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Objective@#To observe the expression changes of Notch and nuclear factor-κB (NF-κB) signaling pathways in rat myocardium post myocardial infarction.@*Methods@#Myocardial infarction was established by ligation of the left anterior descending coronary artery(MI group), sham rats (similar surgical procedure without coronary artery ligation) served as control, the rats were sacrificed at first week, 4th and 8th week after operation, the non-infarct myocardial tissue in both groups was obtained to detect the mRNA expression of Notch1, Dll4 and Hes1 by RT-PCR, the protein expression of NICD1 was detected by Western blot, the nuclear protein p65 content was detected to reflect the activation degree of NF-κB signaling in the cardiomyocytes.@*Results@#The myocardial mRNA expression of Notch1 in MI group was significantly higher than in control group (1.68±0.35 vs. 0.47±0.12, P<0.05) at first week, and tended to be higher at the 4th week and 8th week (P>0.05). The mRNA expression of Dll4 and Hes1 was similar between the two groups at the three time points. NICD1 protein level was increased at the first week in MI group as compared with control group (1.31±0.33 vs.0.45±0.11, P<0.05), which tended also to be higher at the 4th week and 8th week post operation (P>0.05). For NF-κB activation study, the nuclear protein p65 content was higher at first week, 4th week and 8th week in MI group as compared with respective control groups (0.286±0.052 vs.0.049±0.016 (P<0.01), 0.247±0.056 vs. 0.043±0.018 (P<0.01), 0.120±0.033 vs. 0.044±0.009 (P<0.05)), the most significant increase was found in the first week.@*Conclusions@#Notch and NF-κB signaling pathways are actively involved in the process of ventricular remodeling after myocardial infarction. Notch1 and NF-κB signaling pathways are both activated at the first week after myocardial infarction, NF-κB signaling pathway activation after myocardial infarction continues up to 8 weeks. These two signal transduction pathways may thus serve as new targets for future intervention studies to prevent heart failure.
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Objective: To study the effect of berberine (BR) on ventricular remodeling in experimental rats with myocardial infarction (MI) and its mechanisms. Methods: The MI model of experimental rats was established by ligation of the left anterior descending coronary artery and the MI animals were randomly divided into 3 groups: MI+BR group, in which the rats received BR 20 mg/kg.d, Sham group and MI group, the rats in those 2 groups received the same volume of normal saline. All animals were treated for 8 weeks. The cardiac function and structure were assessed by echocardiography, cardiac interstitial collagen deposition was evaluated by Masson stain, the myocardial cell apoptosis was detected by Tunel method, and the activation of nuclear factor (NF-κB) was also examined. Results: For echocardiography, MI group had enlarged left ventricular end diastolic diameter (7.28 ± 0.29) mm than Sham group (6.86 ± 0.36) mm,P0.05. MI group had increased left ventricular end systolic diameter (5.88 ± 0.33) mm than Sham group (4.61 ± 0.31) mm, but it decreased in MI+BR group (4.68 ± 1.17) mm, allP Conclusion: Application of BR may improve the ventricular remodeling and cardiac function in experimental MI rats, it might be because of BR partially inhibit NF-κB activation, reduce collagen deposition and help anti-apoptosis in myocardial cells.
