Protective effect of metformin on H9C2 rat myocardial cell damage induced by saturated fatty acid / 重庆医学

Objective To investigate the mechanisms of metformin (Met) for protecting H9C2 myocardial cells damage induced by saturated fatty acids (palmitic acid,PA) in rats.Methods Rat H9C2 myocardial cell lines in blank control group,PA group and three different concentrations of metformin and PA combination groups were cultured for 24 h.Then Western blot was adopted to detect the protein expression of nuclear factor κB p65 (NFκB p65),intercellular cell adhesion molecule-1 (ICAM1),phosphorylated inhibitor of nuclear factor κB (p-IκBα) and phosphorylated adenosine monophosphate activated protein kinase(p-AMPK);the quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of nuclear factor of nuclear factor κB(NFκB),chemokine (C-C motif) ligand 2 (CCL2) andintercellular cell adhesion molecule-1(ICAM1).Results Compared with the control groups,the protein expression of NFκB p65,p-IκBα and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the protein expression of NFκB p65,IκBα and ICAM1 in the Met+PA combination groups was decreased in various degrees with the Met concentration increase (all P<0.05),while the protein expression of p-AMPK was significantly risen with the Met concentration increase (all P<0.05).Compared with the control group,the mRNA expression of CCL2 and ICAM1 in the PA group was increased (P<0.05);compared with the PA group,the mRNA expression of CCL2 and ICAM1 in the Met+PA combination groups was decreased (P<0.05).Conclusion Met can alleviate H9C2 myocardial cellular damage caused by saturated fatty acid inducing increase of CCL2 and ICAM1 expression.

SIRT1 signaling pathway mediated the protective effects on myocardium of rats after endurance training and acute exhaustive exercise / 中华心血管病杂志

Objective@#To detect the expression of SIRT1 and Ac-FOXO1 in rats after endurance training and acute exhaustive exercise, and explicit the myocardial protective effect of SIRT1.@*Methods@#Rats were randomly divided into four groups: control group(n=20), exhaustive exercise group (E group, n=20), exhaustive exercise group + endurance training (TE group, n=18), exhaustive exercise group + endurance training + selective SIRT1 inhibitor (TSE group, n=17). The Control and E groups were fed routinely for 5 weeks. The TE and TSE groups were subjected to swimming exercise for 5 weeks for endurance exercising. The TSE group was intraperitoneally injected with selective SIRT1 inhibitor Sirtinol(2 mg/kg) at 30 minutes before endurance exercising. The E, TE and TSE groups were subjected to exhaustive exercise. The myocardial tissues of rats were collected after exhaustive exercise. Real-time polymerase chain reaction (PCR) and Western blot analysis were performed to detect the myocardial mRNA and protein expressions of SIRT1 and Ac-FOXO1. The myocardial protein expression of Bax and Bcl-2 was also detected by Western blot. Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay was used to assess the apoptosis of myocardial cells.@*Results@#Compared with Control group, the SIRT1 and Bcl-2 expression in the myocardial tissue was obviously decreased, while the Ac-FOXO1, Bax, and the myocardial cell apoptosis were significantly increased in E group (all P<0.01). Compared with E group, the expression of SIRT1 and Bcl-2 was obviously up-regulated (both P<0.01), while the Ac-FOXO, Bax and the myocardial cell apoptosis was significantly reduced in TE group (all P<0.01). Compared with TE group, the SIRT1 and Bcl-2 expression was obviously lower (both P<0.01), while Ac-FOXO1, Bax, and the cell apoptosis were significantly higher in group TSE (all P<0.01).@*Conclusion@#Endurance training could protect myocardium by reducing the myocardial oxidative stress injury and apoptosis via activating SIRT1 signaling pathway, up-regulating the myocardial expression of SIRT1 and regulating the deacetylation of FOXO1.

Cohort study of effects on lung function of coke oven workers exposured to coke oven emissions / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>Through comparative study on pulmonary function damage of coke oven workers exposed to coke oven emissions with the same group before and after five years, and further explore the relationship between the coke oven emissions and injury in pulmonary function of coke oven worker.</p><p><b>METHODS</b>Select a coking plant in Shanxi 165 coke oven workers (exposed group) and 52 auxiliary workers (control group) for the study, using a uniform questionnaire to collect workers' personal information. Fixed workplace air samples collected periodically. Air samples of benzo (a) pyrene concentrations was measured by high pressure liquid chromatograph. Pulmonary function of research object was measured by portable spirometer respectively in 2009 and 2013, and comparative analysis on it.</p><p><b>RESULTS</b>The concentration of B(a)P was no significant difference in the same area between 5 years in 2009-2013. Compared with 2009, 2013 control workers lung function index and the abnormal rate had no significant difference (P > 0.05). But FVC%, FEV1.0%, MVV%, VC% and FEF25% of exposed workers in 2013 was significantly lower than in 2009, FVC%, FEV1.0%, VC% and FEF25% pulmonary dysfunction rate in 2013 was also significantly higher than in 2009, difference was statistically significant (P < 0.05). Workers emerging pulmonary function abnormalities mainly distributed in furnace roof and side. furnace roof group FVC%, FEV1.0%, VC% additional abnormal number (rate) was significantly higher than furnace floor and the control group (P < 0.05), and furnace side groop was significantly higher than the control group, the difference was statistically significant (P < 0.05). Multivariate Logistic regression analysis showed that after 5 years FVC%, FEV1% and VC% of abnormal lung function emerging adjusted OR of furnace roof workers were 7.939, 5.966 and 4.956. For abnormal of FVC%, FEV1%, VC% and MVV%, the contacting coke seniority is a risk factor. There is a positive interaction between contacting coke seniority and furnace roof (P < 0.05).</p><p><b>CONCLUSION</b>Coke oven workers lung function damage associated with exposureing to coke oven emissions, coke oven emissions exposure level and exposure time are the main factors of coke oven workers in lung function damage, there is a positive interaction between the two factors.</p>

