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Objective: To study influence of glycosylated hemoglobin A1c (HbA1c) on major adverse cardiovascular events (MACE) in patients with diabetes mellitus (DM) complicated coronary heart disease (CHD) after percutaneous coronary intervention (PCI).Methods: A total of 100 DM+CHD patients after PCI were selected from our hospital.According to HbA1c level, they were divided into HbA1c<6.5% group (n=48) and HbA1c≥6.5% group (n=52).Levels of C reactive protein (CRP), tumor necrosis factor α (TNF-α), erythrocyte sedimentation rate (ESR) and interleukin (IL)-6 before PCI, incidence rate of MACE on six and 24 months after PCI were compared between two groups.Results: Compared with HbA1c<6.5% group before PCI, there were significant rise in serum levels of CRP[(18.5±6.2) mg/L vs.(25.8±4.2) mg/L]and TNF-α[(32.4±12.3) ng/L vs.(48.3±11.8) ng/L]in HbA1c≥6.5% group, P<0.01 both.On six months after PCI, incidence rate of myocardial infarction in HbA1c≥6.5% group was significantly higher than that of HbA1c<6.5% group (9.62% vs.0, P=0.028);24 months after PCI, compared with HbA1c<6.5% group, there were significant rise in incidence rates of myocardial infarction (2.08% vs.15.38%) and diseased vessel restenosis (12.50% vs.32.69%) in HbA1c≥6.5% group (P<0.05 all).Conclusion: In DM+CHD patients after PCI, those with lower HbA1c level possess better prognosis.
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Objective:To explore therapeutic effect of atorvastatin on inflammatory factor levels and vascular endothelial function in patients with coronary heart disease (CHD).Methods: A total of 112 CHD patients treated in our hospital were selected.According to random number table, they were randomly and equally divided into routine treatment group and atorvastatin group, and both groups were treated for eight weeks.Serum levels of inflammatory factors and vascular endothelial function before and after treatment, angina pectoris and ECG therapeutic effect after treatment, and incidence of adverse reactions during medication were compared between two groups.Results: Compared with before treatment, after treatment, there were significant reductions in serum levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, C reactive protein (CRP), intercellular adhesion molecule (ICAM)-1 and endothelin (ET)-1, and significant rise in nitric oxide (NO) level, left ventricular ejection fraction (LVEF) and cardiac output (CO) in both groups,P<0.01 all;compared with routine treatment group after treatment, there were significant reductions in serum levels of IL-6 [(157.42±30.13) pg/ml vs.(129.83±27.31) pg/ml], TNF-α [(25.41±2.67) ng/L vs.(21.38±2.13) ng/L], CRP [(19.87±2.78) mg/L vs.(17.13±2.04) mg/L], ICAM-1 [(81.23±19.83) pg/ml vs.(64.31±15.46) pg/ml] and ET-1 [(1.45±0.34) pg/ml vs.(0.87±0.23) pg/ml], and significant rise in NO level [(53.27±5.31) mmol/L vs.(58.72±5.46) mmol/L], LVEF [(52.37±5.38)% vs.(63.19±5.79)%] and CO [(4.58±0.78) L/min vs.(5.13±0.82) L/min] in atorvastatin group, P<0.01 all.Compared with routine treatment group, there were significant rise in total effective rates of angina pectoris (73.22% vs.89.29%) and ECG (66.07% vs.83.93%) in atorvastatin group, P<0.05 both.There were no serious adverse drug reactions in two groups.Conclusion: Atorvastatin can significantly improve inflammation state and vascular endothelial function in patients with coronary heart disease.
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Objective To investigate the impact on renal fibrosis by inhibition of connective tissue growth factor( CTGF) by RNA interference in spontaneous hypertension rat( SHR) . Method Twenty SHR were randomly (random number) divided into SHR group ( n = 10) and RNAi group ( n = 10), eight Wistar-Kyoto rats were set as control. At the end of RNA interference procedure, all the rats were sacrificed and the kidneys were harvested. The mRNA and plasmosin of CTGF and fibronectin(FN) of renal tissue were extracted and measured by RT-PCR and Western Blotting. And the localization of CTGF and FN were analyzed with immunohistochernistry technique. The collagen deposition(shown as collagen volume traction, CVF) were evaluated with 0.1% sirius-picric staining, and the hydroxyproline of myocardium were detected by colorimetry. Results The mRNA and protein expression of CTGF decreased 66% and 62% in RNAi group (P < 0.01). The mRNA and protein expression of FN decreased 56% and 51% in RNAi group.The same inhibition effect was observed by hislological analysis. Immuno-histochemistry showed that CTGF localized both in renal parenchyma and renal interstitium, whereas FN majorly expressed in renal interstitium. Observation with light microscope showed that collagen deposition(CVF)decreased sharply in RNAi group versus SHR group. And the same effect was viewed in hydroxypnoline assay[SHR group: (0.596 ± 0.067) μg/mg, RNAi group: (0.368±0.084) μg/mg, P < 0.01 ] .Further study by polarized microscope displayed that RNA interference mainly suppressed type I collagen synthesis. Conclusions Targeted inhibition of CTGF by RNA interference leads significant decrease of extracellular matrix deposition in kidney. And the anti-fibrotic effect independent of lower the blood pressure. This study indicated CTGF take a key role in the development and progress of renal fibrosis.
