[Objective] To determine the effects and possible mechanism of the thrombin antagonist r-RGD-Hirudin (HIR) on ventricular arrhythmia(VA) after acute myocardial infarction (AMI). [Methods] Seventy adult male Sprague-Dawley rats were randomly subjected to the 10 groups according to duration of left coronary occlusion: HIR 0 min, HIR 5 rain, HIR 10 min, HIR 20 min, HIR 30 min, and normal saline(NS) 0 min, NS 5 min, NS 10 min, NS 20 min, NS 30 min; and the average of every group is 7 rats. Acute myocardial infarction was produced by the occlusion of the left anterior descending coronary artery, then the measurements of arrhythmia and infarction sizing by Evans blue were assessed as well as the expression of three isoforms of inositol 1,4,5-trisphosphate receptors (IP3Rs) mRNA in isehemic myocardium by reverse transeriptase polymerase chain reactions (RT-PCR). [Results] Compared with NS groups, the measurements of VA in HIR were reduced significantly in 5 to 20 minutes after AMI (P<0.05). The incidence of VA was all positive related to the expression of three isoforms of IP3Rs mRNA (P<0.01). Compared with NS groups, the expression of type2,inositol 1,4,5-trisphosphate receptor (IP3R2) mRNA at 10 min and type3, inositol 1,4,5-trisphosphate receptor mRNA (IP3R3) at 10 min and 20 min after AMI were significant decreased (P<0.05) in HIR groups. [Conclusion] The thrombin antagonist r-RGD-Hirudin exerts its myocardial protection against ventricular arrhythmia after acute myocardial infarction possible through IP3R2 and IP3R3 and not typel, inositol 1,4,5-trisphosphate receptor (IP3R1).

AIM:To observe the characterization in neural cells derived from the hippocampus of embryonic rats and to examine the effect of myelin-associated glycoprotein(MAG) on the proliferation,differentiation and neurite growth of neural stem cells(NSCs).METHODS:The hippocampus cells of embryonic rats were isolated and cultured in vitro.The expressions of nestin and doublecortin,the marks of NSCs,were observed by immunocytochemical method.The rate of proliferating cells was examined by BrdU immunocytochemistry.The average neuronal neurite length and the percentage of differentiated neurons were detected by immunocytochemistry staining.RESULTS:The hippocampus cells of 16 days old embryonic rats had the characteristics of NSCs.The percentage of differentiated neurons(?-tubulin Ⅲ-positive cells) was 18.17%?2.79% and the average neuronal neurite length was(136.27?33.66)?m,seven days after the differentiation initiated in vitro in control group.After NSCs were treated with MAG-Fc(200 ?g/L),the percentage of differentiated neurons and the average neurite length were decreased,respectively,to 10.05%?3.42%(P0.05).CONCLUSION:MAG-Fc inhibits the differentiation and neurite growth of the NSCs,but has no effect on the proliferation.

Aim To explore whether edaravone (EDA), a novel free radical scavenger, protects H9c2 cardiac cells against doxorubicin ( DOX )-induced car-diotoxicity. Methods H9c2 cells were treated with 5μmol·L-1 DOX to establish a model of DOX cardio-toxicity. Cell viability was examined by cell counter kit ( CCK-8 ) . Changes in morphology and amount of ap-optotic cells were detected by Hoechst 33258 staining;intracellular level of reactive oxygen species ( ROS ) was measured by DCFH-DA staining and photofluorog-raphy;mitochondrial membrane potential ( MMP) was observed by rhodamine 123 ( RH123 ) staining and photoflurograph; the expression level of caspase-3 was determined by Western blot assay. Results Pretreat-ment of H9 c2 cells with 20 , 40 and 80 μmol · L-1 EDA for 60 min markedly inhibited cytotoxicity in-duced by 5 μmol · L-1 DOX, respectively, as evi-denced by an increase in cell viability. The protective effect induced by 40 μmol · L-1 EDA was maximal. Pretreatment of H9 c2 cells with 40 μmol · L-1 EDA for 30 , 60 , 90 and 120 min significantly attenuated DOX-induced cytotoxicity, respectively, having a max-imal protection at 60 min. Furthermore, pretreatment of H9 c2 cells with 40 μmol · L-1 EDA for 60 min be-fore exposure to 5 μmol · L-1 DOX for 24 h obviously reduced cardiac injuries, as evidenced by decreases in the DOX-induced intracellular ROS generation, num-ber of apoptotic cells, and expression of cleaved caspase-3, as well as loss of MMP. Conclusions EDA can protect H9 c2 cardiac cells against DOX-in-duced cardiotoxicity, this protection may be associated with inhibition of ROS production and preservation of MMP.

