Abstract:Aim To study the effects of vascular adventitial vascular cell adhesion molecule-1(VCAM-1) and intercellular adhesion molecule-1(ICAM-1) on atherosclerotic lesion formation. Methods Apolipoprotein E Knockout(ApoE-/-) mice and wild-type C57BL/6 black mice of 6 weeks were used in this experiment.All animals were fed hyperlipidic diet for 2,4 and 8 weeks.The ascending aorta was removed with the heart attached for serial sectioning.Some sections were stained by Movat method in order to observe the morphological changes of the tissues and measure the thickness of vascular adventitia.Some sections were stained with immunohistochemistry to observe the changes in the expression of vascular adventitial ICAM-1 and VCAM-1 at different stages. Results ApoE-/-mice of 6 weeks and C57BL/6 mice at any time point did not show any changes of adventitial thickness,nor expression of VCAM-1,nor intimal lesion formation.After hyperlipidic diet for 2 weeks in ApoE-/-mice,the adventitial thickness increased and the expression of VCAM-1 was found in the adventitia when there was no visible intimal lesion formation.After hyperlipidic diet for 4 weeks the foam cells were showed in the intima and the atherosclerotic lesion developed after hyperlipidic diet for 8 weeks in ApoE-/-mice.The adventitial thickness and the expression of VCAM-1 in adventitia and intimal lesion of ApoE-/-mice increased.The expression of ICAM-1 in the adventitia and the intima of ApoE-/-mice increased gradually with increasing duration of the hyperlipidic diet.However the expression of ICAM-1 was infrequent and stable in C57BL/6 mice. Conclusion The expression of VCAM-1 and ICAM-1 in the adventitia of ApoE-/-mice increased gradually with increasing duration of the hyperlipidic diet.

Abstract:Aim To observe the changes of distribution of RhoA and phosphorylated RhoA kinase(ROCK) induced by advanced glycation end products(AGE) in human dermal microvascular endothelial cells(HMVEC-1). Methods Cultured HMVEC-1 were treated with AGE-modified human serum albumin(AGE-HSA).The distribution of RhoA and phospho-ROCK were detected by immunohistochemistry using anti-RhoA and anti-phospho-ROCK antibodies and observed under confocal microscope. Results The data revealed that RhoA located around the nucleus in quiescent HMVEC-1.The stimulation of AGE-HSA evoked an increased distribution of RhoA in cytoplasma,even an accumulation at the cellular edge.The administration of AGE-HSA also triggered a significant increase of phospho-ROCK localization in HMVEC-1 cytoplasma.The transfection of dominant negative RhoA N19 attenuated this AGE-induced phosphor-ROCK spreading while constitutive active RhoA L63 mimiced the AGE-induced response in phospho-ROCK distribution. Conclusion AGE stimulation causes the redistribution of RhoA and results in the phosphorylation of ROCK in human microvascular endothelial cells.

Abstract:Aim To investigate the effect of cigarette smoke extract(CSE) on the proliferation of vascular smooth muscle cells(VSMC) and the relevant roles of basic fibroblast growth factor(bFGF). Methods(1)The rat aortic smooth muscle cells were treated with various concentrations of cigarette smoke extract(0%,2.5%,5.0%,10.0%,20.0%),the VSMC treated without CSE were control group,then MTT assay was performed to observe the changes of the proliferation of VSMC.The expression of proliferating cell nuclear antigen(PCNA) and Fibroblast Growth Factor 2(bFGF) were detected by immunocytochemistry.In addition,reverse transcription polymerase chain reaction(RT-PCR) was applied to detect the mRNA expression of bFGF.(2)Treated with 5%CSE(the optimal concentration) at 0 h(control group),4 h,8 h,12 h,24 h,the expression of bFGF mRNA,bFGF and PCNA protein were observed.(3)Treated with bFGF antibody and 5.0%CSE at 24 h,MTT A value,bFGF and PCNA protein were observed. Results(1)CSE can stimulate the increase of MTT absorbance(A)value.The absorbance(A)value of 2.5%(P><0.05),5.0%CSE(P><0.01) group were significantly increased compared to the control group.The absorbance(A)value of 10%,20%CSEgroup were not significantly increased compared to the control group(P>0.05).There was the maximal increase in5.0% CSE group.The VSMC in control group expressed bFGF mRNA,bFGF and PCNA protein at low levels.In-creased bFGF mRNA,bFGF and PCNA protein expression were evident after 2.5%CSE treatment.Maximal increase inbFGF mRNA,bFGF and PCNA protein expression occurred after5.0%CSE treatment.Then expression were still elevat-ed compared with control group’s after 10%,20%CSE treatment.(2)The VSMC in control group expressed bFGF mR-NA,bFGF and PCNA protein at lowlevels.Increased bFGF mRNA,bFGF and PCNA protein expression were evident at4h after CSE treatment.Maximal increase in bFGF mRNAoccurred at8 h,while peak expression of bFGF and PCNApro-tein was at12 h.(3)Treatment with bFGF antibody nearly inhibited CSE-induced MTTA value,bFGF and PCNA proteinexpression.Conclusion The proliferation of VSMC increased gradually in low and middle concentrations(2.5%,5.0%CSE group),while decreased in high and higher concentrations(10%,20%CSE group)on the contrary.CSE maybe in-creased rat VSMC proliferation by high expression of bFGF.