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The effects of cardiomyocyte grafting on left ventricular (LV) remodeling and function in rats with chronic myocardial infarction were evaluated using high-frequency ultrasound. Chronic myocardial infarction was induced in 50 Wister rats by ligating the left anterior descending artery. They were randomized into two groups: a trial group that received neonatal rat cardiomyocyte trans- plantation (n=25) and a control group which were given intramyocardial injection of culture medium (n=25). The left ventricular (LV) geometry and function were evaluated by high-frequency ultrasound before and 4 weeks after the cell transplantation. After the final evaluation, all rats were sacrificed for histological study. The results showed that 4 weeks after the cell transplantation, as compared with the control group, the LV end-systolic dimension, end-diastolic dimension, end-systolic volume and end-diastolic volume were significantly decreased and the LV anterior wall end-diastolic thickness, LV ejection fraction and fractional shortening were significantly increased in the trial group (P<0.01). Histological study showed that transplanted neonatal rat cardiomyocytes were found in all host hearts and identified by Brdu staining. It was suggested that transplantation of neonatal rat cardiomyocytes can reverse cardiac remodeling and improve heart function in chronic myocardial infarction rats. High-frequency ultrasound can be used as a reliable technique for the non-invasive evaluation of the effect of cardiomyocyte transplantation.
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AIM:To observe the secretion of vascular endothelial growth factor(VEGF)when adenovirus induced VEGF165(AdVEGF165)gene transferred into neonatal cardiomyocytes in vitro,and to investigate the impact on heart function after transplanted the transferred cardiomyocytes into infarct myocardium in rats.METHODS:Neonatal cardiomyocytes were cultured in vitro and labeled with BrdU,then transferred by AdVEGF 165.ELISA was applied to assay the expression and secretion of VEGF.Wistar rats,in which left descending branch of coronary artery was ligated,were randomly divided into four groups and transplanted into MI area with transferred cardiomyocytes(group Ⅰ),untransferred cardiomyocytes(group Ⅱ),AdVEGF 165(group Ⅲ)and culture medium(group Ⅳ),respectively.The echocardiograph was applied to evaluate the heart function before and after cell transplantation.Then the rats were executed and the hearts were harvested for histological(hematoxylin-eosin)and immunohistological(anti-BrdU dyeing)examinations.The vessels were also counted in injected area.RESULTS:ELISA indicated that the expression and secretion of VEGF in groupⅠwere higher than those in the rest(P
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AIM:To observe the effect of preconditioning with pioglitazone on ischemia reperfusion/hypoxia reoxygenation-induced mitochondrial ultramicro-structure and membrane potential in rats. METHODS: Sprague-Dawley rats were randomly divided into four groups: sham-operated (SO) group, ischemia reperfusion (IR) group, pioglitazone preconditioning group (Pio-P) and 5-HD+pioglitazone (5-HD+Pio) group. Apart from the SO group, IR, Pio-P and 5-HD+Pio groups were subjected to 30 min ischemia and 4 h reperfusion. The heart was quickly removed for observing the structure of mitochondria and measurement of the apoptosis index (AI) by TUNEL. Primary cultured cardiomyocytes of Sprague-Dawley rats were divided into control, hypoxic reoxygenation (HR) and different concentrations of Pio-P group. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (?m). RESULTS: The injury of mitochondrial structure in IR group was severer than that in Pio-P group, while the difference between 5-HD+Pio group and IR group was not evident. Flameng score in Pio-P group(1.62?0.60) was significantly lower than that in IR group (2.75?1.09), P0.05). CONCLUSION: Pioglitazone protects the heart from ischemia reperfusion/ hypoxia reoxygenation injury evidenced by improving mitochondrial ultrastructure and lessening the loss of mitochondrial membrane potential, and decreasing apoptosis. The cardioprotective effects can be inhibited by the blocker of mitochondrial ATP-sensitive potassium channels.