【Objective】 To explore the significance of electrocard iogram monitoring during the effective application of radiofrequency energy to s low atrioventricular (AV) nodal pathway ablation. 【Methods】 Slow AV nodal pathway ablation was performed in 58 patients with slownfast AV nodal ree-trant tachyca rdi a (AVNRT). The changes of electrocardiogram were monitored during the effective application of low radiofrequency RF energy (15～25 W). A faster rate of junctio nal ectopy (>150 min-1), ventriculoatrial (VA) block in association with j unctional ectopy, and l ong P-R interval during sinus beat were considered as harbingers of atrioventri cular (AV) block. RF energy deliveries were discontinued as soon as the harbinge rs of AV block occurred. Otherwise, RF energy continued until junctional ectopie s were decreased or vanished. If junctionnal ectopies were not decreased, RF ene rgy continued lasted for 90～120 s. 【Results】 Slow AV nodal pathway ablation w as successful in all patients who had junctional ectopy during the effective del ivery of RF energy. The effective ablation time was (128±26) s. 54 patients exp erienced one time successful ablation, and 4 patients experienced two times abla tion. Unsustained AV block occurred in 6 patinets after RF energy deliveries whi ch were immediately terminated because of VA block in association with junctiona l ectopy in 4 patinets and long P-R interval during sinus beats in 2 patients. No patients developed permanent AV block. Recurrent AVNRT requiring second ablat ion occurred in 2 of 58 successfully ablated slow pathway during (18±16) months of follow-up. 【Conclusion】 RF energy deliveries could be instructed b y intracardiac electrocardiogram monitoring during AVNRT ablation, which could e nhance the successful rate of slow pathway ablation, reduce recurrence and avoide permanent AV block.

Aim To investigate the role of ATP-sensi-tive potassium channels-Akt pathway in exogenous hy-drogen sulfide( H2 S) inhibiting the high glucose( HG)-induced injury in H9c2 cardiac cells. Methods The expression level of Akt protein was tested by Western blot assay. The cell viability was measured by cell counter kit-8(CCK-8 assay). The number of apoptotic cells was tested by Hoechst 33258 nuclear staining fol-lowed by photofluorography. The intracellular levels of reactive oxygen species ( ROS ) were detected by DCFH-DA staining followed by photofluorography. Mi-tochondrial membrane potential ( MMP ) was examined by JC-1 staining followed by photofluorography. Results H9c2 cells were treated with 35 mmol·L-1 glucose (high glucose, HG) for 0 ~24 h respectively. After treating for 3 h, the expression level of phosphorated ( p )-Akt protein began to be obviously reduced, the maximum reduced expression level was observed after the cells were exposed to HG for 24 h. Pretreatment of the cells with 50 μmol · L-1 pinacidil ( Pin, a KATP channel opener) or 400 μmol·L-1 NaHS( a donor of H2 S) prior to exposure to HG considerably blocked the down regulation of p-Akt expression level induced by HG. However, pretreatment with 1 mmol · L-1 KATP channel blocker glibenclamide( Gli) obviously attenua-ted the inhibitory effect of NaHS on HG-induced down-regulation of p-Akt expression level. On the other hand, the protective effects of NaHS against the HG-induced cardiomyocyte injury were markedly blocked by 30 μmol·L-1 Ly294002(an inhibitor of Akt), as indicated by the decrease in cell viability and MMP dissipation as well as the increases in the number of apoptotic cells and ROS generation. Conclution KATP channels-Akt pathway mediates the protective effect of H2 S against the HG-induced cardiac injury.

AIM:To investigate the protective effect of N-acetylcysteine (NAC) on H9c2 cells from injuries induced by methylglyoxal (MG) and the potential mechanism.METHODS:H9c2 cells were divided into control group, MG treatment group, NAC +MG treatment group, SP600125 pretreatment +MG group, NAC group and SP600125 group.The viability of the H9c2 cells was measured by CCK-8 assay.The protein levels of p-JNK and t-JNK were tested by Western blot .The changes of intracellular reactive oxygen species ( ROS) were evaluated by 2′, 7′-dichlorofluorescein di-acetate (DCFH-DA) staining.Mitochondrial membrane potential (MMP) was measured by rhodamine 123 (Rh123) stai-ning.The morphological changes in apoptotic cardiomyocytes were detected by Hoechst 33258 staining.RESULTS: Du-ring 100~800 μmol/L concentration range , MG caused significantly reduced viability of the H 9c2 cells in a dose-depend-ent manner.NAC had a protective effect on H9c2 cells against the injuries induced by MG during 500~1 500μmol/L con-centration range through raising cell viability , inhibiting cellular oxidative stress and improving MMP ( P <0.01 ) . SP600125,an inhibitor of JNK, showed the protective effect similar to NAC on H9c2 cells against MG-induced injuries, in-cluding attenuating oxidative stress , improving MMP and suppressing apoptosis .CONCLUSION: N-acetylcysteine offers obvious protective effect on H9c2 cells against the injuries induced by methylglyoxal .The underlying mechanisms may be associated with decreasing the production of ROS , ameliorating MMP , inhibiting the activation of JNK and suppressing ap-optosis.

