AIM:To observe the effects of adiponectin on injury of the 3-4 d SD rat cardiomyocytes induced by the intervention of H2O2.METHODS:Primary cardiomyocytes were obtained from neonatal rat and were cultured by enzymatic digestion methods.The molecular marker was observed by ?-actin immunocytochemistry.Primary cultured 3-4 d cells were used in experiment,and the injury model was established by H2O2,and adiponectin and Ara-A were used for pre-treatment before cell culture.The morphological change of cardiomyocytes was observed under electron microscope.The contents of LDH,MDA and the activity of SOD were measured.The apoptosis of cardiomyocytes was detected by agarose gel electrophoresis and Annexin V/PI staining with flow cytometry.RESULTS:Adiponectin pretreatment significantly decreased the release of LDH(P

AIM: To investigate the effect of hyperhomo cysteine on endothelial cell function. METHODS: By establishing hyperhomocysteinemia model, 18 male New Zealand rabbits were divided into control group (control group) and high-methi o nine-diet group (M group). At the end of 3 weeks, M group was divided again into M+0 group (continuing high methionine-diet) and M+F group (high-methionine-diet plus folic acid, vitamin B 12). At the end of 6 weeks, isolated aortic rin g s were made and the maximum vasodilation of the aortic rings to Ach was investig ated. Meanwhile, the plasma concentrations of Hcy, NO, ET-1, Ang II at 0 week, 3 weeks and 6 weeks and the contents of NO 2-/NO 3-, Ang Ⅱ, ET-1, NOS i n regional vascular tissue at 8 weeks were also measured. RESULTS: (1) In contrast to M+F group and control group, the max imum vasodilation to Ach were decreased (E max=26.73?4.51 vs 47.84 ?5.62, 56.42?7.82, P

Aim To study the effect of adiponectin ( APN) on myocardial ischemia reperfusion( IR) injury in diabetic rats and to explore the role of oxidation-an-tioxidation system. Methods Male Sprague Dawley rats were randomly divided into control group( NS) , IR group ( NIR ) , diabetes group ( DS ) , DS + IR group (DIR), DS +APN +IR group(APN). Experimental diabetes was induced in the animals by a single intrap-eritoneal injection of streptozotocin at a dose of 55 mg ·kg-1 . The IR and NIR group were subjected to myo-cardial I/R injury. APN group was administered APN through intravenous injection 10 min before the reper-fusion, the others were administered normal saline. The rats were considered diabetic and used for the study only if their glucose levels were higher than 15 mmol·L-1. Results All the diabetic rats exhibited increased levels of blood glucose and reduction of body weight ( P <0. 05 ) . Compared with those of NS and DS groups, the myocardial infarct size, cardiomyocyte apoptosis, MDA concentration and ROS in NIR and DIR groups were remarkably increased, activities of SOD and NO were decreased(P<0. 05 or P<0. 01). APN decreased oxidative stress product generation and myocardial apoptosis induced by diabetic myocardial I/R injury ( P <0. 05 ) . Conclusion APN exerts pro-tective effect on myocardial I/R injury in diabetic rats through anti-oxidative mechanism.

Objective To induce adipose-derived mesenchymal stem cells (ADMSCs) differentiation into cardiomyocytes, so as to provide stem cells for myocardial regeneration.Method ADMSCs were isolated and cultured from adult adipose tissue in vitro.They were induced with 10μmol/L 5-azacytidine (5Aza) for 24h.At the 7th, 14th, 21st days after induction, the expression of α-sarcomeric actin, and myosin heavy chain were repeatedly detected by immunocytochemistry.The expression of ANP was detected by RT-PCR.Results At the 7th day after induction, there was no expression of α-sarcomeric actin and MHC.At the 14th day, there was a little expression of α-sarcomeric actin and MHC that could be seen in cells.At the 21st day, there was increased expression of α-sarcomeric and MHC, and the expression of ANP was positive results detected by RT-PCR.Conclusions 5-Aza can induced ADMSCs to differentiate into cardiomyocytes.ADMSCs might be a potential source of cell transplantation for myocardial.

