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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 construct I-Ad/IgG2b Fc baculovirus expression vector and express I-Ad/IgG2b Fc dimer fusion protein in Sf9 insect cells.Methods:I-Ad α,I-Ad β and IgG2b Fc gene sequences were amplified from BALB/c mouse lymphocytes by RT-PCR.I-Ad α and I-Ad β were connected with the leucine zipper sequence Fos and Jun respectively by overlapping PCR to form I-Ad α-Fos and I-Ad β-Jun.I-Ad α-Fos and IgG2b Fc fragments were ligated by restriction sites Xba I to form I-Ad α-Fos-IgG2b Fc recombination sequence.I-Ad α-Fos-IgG2b Fc and I-Ad β-Jun fragments were inserted to PPH and PP10,which were the downstream of the promoters in the plasmid pFastBacTMDual,to form pFastBacTMDual+[I-Ad/IgG2b Fc] recombinant plasmids.The constructed vector was identified by PCR,restriction endonuclease and sequencing.The recombinant plasmids pFastBacTMDual+[I-Ad/IgG2b Fc] was transferred into the DH10Bac competent cell to form recombinant baculovirus Bacmid+[I-Ad/IgG2b Fc].The recombinant baculovirus was transfected into Sf9 insect cells by liposome transfection reagent.After infected with Sf9 insect cells,the supernatant was collected and concentrated by PEG20000 to obtain I-Ad/IgG2b Fc dimer fusion protein.The fusion protein was detected by double-antibody sandwich ELISA and Western blot.Results:PCR,restriction enzyme digestion and sequencing confirmed that the recombinant vector pFastBacTMDual+[I-Ad/IgG2b Fc] had the correct sequence.The double antibody sandwich ELISA and Western blot showed that recombinant bacmid could successfully infect Sf9 insect cells,and the expressed fusion protein had the correct conformation.Conclusion:The pFastBacTMDual+[I-Ad/IgG2b Fc] baculovirus expression vector was successfully constructed and expressed in Sf9 insect cells,laying a foundation for the study of I-Ad-restricted T cells.
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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 value of treadmill test Duke score on diagnosis of coronary heart disease (CHD). Methods: A total of 200 patients suspected CHD were selected. All patients received biochemical examinations, treadmill exercise test (TET) and coronary angiography (CAG) within two weeks. The results of TET, Duke treadmill score（DTS）and CAG were compared and analyzed. Results: The CAG was regard as gold standard diagnosing CHD. （1）Compared with TET alone, there were significant decrease in specificity (72.3% vs.55.4%, χ2=5.161, P=0.021) in positive DTS alone for diagnosing CHD; there were significant increase in sensitivity(72.6% vs. 87.8%，χ2=7.860, P=0.005), negative predictive value(56% vs.76.9%，χ2=6.128, P=0.013) in combined use of TET and DTS for diagnosing CHD; （2）Compared with positive DTS alone, there were significant increase in sensitivity (76.3% vs. 87.8%，χ2=4.334, P=0.037),negative predictive value(52.9% vs. 76.9%，χ2=7.298, P=0.007) and accuracy (69.5% vs. 80.8%，χ2=5.849, P=0.016)in combined use of TET and DTS. Conclusion: Combined use of treadmill exercise test and Duke score can significantly increase sensitivity, negative predictive value and accuracy diagnosing CHD.
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Pim kinases contribute to tumor formation and development of lymphoma, which shows enhanced DNA replication, DNA recombination and repair. Endothelial cells
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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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This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.
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Animals , Male , Rats , Animals, Newborn , Myocardial Ischemia , Metabolism , Myocardial Reperfusion Injury , Metabolism , Myocardium , Metabolism , Oxidative Stress , Physiology , Protein Serine-Threonine Kinases , Genetics , Metabolism , Rats, Sprague-Dawley , Signal Transduction , Up-RegulationABSTRACT
This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.
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Objective To study the effects of Wortmannin, inhibitor of PI3K and SB202190, inhibitor of P38 MAPK and PD98059, inhibitor of ERK1/2 on the migration of epidermal growth factor (EGF)-induced vascular smooth muscle cells (VSMCs). Methods There were fives groups in this experiment, including control group, EGF group, PD98059 (PD) group, SB202190(SB) group and Wortnannin (WT) group. The migration rate of the VSMCs was measured by wound healing assay. Results At the 24th hours after wounding, there was obvious migration in EGF group compared to control group. The migration of VSMCs was significantly inhibited in PD group, SB group and WT group compared to the EGF group, but there were no significant difference among three inhibitor groups. At the 30th hours after woun-ding, there was still obvious migration in EGF group compared to control group. The migration of VSMCs was significantly inhibited in the three iuhibitors group compared to the EGF group, and there were significant difference among three inhibitor groups. Furthermore, inhibiting effect on VSMCs in SB group was more obvious compared to PD group and WT group. Conclusion These results suggested that the migra-tion of EGF-induced VSMCs may play a role through PI3K, P38 MAPK and ERKI/2 signal pathways, and the effect of P38 MAPK signal pathway is very important.
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Objective To investigate the changes of compliance in large arteries and carotid artery intima-media thickness(IMT)in patients with metabolic syndrome.Methods There were 64 patients with metabolic syndrome and 56 age-matched control subjects.Their carotid-femoral pulse wave velocities(C-FPWV)were measured by the Complior SP and their carotid artery IMT were detected by B-mode ultrasound.At the same time their height,weight,waist circumstance,hip girth,blood pressure,blood glucose,blood lipid,BMI and waist to hip ratio(WHR)were measured.Results Compared with the control,the patients with metabolic syndrome had higher C-FPWV(P
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AIM:To observe the effect of spironolactone on myocardial fibrosis of spontaneously hypertensive rats(SHR).METHODS:Sixteen fourteen-week-old male SHRs were randomly assigned to spironolactone and SHR group equivalently(n=8).Rats in each group were given 30 mg ? kg-1 ? d-1 spironolactone and equal sodium chloride respectively for 12 weeks by gavage.Eight fourteen-week-old male SD rats were as control group.Connective tissue growth factor(CTGF),transforming growth factors beta-1(TGF?1),collagenⅠand Ⅲ were measured by qualitative and semiquantitative immunohistochemical staining and semiquantitative reverse transcription polymerase chain reaction.Masson staining was used to determine total collagen in left ventriculum.Alkaline hydrolysis method was used to detect the concentration of hydroxyproline(Hypro)in the myocardium of left ventricle.RESULTS:Left ventricular index(LVI),collagen volume fraction(CVF),Hypro and the expression of TGF?1,CTGF,collagenⅠand Ⅲ in SHR group were significantly higher than those in SD group(P