(-1) or 1 μg/kg over a 10-min period via a computer controlled infusion pump followed by a maintenance infusion of 0.2 μg kg(-1)h(-1) or 0.4 μg kg(-1)h(-1)over the surgery. The heart rate, SpO(2) and mean arterial blood pressure were recorded for each patient in both operation room and PACU. The designated time points: at the start of the anesthetic induction, at the discontinuation of inhalational agents, at first opening of eyes, at time to remove endotracheal tube were recorded. After patient arrival at the PACU, VAS score, RSS, the occurrence of emergence agitation were recorded every 5 min for the first 30 min and every 10 min for the next 30 min after endotracheal tube was removed. There was significant difference in the incidence of emergence agitation between Placebo group and the high concentration group when endotracheal tube was removed (P<0.05). There was significant difference in the VAS pain scores and in the RSS between three groups at the time of extubation, as well as 5 min and 10 min after extubation (P<0.05). Dexmedetomidine appears to be safe and effective to reduce the incidence of early emergence agitation in children after tonsillectomy. Initial loading dose of 1.0 μg kg(-1) followed by a maintenance infusion of 0.4 μg kg(-1)h(-1) is better choice for children received tonsillectomy.
    International journal of pediatric otorhinolaryngology 04/2012; 76(7):1036-41. · 0.85 Impact Factor
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    ABSTRACT: To investigate the effects of ligustrazine on acute lung injury induced by blunt chest trauma. This study was performed in the Animal Center of Renmin Hospital of Wuhan University, Wuhan, China between September 2009 and September 2010. Male Sprague-Dawley rats were randomly allocated into 4 groups: sham control group (group C, n=60), ligustrazine treatment group (group C+L, n=60), blunt chest trauma model group (group T, n=60), and the trauma plus ligustrazine treatment group (group T+L, n=60). The lung contusion was induced as previously described. Animals of the T+L group were intraperitoneally injected with ligustrazine. Acute lung injury was evaluated by histopathology of the lung, and apoptosis was determined by terminal dUTP nick-labeling. Pulmonary edema was estimated using Evans blue dye extravasation and wet/dry ratios of lung tissue. The expression of caspase-3, Bcl-2, and Bax in the lung, as well as blood plasma tumor necrosis factor (TNF)-alpha were also measured. The ligustrazine treatment significantly attenuated lung injury induced by blunt chest trauma, as shown by decreased apoptosis index, and pulmonary edema (p=0.04). The blood plasma TNF-alpha level after blunt chest trauma significantly deceased after the administration of ligustrazine (p=0.03). In addition, the ligustrazine treatment significantly alleviated the expression of caspase-3 (p=0.03), and increased the ratio of Bcl-2 to Bax (p<0.03). Ligustrazine effectively protects lung injury induced by blunt chest trauma, and the protective effects seem to be mediated by attenuation of cell apoptosis via an increased ratio of Bcl-2/Bax and decreased caspase-3 activity.
    Saudi medical journal 02/2012; 33(2):139-45. · 0.62 Impact Factor
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    ABSTRACT: Phosphocreatine (PCr) is an endogenous compound containing high-energy phosphate bonds. It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this study, rat cerebral ischemia-reperfusion injury models were constructed. Apoptotic cells in the cortex region were measured by TUNEL method. Malondialdehyde (MDA) content was detected by chromatometry, and calmodulin (CaM) activity was detected by ELISA. Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia-reperfusion group (I/R group) and PCr preconditioning group (PCr group); compared with I/R group, TUNEL-positive cells, MDA content, and level of CaM activity decreased in PCr group. This study indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain through attenuating abnormalities of calcium balance and production of oxygen free radicals.
    BioMed Research International 01/2011; 2011:107091. · 2.71 Impact Factor
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    ABSTRACT: Diabetes mellitus is associated with decreased NO bioavailability in the myocardium. Ginsenoside Rb1 has been shown to confer cardioprotection against ischemia reperfusion injury. The aim of this study was to investigate whether Ginsenoside Rb1 exerts cardioprotective effects during myocardial ischemia-reperfusion in diabetic rats and whether this effect is related to increase the production of NO via enhancing eNOS expression in the myocardium. The myocardial I/R injury were induced by occluding the left anterior descending artery for 30 min followed by 120 min reperfusion. An eNOS inhibitor L-NAME or Rb1 were respectively administered 25 min or 10 min before inducing ischemia. Ginsenoside Rb1 preconditioning reduced myocardial infarct size when compared with I/R group. Ginsenoside Rb1 induced myocardial protection was accompanied with increased eNOS expression and NO concentration and reduced plasma CK and LDH (P < 0.05). Moreover, the myocardial oxidative stress and tissue histological damage was attenuated by Ginsenoside Rb1 (P < 0.05). L-NAME abolished the protective effects of Ginsenoside Rb1. It is concluded that Ginsenoside Rb1 protects against myocardium ischemia/reperfusion injury in diabetic rat by enhancing the expression of eNOS and increasing the content of NO as well as inhibiting oxidative stress.
    BioMed Research International 01/2011; 2011:767930. · 2.71 Impact Factor
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    ABSTRACT: The objective of the current study is to investigate whether ginsenoside Rb1, a major pharmacological extract of ginseng that could attenuate myocardial ischemia reperfusion (MI/R) injury in non-diabetic myocardium, can attenuate MI/R injury in diabetes that are more vulnerable to ischemic insult. Rats were divided into seven groups: (i) diabetic sham, (ii) diabetic, (iii) normal, (iv) diabetic + ginsenoside Rb1, (v) diabetic + wortmannin, (vi) diabetic + wortmannin + ginsenoside Rb1, (vii) diabetic sham + wortmannin. Ginsenoside Rb1 and/or wortmannin were administered prior to inducing MI/R (30 min of coronary artery occlusion followed by 120 min reperfusion). At the end of the experiment, postischemic myocardial infarct size was significantly higher in the diabetic untreated group as compared to normal (P < 0.05), accompanied with increased myocardial apoptosis, elevated plasma CK-MB and LDH release and reduced blood pressure. Ginsenoside Rb1 reduced infarct size, cardiomyocyte apoptosis and caspase-3 activity compared to the diabetic group. The cardioprotective effects of ginsenoside Rb1 were cancelled by wortmannin. Ginsenoside Rb1 significantly upregulated phosphorylated Akt expression, which was attenuated by wortmannin. Ginsenoside Rb1 exerts cardioprotective effects against MI/R injury in diabetic rats, which is partly through activation of phosphatidylinositol 3-kinase (PI3 K)/Akt pathway. Thus this study shows a novel pharmacological preconditioning with ginsenoside Rb1 in the diabetic myocardium.
    Molecular Biology Reports 11/2010; 38(7):4327-35. · 2.51 Impact Factor
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    ABSTRACT: A simple and rapid CZE method was established for the simultaneous determination of valienamine, acarbose and validamycin A, using a 20-kV CZE with the detection wavelength of 193 nm and 50 mM phosphoric acid-20 mM Tris (pH 5.3) as a running buffer. The calibration curves of valienamine, acarbose, and validamycin A showed a good linear relationship at a concentration range of 5-1000 microg/mL. The detection limits of valienamine, acarbose, and validamycin A were 0.3, 0.6, and 0.6 microg/mL, respectively, and the average recoveries of each of the above were 99.9, 99.5, and 100.3%. The method has been successfully applied for simultaneous determination of substrate and product in the process of preparation of valienamine.
    Journal of Separation Science 07/2010; 33(13):1997-2001. · 2.59 Impact Factor