Objective To study the effect on renal function about repeated use of contrast media , and whether alprostadil has protective effect towards contrast-induced nephropathy ( CIN) .Methods 80 adult patients who had ever received contrast examination and scheduled to have PCI within 1 month were randomly divided into two groups: the simple hydration group and the hydration plus alprostadil therapy group.The serum level of creati-nine,urea, Cystatin C, Urineβ-microglobulin and creatinine clearance were recorded and compared between the two groups , and were observed before and after repeated exposure of contrast medium.The incidence of CIN was analyzed .Results Compared with pre-contrast levels , serum levels of urea, creatinin, Cystatin C and Urine β-microglobulin all elevated after single and repeated contrast media use in patients in the simple hydration group ( P<0.05 ) .The incidence of CIN did not differ after single or repeated contrast used (2.5%vs.15.0%, P>0.05).After repeated contrast exposure compared with patients with simple hydration , patients in the alprostadil group had repeated serum levels of urea [(7.4 ±2.3) mmol/L vs.(9.1 ±2.6) mmol/L], creatinia [(87.2 ±25.6) μmol/L vs.(96.9 ± 25.8) μmol/L], Cystatin C [(0.8 ±0.3) mg/L vs.(1.4 ±0.3) mg/L] and Urine β-microglobulin [(207.0 ±31.9 ) μg/L vs.(279.3 ±37.3 ) μg/L] were all lower with higher creatinin clearance [(92.2 ±24.2) ml/min vs.(78.2 ±27.5) ml/min](all P<0.05).The incidence of CIN in patients with alprostadil did not differ after single or repeated contrast used (2.5%vs.7.5%, P>0.05).The incidence of CIN in patients treated with alprostadil had no difference compared with patients with simple hydration after repeated contract (7.5% vs.15.0%, χ2 =0.501,P=0.479).Conclusions Contrast media can cause damage to renal function .Short-term repeated use of contrast media can further worsen renal function without significant increase in CIN rates .Alprostadil may have renoprotective effect towards CIN .

AIM: Using simvastatin and vitamine E (Vit-E) treatment to coronary artery disease (CAD) patients with low HDL, to investigate the relationship between Ox-LDL, platelet activation and HDL. METHODS: 40 CAD patients with low HDL were divided into two groups (A and B): A group oral simvastatin, B group oral simvastatin and Vit-E. The level of serum Ox-LDL, TXB 2 and GMP-140 were measured before and after treatment. The relationship between Ox-LDL, TXB 2, GMP-140 and HDL were analysed. RESULTS:The level of serum HDL was significantly increased in A and B group after treatment and attained normal level. The level of serum Ox-LDL, TXB 2 and GMP-140 were decreased significantly after simvastatin and Vit-E treatment and neared normal. CONCLUSIONS:This study confirmed that HDL can effectively refrain LDL oxidation. It also revealed that Vit-E and simvastatin treatment were more effectively refrained platelet activation by increasement of HDL and decreasement of Ox-LDL.

Objective To investigate the effect of Ang-(1-7) on the apoptosis in human umbilical vein endothelial cells (HUVECs) induced by Ang Ⅱ.Methods HUVECs were isolated and cultured.Cultured HUVECs were incubated for 24 h with Ang-(1-7), Ang Ⅱ, Ang-(1-7) A-779, Ang-(1-7) + Ang Ⅱ, A-779 + Ang Ⅱ + Ang-( 1-7), respectively.Cultured HUVECs without incubating stimulator were chosen as controls.The apoptosis of endothelial cells were detected by flow cytometry.Results The apoptosis of endothelial cells in HUVECs were upregulated by AngⅡ ( 10-6 mol/L) (25.60% ±3.17% vs 2.32% ±0.24%, P ＜0.005).Compared with the AngⅡ group, Ang-(1-7) dose-dependently inhibited the apoptosis of endothelial cells in HUVECs ( (20.04% ± 2.21% ,16.04% ± 1.32 %, 10.04% ±2.05,7.79% ±1.50% vs AngⅡ group 25.60% ±3.17%, P ＜0.05 , P ＜0.05).The effects of Ang-(1-7) could be blocked by A-779 (23.37% ±0.75% vs 20.04% ± 2.21%, 16.04% ± 1.32,10.04% ± 2.05% ,7.79%± 1.50%, P ＜ 0.05 ).Conclusion Ang-(1-7) can attenuate the apoptosis of endothelial cells induced by Ang Ⅱ in HUVECs in a dose-dependent manner.The effects of Ang-(1-7) could be blocked by A-779( P＜0.05).