Abstract:Aim To investigate the effect of pinocembrin on apoptosis of human umbilical vein endothelial cells(HUVEC) induced by lipopolysaccharide(LPS). Methods HUVEC were collected by digestion-perfusion culture.An apoptotic model of HUVEC was established by 10 mg/L LPS.The apoptosis of HUVEC induced by LPS was mixed with culture medium of 50 mg/L,100 mg/L and 200 mg/L pinocembrin,after treatment of 24 hours,HUVEC apoptotic rate was detected by TUNEL assay.Cell-morphosis was observed by light microscope.Cell survival rate was measured by MTT assay.Expression of nuclear factor–kappa B p65(NF-κB p65) was detected by immunocytochemistry staining. Results HUVEC apoptotic rate of model group increased obviously than control group,and different dosage pinocembrin group discreased significantly than model group(P><0.01).Meanwhile,cell survival rate was increased after pinocembrin treatment.Expression of NF-κB p65 in LPS induced HUVEC was reduced significantly after pinocembrin treatment compared with those induced apoptosis group by LPS(P><0.01). Conclusion Pinocembrin may inhibit the apoptosis of HUVEC,the protection mechanism of pinocembrin on HUVEC may be related to reducing the activity of NF-κB.Thereby it plays a role in protecting the vascular endothelial cells.

Abstract:Aim To study the effect of ligustrazine on hypertrophy of cardiomyocytes induced by angiotensin Ⅱ(AngⅡ). Methods The cultured cardiomyocytes were treated with AngⅡ to induce hypertrophy and given with ligustrazine of different densities.The cell size,3H-Leucine incorporation and the mRNA levels of β-myosin heavy chain(β-MHC) were examined. Results Stimulated by AngⅡ,the cardiomyocytes were enlarged under the contrast phase microscope.After stimulated by AngⅡ,3H-Leucine incorporation and the mRNA levels of β-MHC increased in the hypertrophic cardiocytes.Given by ligustrazine,these data decreased accordingly as the ligustrazine densities increased. Conclusion AngⅡ may induce the cardiomyocytes hypertrophy.Ligustrazine P could partly inhibit the cardiomyocytes hypertrophy induced by AngⅡ.

Abstract:Aim To observe the effect of ghrelin on human umbilicus endothelial cell(HUVEC) proliferation and migration. Methods Different concerntration of angiotesionⅡ(AngⅡ)(10-9～10-6 mol/L) was adopted to excite HUVEC for 24 hours,and the best concerntration of 10-6 mol/L was acquired,and used to stimulate HUVEC for 0,6,12,24 hours respectively to observe human umbilicus endothelial cell proliferation and migration.(10-9～10-6 mol/L) ghrelin was pretreated for 2 hours and cultivated for 24 hours with HUVEC and 10-6 mol/L ghrelin was used to pretreat for 0,0.5,1,2 hour and cultivate HUVEC for 24 hours to observe the cells proliferation and migration.MAPK /ERK1/2 singal pathy inhibitor PD98059(25 μmol/L),GHSR1a receptor inhibitor(GHRP-6 25 μmol/L) were added to pretreat HUVEC to observe ghrelin effect on AngⅡ induced endothelial cell injury.Cell proliferation was measured with WST-8,and cell migration with Transwell;ERK1/2 and p-ERK1/2 protein expression with western blot. Results AngⅡ promoted HUVEC proliferation and migration with dose and time dependent manner.Ghrelin inhibited AngⅡpromoting effect on cell migration and proliferation with dose and time dependent manner.Pretreatment with PD98059(25 μmol/L) can inhibit the promoting effect of HUVEC proliferation and migration;pretreatment with GHRP-6(25 μmol/L) can block ghrelin's inhibiting effect on cell migration and proliferation effect.Ghrelin can decrease the p-ERK1/2 expression. Conclusion Ghrelin can inhibit AngⅡinduced HUVEC proliferation and migration,and the mechanism was involved in ERK1/2 pathway.