Relationship between HSP70 gene polymorphisms and susceptibility to lung function injury of cock-oven workers / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>In this study, we investigate the relationship between HSP70 and lung function injury. To study on the feasibility of HSP70 genes polymorphisms as biological marker of the damage of pulmonary dysfunction susceptibility.</p><p><b>METHODS</b>183 cock-oven workers were selected as exposure groups and 143 workers unexposed workers were selected as control groups. We investigated their general information with uniform questionnaire. Pulmonary dysfunction indicators were determined using portable spirometer. HSP70-1 G190C, HSP70-2 A1267G, HSP70- hom T2437C genotypes were analyzed by using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The haplotypes were calculated using PHASE 2.0 software.</p><p><b>RESULTS</b>VC%, FVC%, MVV%, FEV(1.0%) in exposed group were lower than in non-exposure group, the difference were significantly (P < 0.05). VC%, FVC%, MVV%, FEV1.0% in exposed group with HSP70-1, HSP70-2, HSP70-hom genotypes were lower than in non-exposure group (P < 0.05); FVC% in exposed group with HSP70-hom T/C genotypes were lower than that with HSP70-hom T/T genotypes, MVV% were lower than that with HSP70-hom T/T, C/C genotypes. There's no difference in pulmonary dysfunction index of HSP70-1, HSP70-2 genotypes (P>0.05), but significant difference between the exposed group with HSP70-1, HSP70-hom genotypes; The adjust OR (95%CI) of exposed group with HSP70-1 G/C genotypes and HSP70-homT/C genotypes were 2.516 (1.012 ∼6.252) and 2.284 (1.033∼5.053). Exposed group with CGT haplotype pulmonary dysfunction were significantly higher than in non-exposure group (P < 0.05).</p><p><b>CONCLUSION</b>Coke oven exposure may increase pulmonary dysfunction injury, Coke oven workers who have the HSP70-1 G/C genotypes, HSP70-hom T/C genotypes and CGT haplotypes may increase the susceptibility of pulmonary dysfunction. There must be some relationship between HSP70-1, HSP70-hom gene polymorphisms and lung function injury of Cock-oven Workers.</p>

Correlation between PPARγand coronary stenosis and plaque stabilit of patients with ACS and T2DM / 中国介入心脏病学杂志

Objective To investigate the effect of PPARγ in acute coronary syndrome (ACS) patients with type 2 diabetes (T2DM) for the severity of coronary atherosclerosis and plaque stability. Methods We selected 102 patients with ACS, including 52 patients with type 2 diabetes mellitus (ACS+T2DM group) and 50 patients with simply ACS (ACS group). Meanwhile, we selected 30 patients without coronary heart disease and T2DM as the control group. All basic clinic data, CAG and the Gensini score were compared among all groups. To all patients, blood was drew when they were enrolled to detect the level of PPARγ and MMP-9. Results Gensini points in the ACS+T2DM group was much higher than that of the ACS group (P < 0.05). The levels of PPARγ of the ACS group and the ACS+T2DM group, when compared with the control group, were decreased significantly, but the level of MMP-9 were increased (all P < 0.05). The level of PPARγ in the ACS+T2DM group was much lower than the ACS group, and the level of MMP-9 was much higher (P<0.05). Gensini scores (r=-0.416, P<0.05), the level of MMP-9(r= - 0.503, P < 0.05) were correlated negatively with the level of PPARγ. Conclusions Complicating with T2DM can aggravate coronary artery disease and plaque instability degree in ACS patients, and PPARγpossibly make an protective effect.