AIM: To investigate the effects and mechanisms of angiotensin-(1-7) on cardiac hypertrophy in pressure-overloaded rats. METHODS: Ar at model of pressure-overloaded heart was induced by constriction of abdominal aorta. Seventy-five male Sprague Dawley rats were randomized to sham-operated group, model control group and angiotensin-(1-7) treatment group. They were treated with intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour) or saline by minipump. RESULTS: Abdominal aortic banding resulted in a significant increases in LVW/BW, myocardial angiotensinⅡlevels, and p-ERK1/2 expression. Angiotensin-(1-7) had no effect on aortic banding-induced increases in myocardial angiotensinⅡlevels, but it significantly attenuated aortic banding-induced increases in LVW/BW and p-ERK1/2 expression. CONCLUSION: Angiotensin-(1-7) attenuates the development of cardiac hypertrophy in pressure-overloaded rats. It may be associated with the inhibition of p-ERK1/2 expression in cardiac tissue.

AIM:To evaluate complement activation in patients with all forms of acute coronary syndromes(ACS)and to examine the relationship between the degree of complement activation and myocardial injury.METHODS:The subjects were divided into 2 groups:110 ACS patients(group ACS)and 18 healthy persons(group control).One hundred and ten patients with ACS were divided into 3 sub-group:51 patients with ST-segment elevated myocardial infarction(STEMI),28 patients with non-ST-segment elevated myocardial infarction(NSTEMI)and 31 patients with unstable angina(UA).Complement 3(C3),complement 4(C4),troponin T(TnT)as well as creatine kinase MB(CK-MB)were evaluated.RESULTS:Plasma C3 and C4 peak levels were significantly higher in patients with STEMI [(1 525?302)mg/L and(423?123)mg/L] and NSTEMI [(1 516?289)mg/L and(396?68)mg/L] than those in patients with UA [(1 275?172)mg/L and(356?91)mg/L] and the control subjects [(1 072?196)mg/L and(182?73)mg/L](P

AIM: To explore the role of extracellular signal-regulated kinases ERK1/2-STAT3 pathway in adaptive cytoprotection induced by H2O2 preconditioning in PC12 cells.METHODS: In PC12 cells,the experimental model of cytoprotection by H2O2 preconditioning against oxidative stress-induced injury was set up.The morphological changes in the apoptotic cells were observed by using of chromatin dye Hoechst 33258.The percent of apoptotic cells was determined by flow cytometry(FCM) with propidium iodide staining.The levels of p-ERK1/2 and p-STAT3 expression were detected by Western blotting assay.RESULTS: Preconditioning with H2O2 at concentration of 100 ?mol/L for 90 min obviously inhibited apoptosis induced by 300 ?mol/L H2O2,and both ERK1/2 and STAT3 were activated.UO126(10 ?mol/L,an inhibitor of ERK1/2) or AG-490(10?mol/L,an inhibitor of JAK2) significantly blocked the cytoprotection effect of H2O2 preconditioning.Moreover,UO126(10 ?mol/L) also markedly inhibited the up-regulation of p-STAT3 expression by H2O2 preconditioning.CONCLUSION: H2O2 preconditioning activates ERK1/2-STAT3 signal pathway,which may be one of the mechanisms underlying H2O2 preconditioning-induced cytoprotection.

AIM: To study the reactions of human platelet to active complement and the effects of anti-CD59 on human platelet activation induced by complement. METHODS: By applying CVF to activate complement, the platelet aggregation and release reactions induced by activated complement with or without appling anti-CD59 with different doses to block the complement modulative protein CD59 in healthy individuals, were observed. RESULTS: CVF induced platelet release and significant and lasting metamorphosis in healthy individuals, but platelet aggregation was not observed. CVF-induced platelet metamorphosis showed positive linear correlation to lg concentration of CVF (r=0 970. P