Abstract:Aim To explore effects of hypoxia-reoxygenation on glucose oxidation and fatty acid oxidation(FAO) of hypertrophied cardiomyocytes. Methods Cultured rat cardiomyocytes were induced to be hypertrophy by angiotention Ⅱ(AngⅡ) and norepinephrine(NE),which was confirmed by -Leu incorporation in cardiomyocytes and detection surface area of cells.We established a model of post-hypoxia reoxygenation of cultured cardic cells in vitro.Glucose oxidation,FAO and acitivity of pyruvate dehydrogenase(PDH) and carnitine palmitoyltransferase(CPT) were determined by liquid scintillation counting. Results Surface area of cells increased by 63.94% and -Leu incorporation by 181.54%,when 0.1 μmol/L Ang Ⅱand 1 μmol/L NE were added in vitro.Activity of PDH decreased,and glucose oxidation decreased by 48%;Activity of PDH and glucose oxidation recovered to the level of prehypoxia at 8 hours of reoxygenation.Activity of CPT decreased,and FAO decreased by 60%;Activity of FAO and CPT recovered gradually to the level of prehypoxia during reoxygenation. Conclusion Glucose oxidation and fatty acid oxidation of hypertrophied cardiomyocyte decreased during hypoxia,and both recovered during reoxygenation.Activity of PDH and CPT was involved in these changes.

Abstract:Aim To investigate the role of integrin-linked kinase(ILK) during progressive heart dysfunction after acute myocardial infarction(AMI),and observe the changes of heart function as well as ILK expression at different time points after AMI. Methods Left anterior descending arteries of adult male SD rats were ligated to form AMI models.Cardiac function was evaluated by echocardiography and left ventricular catheter.Real time PCR and Western blotting were used to assess ILK expression in non-infarct area.The above parameters were examined in different time points after post AMI. Results After AMI,heart function was significantly decreased.Lower of ±dp/dtmax and higher left ventricular end diastolic pressure(LVEDP) of 8 weeks group was observed,compared with 1 and 4 weeks groups post AMI.On the other hand,ILK expression of non-infarct area was increased in 1 and 4 weeks groups and decreased significantly in 8 weeks group post AMI. Conclusion Although temporary ILK up-expression in non-infarct area post acute myocardial infarction maintains compensatory cardiac function,long-term down-regulation of ILK pathway finally lead to cardiac decompensation.

Abstract:Aim To investigate the effect of chlorpyrifos on relaxation function of artery and explore the potential mechanism. Methods Organ baths in basilar aortic rings of New Zealand rabbits were used to investigate the effect of different concentration chlorpyrifos on vascular relaxation function induced by acetylcholine(Ach) and sodium nitroprusside(SNP). The level of nitric oxide(NO) was measured in basilar artery and cultural human umbilical vein endothelial cells.The expression of endothelial nitricoxide synthase(eNOS) was detected by Real-time PCR and Western blot in cultural human umbilical vein endothelial cells(HUVEC). Results Endothelium dependent relaxation and NO content of rabbits basilar aortic rings were decreased in concentration-dependent manner by pre-treatment with chlorpyrifos(0.001 mmol/L,0.01 mmol/L,0.1 mmol/L) for 30 minutes. But chlorpyrifos had no effect on SNP-induced endothelium-independent relaxation of basilar aortic rings.Pre-treatment with atropine had no influence on the action of chlorpyrifos.The level of NO in culture medium and the expression of eNOS in HUVEC were decreased by pre-treatment with chlorpyrifos(0.001 mmol/L,0.01 mmol/L,0.1 mmol/L) for 30 minutes in concentration-dependent manner. Conclusion Chlorpyrifos decreases endothelium dependent relaxation of basilar aortic rings,which the mechanisms may relate to down-regulating of eNOS and decrease of NO induced by chlorpyrifos.