The expression of resistin-like molecules-a in atherosclerotic plaque / 中华急诊医学杂志

Objective To explore the expression of resistin-like molecules-a (RELMa) in atherosclerotic plaque of ApoE-/- mouse, and to study the effects of RELMa on the proliferation and migration of vascular smooth musclee cells (VSMCs) . Method Nine ApoE-/- mice and nine C57BL/6J mice were fed with high fat diet. All mice were sacrificed 24 weeks after force feeding. Vessels were dissected from to abdominal aorta. Sections of aortic tissue were stained with HE dyeing and RELMa in aortic tissue was assayed by immunohistochemistry. The expression of RELMa mRNA in vessels was detected by RT-PCR. The effects of different concentration RELMa in different concentrations on the proliferation and migration of VSMCs were detected. Data was expressed as mean ± standard deviation. ANOVA were used for comparison in SPSS 11.0, and changes were considered as statistically significant if P value was less than 0.05. Results Atherosclerosis plaque formed in aortic root of ApoE-/- mice after they were fed with high fat diet for 24 weeks. RELMa protein and RELMa mRNA were found by immunohistochemistry and RT-PCR in atherosclerotic plaque of ApoE-/- mouse. RELMa protein didn't be found in vessels of control mouse. RELMa promoted the proliferation of VSMCs (RELMa groups: 2811. 21 ± 216. 89,4056. 87 ±220.65,5061.45 ± 335.86, vs. control 1609.58 ± 203.53, P < 0.01). RELMa promoted the migration of VSMCs (RELMa groups: 130.54±12.98,158.39±11.58,203.50± 17.37 vs. control:70.54± 11.92, P<0.01).Conclusions RELMa expresses in atherosclerotic plaque of ApoE-/- mouse. RELMa enhances the proliferation and migration of VSMCs of aorta.

The Expression of FIZZ1 in Atherosclerotic Plaque of ApoE~(-/-)Mouse / 中华高血压杂志

Background FIZZ1 is a newly found protein associated with pulmonary inflammation. It has been shown to involve in proliferation of pulmonary arterial vascular smooth cells, contriction of vascular vessels, and stimulation of fibroblasts. Objective This study was designed to investigate the expression of FIZZ1 in atherosclerotic plaque of C57BL/6J ApoE-/-mice and the role of FIZZ1 on the proliferation of vascular smooth muscle cells obtained from aorta. Methods Nine C57BL/6J ApoE-/-mice were fed with high fat diet and nine C57BL/6J wild type mice with normal chow for 24 weeks. All mice were euthanized and the aortas were collected. HE stain histological examination and FIZZ1 immunohistochemistry were used in vivo study. In vitro, smooth muscle cells were treated with normal saline (control groups) or recombinate FIZZ1 at different concentrations (final concentration 3?10-6, 9?10-6, 2.7?10-5 mmol/L) respectively. The proliferation of smooth muscle cells were detected by MTT. Results After 24 weeks of high fat diet treatment, large atherosclerotic plaques were found in aortic root of ApoE-/-mice. FIZZ1 was found in atherosclerotic plaques of C57BL/6J ApoE-/-mice, however, no FIZZ1 was expressed in the arteries of C57BL/6J wild type mice. Cell culture study showed FIZZ1 promoted the proliferation of smooth muscle cells in a dose dependent manner(P

Isolation and Characterization of Bacteriophage for Klebsiella pneumoniae / 中华医院感染学杂志

OBJECTIVE To characterize bacteriophage isolated from sewage with indicator of Klebsiella pneumoniae subsp pneumoniae.METHODS Bacteriophage was isolated from sewage by double-layer agar plate method,identified lytic or lysogenic capacity by induced methods of ultraviolet ray and mitomycin C,performed one-step growth experiments,decided the optimal multiplicity of infection,and its structure was observed with electron microscope.RESULTS The study found a strain of bacteriophage against the K.pneumoniae subsp pneumoniae.The phage had a head of 180 nm in diameter and a tail of 210 nm in length.The plaque was transparent and 4-7 mm in diameter.the optimal multiplicity of infection was 4,latent period was 35 min and burst period was 40 min,the average burst size was about 94 PFU/cell.CONCLUSIONS The isolated bacteriophage belongs to Stylovinidae,and it is a lytic bacteriophage with narrow host spectrum.Moreover,it is only sensitive to a part of K.pneumoniae subsp pneumoniae and a few of Escherichia coli strains.

Found in Inflammatory Zone 1 Enhance Scavenger Receptor-A Expression in Vascular Smooth Muscle Cells / 中华高血压杂志

Background Found in Inflammatory Zone 1(FIZZ1)is a newly found protein associated with pulmonary inflammation.We previously had reported its role in the development of atherosclerosis,but its detailed mechanism has not been explored.Objective This study was designed to delineate the effect of FIZZ1 on the expression of scavenger receptor(SR-A)in vascular smooth muscle cells(VSMC)scavenger receptor(SR-A)induced by ox-LDL.Methods Smooth muscle cells were treated with ox-LDL(20 mg/L)or cocultured with recombinate FIZZ1 at different concentration(final concentration 3?10-6,9?10-6,2.7?10-5 mmol/L).The expression of SR-A of smooth muscle cell was detected by flow cytometry and laser confocal microscopy.Results SR-A positive expression was found in VSMCs treated with ox-LDL after 24 hours,which were located mainly in cell membrane by laser confocal microscopy.FIZZ1 significantly accentuate the LDL induced increases in SR-A positive rate in VSMC in a dose dependent manner(P