Oxidative stress played an important role in the development of diabetes and its complications. Nuclear factor erythroid 2-related factor 2 (NRF2) pathway is one of the most vital endogenous antioxidant pathways. Accumulated evidences indicated that the relationship between diabetes and NRF2 pathway attracted more and more attention in recent years. Our group has devoted ourselves to the researches concerning the chronic complications of diabetes and NRF2 pathways. This review highlighted our recent progresses in the underlying mechanism of the protective role of NRF2 in diabetic nephropathy, diabetic ulcers and diabetic amyotrophy. Finally, the possibility of NRF2 agonists applied to clinical therapy for diabetic chronic complications was explored.

Aim To study the effects of preconditioning with desflurane, sevoflurane and isoflurane on adenosine triphosphate (ATP) in anoxia-reoxygenation myocardial cells. Methods Rat ventricular myocytes, cultured for 4～5 days, were randomly allocated to five groups: Control group, anoxia-reoxygenation group and groups preconditioned with 1.5 MAC desflurane, sevoflurane or isoflurane following anoxia-reoxygenation. The content of intracellular ATP ,the activities of lactic dehydrogenase(LDH) and creatine kinase(CK), and the cell viability were measured at the end of experiment.Results Preconditioning with 1.5 MAC desfllurane, sevoflurane or isoflurane significantly attenuated the great reduction in ATP and cell viability and the increase of LDH and CK caused by anoxia-reoxygenation. There was a positive correlationship between ATP and cell viability,and a negatiue correlationship between LDH and CK (r was 0.83, -0.87 and -0.82 respectively, P

ObjectiveTo investigate the effect of mild hypothermia on neuron specific enolase (NSE) and superoxide dismutase (SOD) in serum of patients with large-area cerebral infarction.Methods160 cases with large-area cerebral infarction were divided into the treatment group and control group with 80 cases in each group. Patients of the control group were treated with routine therapy. Those of the treatment group were added with mild hypothermia therapy (MHT). The scores of NIHSS were assessed and NSE and SOD in serum were examined before treatment and 7, 14 and 30 days after treatment in two groups.ResultsThe NIHSS score of the treatment group was significantly lower than that of the control group ( P<0.05), and NSE level decreased, SOD vitality increased in the treatment group. Other indexes such as respiratory, pulse, serum kalium and etc of two groups were not different ( P>0.05).ConclusionMHT can improve he nerve function of patients with large-area cerebral infarction recovering and improve prognosis.

Humans ; Inflammation ; drug therapy ; metabolism ; MicroRNAs ; metabolism ; Stilbenes ; pharmacology ; therapeutic use

Objective To investigate the biocompatibility between collagen- polyglycolic acid (PGA) and bone marrow mesenchymal stem cells (MSCs) in vitro to provide some experimental basis for further study in tendon tissue engineering. Methods MSCs were isolated, cultured and characterized. In the experimental group the MSCs were cultured in DMEM containing type-I collagen and PGA suture, and in the control group the MSCs were cultured in DMEM. The cell growth was compared between the two groups, and the cell ultramicroscopic structure of experimental group was observed. Results MSCs grew well in the collagen-PGA scaffold, and 2 weeks after incubation they still kept secretion potential and more than cell 89% vitality, which were not significantly different compared with the control group. There is no statistical difference in the MSCs count in the experimental group during 2 weeks culture, while in the control group MSCs began to proliferate at the 4th day after culture. Conclusion Collagen-PGA has a good biocompatibility with mesenchymal stem cells. It is possible to fabricate a tissue-engineered tendon in vitro using mesenchymal stem cells as seed cells and collagen-PGA as scaffold.

Objective Protection afforded by ischemic preconditioning (IPC) against myocardial ischemia in adult heart has been investigated. This study was designed to examine the effects of IPC on myocardial tolerance to ischemia in immature hearts.Methods The aorta of isolated immature rabbit heart (14-21d old) was connected to Langendorff preparation within 30 s after excision. The hearts were perfused with oxygenated (95%O 2:5%CO 2) Krebs-Henseleit buffer(KHB) at 60 cmH 2O. 16 immature rabbit hearts were equally divided into 2 groups: control group and IPC group. In IPC group the hearts were first subjected to IPC stimulus consisting of 5 min global ischemia followed by 10 min reperfusion. The hearts in both groups were made globally ischemic for 30 min(no perfusion) followed by 40 min reperfusion. At the end of 40 min reperfusion the hearts were harvested for ATP analysis. The coronary flow(C), HR, left ventricle developed pressure(LVDP) and ?dp/dt were monitored and recorded before ischemia and at 5,10,20,30 and 40 min of reperfusion, and calculated as % of pre-ischemia levels. Coronary flow was collected before and after reperfusion for CK-MB determination.Results There were no statistically significant differences in the four parameters between the two groups. Arrhythmia scores were also comparable betweeen the two groups. The CK-MB leakage in IPC group was increased but not significantly different from that in control group. The ATP levels of myocardium at the end of reperfusion was significantly lower than that in the control group [(123.85?17.42)?g/g versus (167.21?16.53)?g/g].Conclusions IPC can not protect immature rabbit hearts from ischemia-reperfusion injury. On the contrary it may lead to myocardial injury due to more energy consumption.