Abstract:Aim To investigate the effect of JNK in the proliferation and β-catenin nuclear accumulation stimulated by platelet derived growth factor-BB(PDGF-BB). Methods The inhibitory effect of JNK inhibitor-SP600125(10,20,40 μg/L) in the PDGF-BB stimulating vascular smooth muscle cell proliferation was detected by CCK8 assay.Expression of JNK,p-JNK,nuclear and cytosolic β-catenin stimulated by PDGF-BB at different time point was examined.The effect of SP600125 on the nuclear accumulation of β-catenin was detected by Western Blotting and immunofluorescence. Results CCK8 OD value was greatly enhanced after stimulated by PDGF-BB(50 μg/L)(0.876±0.041 vs 0.370±0.082,P><0.01),it was significantly inhibited by JNK inhibitor-SP600125(10,20,40 μg/L)(0.635±0.063,0.470±0.044,0.381±0.054 vs 0.876±0.041,P><0.01) in a concentration-dependent manner.After stimulated by PDGF-BB,expression of p-JNK and nuclear β-catenin increased over time,and p-JNK at 15 minute and nuclear β-catenin at 60 minute reached its peak.The expression of p-JNK at 15 minute and nuclear β-catenin at 60 minute was inhibited by using SP600125(10,20,40 μg/L)in a concentration-dependent manner.The immunofluorescence test also showed that nuclear accumulation of β-catenin in vascular smooth muscle cell was significantly inhibited by SP600125. Conclusion The phosphorylation of JNK was a key step in the nuclear accumulation of β-catenin induced by PDGF-BB.

Abstract:Aim To explore the effects of probucol combined with atorvastatin on carotid atherosclerosis of cerebral infarction patients. Methods 120 acute cerebral infarction patients included 68 males and 52 females,whose average age were 74±15 years.They all had atherosclerosis plaques detected by carotid artery ultrasonography.All subjects were divided randomly into 2 groups: atorvastatin group were treated with atorvastatin(20 mg/d) which included 35 males and 25 females,whose average age were 73±16 years;combined treatment group were treated with atrovastatin(20 mg/d) combined with probucol(500 mg/d) which included 33 males and 27 females,whose average age were 76±18 yeares.The lipoprotein-associated phospholipase A2(Lp-PLA2) activities in serum,characters of carotid atherosclerosis plaques of the two groups were assayed before treatment,6 month,12 month and 24 month after treatment. Results Lp-PLA2 activities in the two groups pretreatment were 18.43±8.01(mmol/(min.L)) and 18.65±8.12(mmol/(min.L)) respectively and there were no significant difference in the two groups.It decreased distinctly to 14.98±4.21(mmol/(min.L)) and 12.68±2.04(mmol/(min.L)) 6 month after treatment in the two groups,especially in com-bined treatment group;and it decreased further to 11.57±1.62(mmol/(min.L)) and 11.98±1.43(mmol/(min.L)) respectively 12 months after treatment and kept on the comparable level as 12 month on the 24 month time point:12.06±1.68(mmol/(min.L)) and 11.34±1.61(mmol/(min.L)).The magnitude of varieties in atorvastatingroup was much larger than that in combined treatment group(P><0.05).In atorvastatin group the average integral ofstable plaques were 2.73±0.31,2.68±0.46,3.92±0.28 and 3.84±0.35 respectivly on pretreatment,6 month,12month and 24 month time point after treatment.The average integral on the 6 month time point dropped compared withpretreatment but had no significant difference.The average integral on 12 month and 24 month after treatment increasedremarkably than those on the two former time point(P><0.05);the average integral of vulnerable plaques were 6.82±0.37,4.38±0.42,3.02±0.43 and 3.28±0.29 respectively.The integral on 6 month after treatment dropped distinctlythan before(P><0.05) and it dropped continuately on 12 month and 24 month after treatment(P><0.01).In combinedtreatment group the average integral of stable plaques were 2.68±0.34,2.73±0.50,3.01±0.44 and 2.89±0.42 re-spectivly on pretreatment,6 month,12 month and 24 month after treatment.There were no difference significantly.Theaverage integral of vulnerable plaques were 7.08±0.39,4.92±0.33,3.11±0.46 and 2.28±0.41 respectively.Theintegral dropped progressively by time and there were significant differences between integrals in every two time point.There was no significant difference of the carotid atherosclerosis plaque integral before treatment in two groups.For stableplaques,the average integral increased on 12 month and 24 month after treatment in atorvastatin group than that in com-bined treatment group(P><0.05).For the vulnerable plaques,the average integral after treatment dropped remarkblythan pretreatment.And the decrease apitude in combined treatment group on 12 month and 24 month were more obviousthan those in atorvastatin group(P><0.01).Conclusion It is an important strategy to stablize plaques for treatmentof atherosclerosis of cerebral infarction.Protocol combined with atorvastatin was an important treatment to antiatheroscle-rosis in secondary prevention from ischemic stroke.It could degrade level of LDL,inhibit the information of ox-LDL,bring down the Lp-PLA2 activities in circulation especially surpress the secretion of Lp-PLA2 from macrophagocyte.Theantiatherosclerosis role is multiaspect and multiple-target-point.

