AIM: To investigate the effects of Chlamydia pneumoniae infection and hyperlipidemia on the expression of NF-?B and AP-1 in the myocardium. METHODS: The indirect immunofluorescence method was used to examine wild C57BL/6J mice infected with Chlamydia pneumoniae and fed with an atherogenic diet. The expression of the subunit of NF-?B, P50, and c-Fos in the murine myocardium was observed. RESULTS: Chlamydia pneumoniae infection and hyperlipidemia induced the activation of NF-?B and AP-1 in murine myocardium. P50 and c-Fos were not detected in the controls, but there were different levels of positive expression in the experiments (P

Objective To evaluate the predisposition effects of angiotensin-converting enzyme (ACE) ,angiotensinogen (AGT) and endothelial nitric oxide synthase (eNOS) gene polymorphisms on coronary disease (CHD) as well as their possible synergistic effect in the development of CHD in Chinese aged people. Methods The study included 191 subjects (100 CHD and 91 controls). Gene chip technology was performed. The allele frequency and genotype distribution were compared between groups. Results A significantly higher frequency of the DD genotype of ACE gene was observed in CHD group (28.0% vs 15. 4%, P0. 05). Subjects carrying ACE DD and AGT TT genotypes or those carrying AGT TT and eNOS TT genotypes showed a stronger association withCHD(OR=2. 9, P

[Objective] To observe the preventive effect of Huanglian Jiedu Decoction (HJD), a prescription with the actions of clearing heat and removing toxicity, on rabbits atherosclerosis (AS) induced by Chlamydia pneumoniae (CP) infection. [Methods] Fifty two New Zealand rabbits were fed with forage containing 2. 5g/kg cholesterol and were infected with CP via nasopharynx for three times during 6 weeks. At the end of the sixth week, forty four rabbits with serum CP-IgG positive were randomized into 4 groups: group A treated with HJD 2g?kg-1 ?d-1 by gastric gavage, group B with HJD 1g?kg-1?d-1, group C with azithromycin 20 mg?kg-1?d-1 and model group D with normal saline for 6 weeks. Group E was set up in 8 rabbits fed with fatty forage and served as the control. Serum levels of high-sensitive C reactive protein (hs-CRP) and CP-IgG were detected before infection, after infection and after treatment. At the end of the 18th week, the rabbits were executed and the pathological features of aortic tissue were observed under microscope. Meanwhile, the expression of CP-DNA and tumor necrosis factor ?(TNF-?) in the aortic tissue was detected with polymerase chain reaction (PCR) and immunohistochemical method respectively. [Results] At the end of the experiment, atherosclerotic changes were obvious in groups D and E, particularly in group D. Compared with group D, the atherosclerotic damage was much relieved, and AS indexes such as maximum intimal thickness (MIT), atherosclerotic damage percentage and plaque area index were much improved in groups A and C (P

This paper analyse the problem of medical probation,suggests solutions with the application of new medical education methods to improve teaching quality and cultivate the high quality talents that can meet the fundmental requirement of global medical education.

[Objective]This study was designed to investigate the effects of 5-aminoimidasole-4-carboxamide ribonucleoside (AICAR)on activity of transcription factor Forkhead O 3a(FOXO3a)and expression of ubiquitin ligase muscle atrophy F-box (MAFbx),and to explore the role of adenosine monophosphate-activated protein kinase(AMPK)on proteolysis pathways in eardiomyocytes.[Methods]The effect of AICAR on activation of AMPK was observed.Cultured neonatal rat cardiomyocytes was treated with AICAR in different concentration.Cultured cardiomyocytes were then divided into three groups:control group,AICAR group,AICAR+Compound C group.Effects of AMPK activation on phosphorylation of FOXO3a and expression of MAFbx in cardiomyocytes were detected using Western blot.[Results]①Compared with control group,activity of AMPK in cultured cardiomyocytes was increased after treatment with 0.25 mmol/L or 0.5 mmol/L AICAR for 6 h(P＜0.05),and the activity of AMPK was further enhanced after treatment with 1.0 mmol/L or 2.0 mmol/L AICAR for 6 h(P＜0.01).②Activation of AMPK by AICAR significantly increased the transcriptional activity of FOXO3a(P＜0.01),and enhanced MAFbx protein expression in cardiomyocytes when comparing with control group(P＜0.01),however,specific AMPK antagonist Compound C markedly reversed these effects induced by AICAR.[Conclusion]AMPK may regulate cardiomyocytes proteolysis by activation of FOXO3a transcription factor,and up-regulation of MAFbx protein expression.