Objective To evaluate the effects of the short-term intervention lifestyle intervention on metabolic measurements of community patients with impaired glucose regulation (IGR). Methods A total of 90 IGR participants were randomly assigned to the control group (n=45) or the intervention group (n= 45). The subjects in the control group received routine diet and physical exercise advice once a month. The subjects in the intervention group received additional individualized diet counseling and circuit-type resistance training. Metabolic parameters were compared before or after the intervention between the two groups. Results In oral glucose tolerance test (OGTT),2-h plasma glucose (PG) and homeostasis model of insulin resistance index (HOMA-IR) were significantly decreased in the intervention group at 3 months(F= 13.47 or 82.25 ,both P < 0.05). Body mass index (t=-2.44, P<0.05), systolic blood pressure (t= -3.39, P<0.05), diastolic blood pressure (t=-3.97, P<0.05), fasting plasma glucose (t=-3.89, P<0.05),2-h PG (t=-7.22,P <0.05) ,total cholesterol (t=-2.72,P<0.05),low-density lipoprotein cholesterol (t=-2.74, P<0.05), and glycosylated hemoglobin A1 C (t=-3.73, P<0.05) were significantly declined in the intervention group compared to the control group (all P<0.05). Conclusions Intensive lifestyle intervention can significantly improve the metabolic markers of IGR subjects and should be used to prevent type 2 diabetes.

Objective To explore the activity of thioredoxin reductase (TrxR) in chronic myeloid leukemia cell line K562 and the anti-leukemia effect of BBSKE (a novel inhibitor of TrxR) in vitro. Methods The activity of TrxR on K562 cell lineage and fresh bone marrow cell from healthy adult was analyzed by insulin reduction assay. The inhibition of proliferation was measured by CCK-8 assay. The anti-leukemia effect of BBSKE was detected by laser scanning confocal microscope,agarose gel electrophoresis and flow cytometry with Annexin V -FITC/PI staining. Results TrxR activity of K562 cell lineage was significantly higher than that of normal bone marrow mononuclear cells. The apoptosis of K562 cells could be induced at concentrations of 10 μmol/L BBSKE after treated for 24 hours. The typical DNA ladder bans were observed by agarose gel electrophoresis. The apoptotic rates of K562 cells were (10.28±2.74) %. Application of 10 μmol/L BBSKE for 48 hours could also induce apoptosis of fresh bone marrow cell from chronic myeloid leukemia patients, and the apoptotic rates were (5.70±0.48) %. Conclusion TrxR activity in chronic myeloid leukemia cells was significantly higher than that of normal cells. BBSKE inhibits the TrxR activity and the proliferation of K562 by inducing apoptosis.It might be a potential medication for chronic myeloid leukemia.

Myocardial infarction is one of the leading causes of mortality globally.Currently, the pleiotropic inflammatory cytokine interleukin-6 (IL-6) is considered to be intimately related to the severity of myocardial injury during myocardial infarction. Interventions targeting IL-6 are a promising therapeutic option for myocardial infarction, but the underlying molecular mechanisms are not well understood. Here, we report the novel role of IL-6 in regulating adverse cardiac remodeling mediated by fibroblasts in a mouse model of myocardial infarction. It was found that the elevated expression of IL-6 in myocardium and cardiac fibroblasts was observed after myocardial infarction. Further, fibroblast-specific knockdown of Il6 significantly attenuated cardiac fibrosis and adverse cardiac remodeling and preserved cardiac function induced by myocardial infarction. Mechanistically, the role of Il6 contributing to cardiac fibrosis depends on signal transduction and activation of transcription (STAT)3 signaling activation. Additionally, Stat3 binds to the Il11 promoter region and contributes to the increased expression of Il11, which exacerbates cardiac fibrosis. In conclusion, these results suggest a novel role for IL-6 derived from fibroblasts in mediating Stat3 activation and substantially augmented Il11 expression in promoting cardiac fibrosis, highlighting its potential as a therapeutic target for cardiac fibrosis.