Abstract:Aim To investigate the relationship between paraoxonase-1(PON1) polymorphisms and essential hypertension with carotid atherosclerosis. Methods The study comprised 527 participants who were divided into two groups: essential hypertension with carotid atherosclerosis(case group,n=321) and essential hypertension without carotid atherosclerosis(control group,n=206).The case group was consisted of Han people(n=230) and Uighur people(n=91).The control group was consisted of Han people(n=123) and Uighur people(n=83).Genotypes were detected by polymerase chain reactions followed by restriction analysis with specific endonucleases and their frequencies were determined. Results The M allele frequency of the PON1 L55M gene exihibited a significant difference between case group and control group in Han people(χ2=4.038,P>=0.044).LDL exhibited a difference in Han people between LL genotype and M allele carriers(P>=0.029).The M allele might be a risk factor for carotid atherosclerosis in Han people(P>=0.016). Conclusion The single nucleotide polymorphism of PON1 L55M is probably associated with carotid atherosclerosis in essential hypertension people of Chinese Han population in Xinjiang.The M allele might be a risk factor.

Abstract:Aim To explore the clinical value of the content of Angiopioetin-like protein 3(ANGPTL3)in patients with hyperlipoidemia by ELISA. Methods Serum ANGPTL3 was examined by ELISA in the patients with hypercholesterolemia(HTC),hypertriglyceridemia(HTG) and patients with both of them,and compared with normal group. Results In comparison with the normal group,the content of serum ANGPTL3 of patients with HTG was increased significantly(P>0,05),and there was no significant difference in diagnosis of HTG between detecting ANGPTL3 by ELISA and TG by GOD-POD method.But the content of serum ANGPTL3 of patients with HTC made no difference with normal group(P>0.05).And variance in the contents of serum ANGPTL3 of patients with both of HTC and HTG was not significant. Conclusion ELISA method can detect the increase in the patients with HTG,and there was no difference in the patients with HTC sensitively,which laid a foundation for application of ANGPTL3 ELISA kit in clinical laboratory.

Abstract:Aim To investigate the association between plasma lysophosphatidic(LPA) and coronary stenosis with coronary heart disease(CHD) as well as the roles of LPA in inflammation and lipidperoxidation. Methods Eighty-five patients were diagnosed as CHD according to the results of coronary angiography and ACC/AHA diagnostic criteria.The patients were divided into 3 groups: acute myocardial infarction(AMI) group(n=31),unstable angina(UA) group(n=30),stable angina(SA) group(n=24).Another 20 patients with normal coronary artery served as control.All patients underwent coronary angiography and the results were further evaluated by Jenkins score.The levels of plasma LPA and serum high sensitivity C-reactive protein(hs-CRP) and low density lipoprotein cholesterol(LDLC) were measured. Results The levels of LPA in AMI,UA and SA(4.85±0.36 μmol/L,3.67±0.84 μmol/L and 3.11±0.76 μmol/L) were significantly higher than that in the control group(2.15±0.57 μmol/L),the levels of LPA in AMI group were significantly higher than that in UA and SA,the levels of LPA in UA were significantly higher than that in the SA group(P><0.01).The levels of plasma LPA were positively correlated with Jenkins score(r=0.901,P><0.01),hs-CRP(r=0.755,P><0.01) and LDLC(r=0.549,P><0.01). Conclusion The levels of plasma LPA increased significantly in CHD patients and was positively related with coronary stenosis and serum hs-CRP and LDLC.