AIM: To study the effects of metformin on the pressure overload-induced cardiac hypertrophy in rats. METHODS: Transverse aortic constriction (TAC) model of rat was made through laparotomy. One week after TAC surgery, the rats were randomly divided into 5 groups (n=8 in each group) and were administered with the corresponding drugs orally every day for 8 weeks: sham group (sham surgery, administered with 2 mL distilled water);TAC group (TAC rats, administered with 2 mL distilled water);metformin(MET) group (TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1));MN group [TAC rats, administered with MET at dose of 300 mg·kg~(-1)·d~(-1) plus NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) 50 mg·kg~(-1)·d~(-1)] and L-NAME group (TAC rats, administered with L-NAME at dose of 50 mg·kg~(-1)·d~(-1)). After treated for 8 weeks, the echocardiography, hemodynamics, the ratio of heart weight to body weight (HW/BW) and histological examination of the heart were performed. The levels of myocardial AMP-activated protein kinase subunit α (AMPKα), p-AMPKα~(Thr172), endothelial nitric oxide synthase (eNOS) and p-eNOS~(Ser1177) were detected by Western blotting. Plasma and myocardial nitric oxide (NO) were detected biochemically. RESULTS: After 8 weeks treatment, the wall thickness of left ventricle, the heart weight/body weight ratio (HW/BW), and the left ventricular myocardial perivascular fibrosis and myocardial interstitial fibrosis of the animals in TAC group were significantly increased as compared to those in sham rats. Treatment with MET for 8 weeks significantly attenuated left ventricular hypertrophy and improved cardiac function in TAC rats. These effects of MET were mostly abolished by L-NAME. Molecular biology and biochemical testing revealed that the levels of left ventricular myocardial p-AMPKα~(Thr172) and p-eNOS~(Ser1177), as well as the levels of myocardial and serum NO were significantly increased in MET group. CONCLUSION: Long-term MET treatment significantly inhibits the cardiac hypertrophy and the myocardial fibrosis and improves the cardiac functions in pressure-overload rats. The anti-hypertrophic effects of MET may be mediated via activation of AMPK-eNOS signaling pathway.

AIM: To investigate the effects of simvastation on homocysteine-induced endothelial dysfunction and inflammatory response and the underlying mechanisms of such effects. METHODS: MTT assay was used to detect cell viability, and DCFH-DA assay was used to examine the levels of reactive oxygen species (ROS). Furthermore, Western blotting was performed to detect protein expression and electrophoretic mobility shift assay (EMSA) was used to detect NF-?B DNA binding activity. RESULTS: Homocysteine (0.1-1 mmol/L) decreased the human umbilical vein endothelial cell (HUVEC) viability and increased the levels of ROS. Western blotting and ELISA showed that homocysteine significantly increased the expression of TNF-?, IL-6, MCP-1 and ICAM-1. However, pretreatment with simvastation (1-20 ?mol/L) reversed the decreased cell viability and markedly suppressed an increase in the ROS level and the expression of TNF-?, IL-6, MCP-1 and ICAM-1 induced by homocysteine. Homocysteine induced p38 phosphorylation and such phosphorylation was also inhibited by simvastation and antioxidant NAC. EMSA and Western blotting showed that homocysteine induced NF-?B activation due to the increased phosphorylation of the inhibitory protein (I?B?) as well as the degradation of I?B?, while simvastation pretreatment almost completely blocked the NF-?B activation as well as the phosphorylation and degradation of I?B?. CONCLUSION: Simvastation inhibits homocysteine-induced endothelial dysfunction and inflammatory response through interfering with ROS-p38-NF-?B pathway.

Objective To investigate the prevalence and the risk factors of gastroduodenal damages induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Methods One hundred and eighty-four patients who were prescribed NSA1Ds for long time in rheumatology and cardiovascular clinics were enrolled. Clinical data such as age, sex, medication history and body mass index were recorded. The lesions were estimated by endoscopy and the specimens were tested for Helicobacter pylori (H. pylori) infection. Results Peptic ulcer was found in 63 (34. 24%) patients including gastric ulcer in 22, duodenal ulcer in 34 and compound ulcer in 7. The endoscopic examination showed that 57 out of 121 patients without peptic ulcer had ≥3 erosive lesions. Logistic regression analysis revealed that H. pylori infection was important risk factor that induced the peptic ulcer in those who were taking NSAIDs for long time (OR = 13. 86, 95% CI: 6. 53 ～ 29. 43). The incidence of gastroduodenal damage was similar in patients taking NSAIDs and low dose aspirin (OR =0.45,95CI:0.16～ 1.28). Conclusions NSAIDs may cause gastroduodenal damages in long-term users and H. pylori infection was an important risk factor. The effect of low dose aspirin on gastroduodenal damages is as same as NSAIDs.

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

Objective To evaluate the value of the TIMI risk index in predicting 30-day and one-yosr mortality and incidence of heart failure in patients with ST-elevation myocardial infarction (STEMI).Method Data of 229 patients with STEM1 from August 1999 to March 2006 in the First Affiliated Hospital,Sun Yat-sen University,were retrospeclively collected,analyzed and scored with TIMI risk index.When categorized into quintiles(≤12.5,12.5～17.5,17.5～22.5,22.5～30,>30) and modeled as a continuous variable,difference of prediction of 30day and one-year mortality and 30-day incidence of heart failure of patients were compared respectively.Results When categorized into quintilos and modeled as a continuous variable,30-day and one-year mortality and 30-day incidence of heart failure were increasing with increasing score of risk index (P<0.05).The area under the recewer operating characteristic curve were 0.65,0.68,0.67 and 0.70,0.72,0.70,respectively.Conclusions The TIM1 risk index can be used as a simple,rapid and practical tool to risk-stratify patients with STEMI.