Objective To investigate whether ischemic preconditioning( IPC) could protect against ischemia-reperfusion injury in immature rabbit heart and the role of KATP channel in the mechanism of myocardial protection. Methods New Zealand rabbits aged 14-21 days weighing 220-280g were used. The animals were anesthetized and heparinized. Chest was opened and heart was quickly removed and aorta was connected to Langendorff preparation within 30 s. The hearts were perfused with Krebs-Henseleit buffer balanced with gas mixture(O2: CO2 = 95% : 5% ) at 60cmH2O2(perfusion pressure) . IPC consisted of 5 mm global ischimia plus 10 mm reperfusion. Glibenclamide was used as KATP channel blocker. Cardiac arrest was induced with cold(4℃ ) St Thomas Ⅱ cardioplegic solution and heart was made globally ischemic by withholding perfusion for 45 mm followed by 40 mm reperfusion. Thirty immature rabbit hearts were randomly divided into four groups: group Ⅰ( n= 9 control) was subjected to ischemia-reperfusion only; groupⅡ(n= 9 IPC + ischemia-reperfusion); group Ⅲ(n = 6 glibenclamide + ischemia-reperfusion) and group Ⅳ( n= 6 glibenclamide + IPC + ischemia-reperfusion) . Coronary flow(CF), HR, left ventricle developed pressure( LVDP) and ? dP/dt max were monitored before ischemia/IPC/glibenclamide( baseline value) and 5, 10, 20 and 40 mm after reperfusion and were expressed as percentage of their baseline values. Arrhythmia scores were recorded. Coronary effluent was collected at 10 miii after reperfusion was started for determination of CK-MB level. At the end of reperfusion 200mg myocardium was taken from apex for determination of ATP content. Results The group Ⅱ(IPC group) showed best results. The recovery of CF, HR, LVDP and ?dp/dt max, was best among the four groups. The incidence of arrhythmia was low and less CK-MB leaked out. Myocardial ATP content was better preserved. Pretreatment with glibenclamide completely abolished the myocardial protection provided by IPC but did not affect ischemiareperfusion injury. Conclusions IPC can protect against ischemia-reperfusion injury in immature rabbit bean. Activation of KATh channel is involved in the mechanism of myocardial protection of IPC.

Objective To investigate whether diazoxide preconditioning can exert protective effect on myocardium against ischemia-reperfusion injury in immature rabbits and the possible mechanism. Methods Twenty-one healthy 3-4 week old white rabbits of either sex were randomly divided into 3 groups : group Ⅰ control ( n = 8) ; group Ⅱ diazoxide preconditioning ( n = 8) and group Ⅲ diazoxide + 5-HD preconditioning ( n = 5) . The animals were anesthetized with intraperitoneal pentobarbital 50 mg?kg-1 and heparized (150 IU?kg-1). The hearts were excised and connected to Langendorff apparatus and passively perfused with normothermic (37℃), oxygenated (95% O2 , 5% CO2) Krebs-Henseleit buffer (KHB) at a constant perfusion pressure of 70cmH2O. A latex balloon was inserted via left atrium into left ventricle and filled with water. The left ventricular end-diastolic pressure (LVEDP) was maintained at 10 mm Hg. In group I cardiac arrest was induced with St Thomas Ⅱ solution after the heart was perfused with KHB for 30 min. In group 11 after being perfused with KHB for 15 min, the hearts were perfused with diazoxide 100?mol?L-1 for 5 min followed by 10 min wash-out with KHB , then cardiac arrest was induced as in group Ⅰ . In group Ⅲ after being perfused with KHB for 15 min, the hearts were perfused with diazoxide 100?mol?L-1 and 5-HD 100?mol?L-1 for 5 min, followed by 10 min wash-out with KHB, then the cardiac arrest was induced as in group Ⅰ and Ⅱ . All hearts were subjected to 30 min ischemia followed by 45 min reperfusion after cardiac arrest. Coronary flow (CF), HR, left ventricular developed pressure (LVDP) and dp / dt max were measured after the hearts were perfused with KHB for 15 min (baseline) and at 5, 10, 15, 30, 45 min after reperfusion was resumed. Coronary effluent was collected at 5 min after reperfusion was resumed for determination of myocardial enzymes, CK, LDH and AST. At the end of experiment myocardial specimen was obtained for determination of ATP content and ultrastructure examination. Results There was no significant difference in the baseline hemodynamic parameters among the three groups. The rates of recovery of LVDP and ? dp / dt max after reperfusion were significantly higher in group Ⅱ than those in group I and Ⅲ ( P 0.05 ) , Conclusion Diazoxide can protect myocardium from ischemia-reperfusion injury by opening the mitochondrial KATP channel in immature rabbits.

Angioplasty, Balloon, Coronary ; instrumentation ; Female ; Humans ; Middle Aged ; Prosthesis Failure ; Stents

Objective To explore the correlation between serum level of cystatin C and coronary slow flow (CSF).Methods Thirty-four patients with CSF were enrolled in CSF group and thirty-five patients with normal coronary flow and angiographically normal coronary arteries were enrolled in control group.Coronary flow patterns was assessed by corrected thrombolysis in myocardial infarction (TIMI) frame count.The change of serum high sensitivity C-reactive protein,uric acid,cystatin C were measured.Results There was no significant difference between two groups with respect to gender,age,history of smoking,prevalence of hypertension and diabetes mellitus,family history of coronary heart disease,low density lipoprotein,α-lipoprotein (P ＞0.05).Compared with control group,the level of serum high sensitivity C-reactive protein,cystatin C,uric acid in CSF group were obviously higher [(4.85 ± 6.39) mg/L vs.(2.55 ± 2.18) mg/L,(0.87 ± 0.22) mg/L vs.(0.75 ± 0.16) mg/L,(329.68 ± 85.46) μ mol/L vs.(278.97 ± 76.74) μ mol/L] (P ＜ 0.05 or ＜ 0.01).Logistic regression analysis showed that cystatin C increased as independent risk factors for CSF (P =0.002,OR =0.009).Conclusion High level of cystatin C may play an important role in the occurrence and development of CSF.