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Objective: To observe the impact of vareniline tartrate on vascular endothelial function and inlfammatory factor releasing in acute coronary syndrome (ACS) patients with nicotine dependence after smoking withdrawal treatment. Methods: We recruited the in-hospital ACS patients who were smoking ≥10 cigarettes/day for more than 10 years with at least moderate nicotine dependence, and randomly divided them into 2 groups: Varenicline group, the patients received oral medication for 2 weeks and Self withdrawal group, the patients without medication assistance.n=52 in each group. All patients received (10-30) min daily mission and consulting for quit smoking for 2 weeks. The basic information was recorded and blood levels of NO, IL-6 and ET-1 were compared before and after withdrawal treatment. Results: Compared with they were before, after 2 weeks withdrawal treatment, in Varenicline group, blood levels of ET-1 decreased as (33.950 ± 1.439) ng/L vs (170.198 ± 12.602) ng/L and IL-6 decreased as (0.103 ± 0.020) ng/L vs (0.307 ± 0.051) ng/L; in Self withdrawal group, ET-1 decreased as (60.795 ±7 .036) ng/L vs (170.511 ± 12.374) ng/L, all P0.05. After treatment, ET-1 level in Varenicline group (33.950 ± 1.439) ng/L was lower than Self withdrawal group (60.795 ± 7.036) ng/L and IL-6 level in Varenicline group (0.103 ± 0.020) ng/L was also lower than Self withdrawal group (0.258 ± 0.042) ng/L, allP0.05. Conclusion: Compared with self withdrawal, varenicline tartrate may effectively inhibit inlfammatory factor releasing in ACS patients with nicotine dependence, and therefore improve the vascular endothelial function.
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Objective To investigate the effects of trimetazidine on renal function in patients with shock.Methods A prospective randomized controlled double-blind study was conducted.128 patients with shock admitted to intensive care unit (ICU) of Guangzhou Red Cross Hospital from April 2011 to April 2013 were enrolled and randomly divided into control group and trimetazidine treatment group,each n＝64.All patients received anti-shock treatment,while the patients in trimetazidine group received trimetazidine treatment (20 mg orally,tid) for 7 days,and patients in control group received placebo (10 mL of sterile water for injection,tid) for 7 days.The urinary output,serum creatinine (SCr),blood urea nitrogen (BUN),cystatin C,and creatinine clearance (CCr) reflecting renal function were recorded in both groups,and the values were compared before treatment,48 hours after treatment,and 1 week after the treatment.At the same time,dynamic mean arterial pressure (MAP) was monitored,and 48-hour and 1-week mortality rates were recorded.Results There was no significant difference in results in all the renal function parameters before the treatment between two groups.The levels of SCr,BUN,cystatin C were gradually decreased after treatment in both groups,but CCr and MAP were gradually increased.Compared with the control group,cystatin C at 48 hours after treatment was significantly decreased,while CCr was significantly increased in treatment group [cystatin C (mg/L):0.85 ± 0.81 vs.1.01 ± 0.91,t=2.562,P=0.017; CCr (mL/s):0.93 ± 0.64 vs.0.69 ± 0.40,t=2.155,P=0.033].SCr and BUN at 1 week after treatment were significantly decreased in treatment group [SCr (lμmol/L):94.23 ± 88.31 vs.104.99 ± 98.37,t=2.921,P=0.003 ; BUN (mmol/L):9.46 ± 8.24 vs.11.87 ± 8.65,t=2.611,P=0.010].Urine output per hour and MAP was improved after treatment in both groups,and no significant difference was found between treatment group and control group [urine output (mL):48 hours after treatment 55.67 ± 31.43 vs.45.34 ± 11.79,t =0.934,P=0.323 ; 1 week after treatment 71.67 ± 37.23 vs.75.35 ± 22.88,t=1.280,P=0.210; MAP (mmHg,1 mmHg=0.133 kPa):48 hours after treatment 72.13 ± 33.24 vs.69.28 ± 39.98,t=1.408,P=0.179; 1 week after treatment 71.44 ± 21.98 vs.72.32 ± 31.11,t =1.184,P =0.252].Mortality rate in treatment group was lowered compared with control group,however no statistical significance was found [48 hours after treatment:31.2％ (20/64) vs.32.8％ (21/64),x2=0.084,P=0.785; 1 week after treatment:32.8％ (21/64) vs.35.9％ (23/64),x2=2.084,P=0.173].Conclusions Trimetazidine can improve renal function in patients with shock.
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ObjectiveTo research the endothelial dysfunction and early changes in arterial elasticity in patients with hyperlipidemia and effects of atorvastatin on these changes.Methods40 patients with hyperlipidemia but without any treatment in our hospital were selected as a study group,and 30 healthy people were selected as control group.Use the Flow mediated dilation,FMD detection which bases on the echo-trackingtechnology,eTRACYING to evaluate the right brachial atherosclerosis parameters and vascular diastolic parameters,including the pressure strain elastic modulus(Ep) ;stiffness index (β) ;compliance (AC) ;FMDs and FMDd.The study group take atorvastatin 20mg per day,then retested above parameters and TC,LDL-C after 12 weeks and analyzed all parameters.ResultsThe values of β and Ep in study group are significantly higher than the control group (all P ＜ 0.001 ),but AC;FMDs and FMDd are significantly lower than the control group( all P ＜ 0.001 ).The results of the study group after the treatment of atorvastatin are as follwing:TC,LDL-C,β and Ep are lower than before,AC,FMDs and FMDd are higher than before;and the differences are of significance in statistics ( all P ＜ 0.001 ).ConclusionHyperlipidemic patients had shown the vascular endothelial injury and vascular early hardening before the abnormal changes in intimal,but the atorvastatin intervention could reverse these changes.
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ety, reduce the risk of infection and improve the efficiency of nursing service.
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Objective To observe the effect of aspirin on phtelets activation markers in patients with coronary heart disease and set up a diagnostic criteria of aspirin resistance.To preliminarily predict the incidence of aspirin resistance in hospital patients.Methods The subjects were divided into 3 groups:aspirin group(103 cases),control group(24 eases),and healthy control group(23 cases).Using whole blood samples,we detected the ratio of CD62P,PAC-1 expression by flow cytometry(FCM)before and after 7-day treatment and compared the changes of CD62P and PAC-1 expression ratio,then calculated the inhibition ratio of platelets glycoprotein,set up the diagnostic criteria of aspirin resistance with receiver operator characteristic curve(SOC)and calculate the incidenee of aspirin resistance in hospital patients.Results The statisticsl reaults are listed as below:in asptirin group,before treatment CD62P(10.16±6.80)%,PAC-1(14.66±10.56)%,and after treatment CD62P(5.70±4.28)%,PAC-1(8.93±7.08)%,P＜0.01.In control group,before treatment CD62P(9.14±6.52)%,PAC-1(17.67±11.53)%,and after treatment CD62P(7.81±5.72)%,PAG-1(14.97±8.05)%,P＜0.05.According to ROC,the inhibition ratio of CD62P＜21.5% or PAG-1＜17.7% was individually set up asdiagnostic criteria of AR.Our study indicate that the incidence of aspirin resistance in hospital CHD patients is 17.5%.Conclusion There exists platelet activation in CHD patients.CD62P and PAC-1 could be considered as the sensitive index of platelet activation and used in the evaluation of anti-platelet therapy.Aspirin can decrease the expression of CD62P and PAC-1,and inhibit the activation of platelet.According to this study,aspirin resistance really exists in CHD patients.By FCM,the diagnostic criteria of aspirin resistance in CHD is the inhibition ratio of CD62P＜21.5% or PAC-1 ＜17,7% due to aspirin.The incidence of aspirin resistance in hospital CHD patients is 17.5%.
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Objective To investigate the effects of ischemic preconditioning(IPC)on aged patients with acute myocardial infarction(AMI). Methods 124 cases of AMI during hospitalization were divided into two groups: ischemic precondition group(IPC, n =68)with angina 48 hours before AMI; no ischemic precondition group (NIPC, n =56) without angina. The clinical data of the two groups were compared. Results The infarction size was smaller in the group IPC than that in the group NIPC ( P
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AIM:To investigate the affecting factors of detecting platelet activation by flow cytometry (FCM). METHODS:Using decoagulant of natrium citricum,anticoagnlated peripheral venous bloods from 6 healthy donors were labeled with the method of three-colour immunofluorescence assay. Platelet activation markers fibrinogen receptor (Fib-R,PAC-1) and P-selectin (CD62P) were measured. In the same time,the reproducibility of FCM was assessed.RESULTS:The platelet activation markers PAC-1 and CD62P at each time point showed significant difference(P