Abstract:Aim To explore the distribution of intracranial artery stenosis in patients with lacuna infarct and cerebral thrombosis. Methods Magnetic resonance angiograghy was used to assess intracranial artery stenosis in 222 patients with lacuna infarct and 228 cerebral thrombosis. Results 112 subjects with intracranial artery stenosis were found in 222 patients with lacuna infarct(50.45%),being composed of 38 subjects with simplex artery stenosis and 74 subjects with complex artery stenosis.The prevalence of intracranial artery stenosis in the patients aged 30 to 44 years,45 to 59 years and 60 years and over was 16.67%,21.43% and 60.12%,respectively.The incidence of intracranial artery stenosis in grade 1,grade 2 and grade 3 and above was 59.82%,30.36% and 9.82%,respectively.The 191 subjects with intracranial artery stenosis were found in 228 patients with cerebral thrombosis(83.77%),being composed of 83 subjects with simplex artery stenosis and 108 subjects with complex artery stenosis.The prevalence of intracranial artery stenosis in the patients aged 30 to 44 years,45 to 59 years and 60 years and over was 42.86%,80.77% and 86.39%,respectively.The incidence of intracranial artery stenosis in grade 1,grade 2 and grade 3 and above was 34.56%,41.36%,24.08%,respectively.The proportion of simplex artery stenosis in anterior circulution was high in the patients aged 30 to 44 years with lacuna infarct and cerebral thrombosis.In contrast,the complex artery stenosis and the posterior circulation artery stenosis was frequently encounted in the patients aged 60 years and over. Conclusion The prevalence of intracranial artery stenosis with cerebral thrombosis was higher than that of lacuna infarct.The intracranial artery stenosis in grade 1 was the most frequently encounted in the patients with lacuna infarct and the stenosis in grade 2 and above was frequently encounted in the patients with cerebral thrombosis.The complex artery stenosis increased with the ages significantly in the patients aged 60 years and over.

Abstract:Aim To study the detection of carotid artery intima plaque in elderly hospitalized patients with hypertension and its influencing factors. Methods A total of 328 elderly hypertensive patients were selected,and color Doppler ultrasound was used to detect all patients' carotid artery intima plaque and grading.Patients' sex,age,the course of hyperpiesia,the controls of high blood pressure in the past,the smoking history,family history of hypertension,history of stroke and other messages were noted by clinical records. Results The detection rate of carotid artery intima plaque was 77.4%,in which class 1,class 2 and 3 accounted for 32.0%,36.9% and 8.5%(plague score).Ordered Logistic regression univariate cumulative analysis showed that male,old,poorly controlled blood pressure,longer duration of hypertension were risk factors for plaque.Multivariate analysis showed that the major risk factors for plaque were male,old age and poor control of blood pressure. Conclusion Hypertension in the elderly patients with higher rate of carotid artery intima plaque,and male patients,old age,patients whose blood pressure was in poor control were the high-risk groups.

Abstract:Aim To evaluate the correlation among the level of peroxisome proliferator-activated receptors δ(PPARδ) expression in peripheral blood monocytes,serum levels of transforming growth factor-β1(TGF-β1) and interleukin-1β(IL-1β) in patients with acute coronary syndrome(ACS). Methods Peripheral blood monocytes were collected from 55 patients with ACS and 47 healthy controls.The PPARδ mRNA expression was detected by reverse transcription polymerase chain reaction(RT-PCR),while the serum level of TGF-β1 and IL-1β were measured by enzyme linked immunosorbent assay(ELISA). Results The PPARδ mRNA expression level(0.13±0.09)was markedly reduced in peripheral blood monocytes from patients with ACS compared with healthy controls(0.34±0.08,P><0.01).The serum IL-1β level(142.7±39.3 ng/L)was significant higher while the TGF-β1 level(11.4±4.6 μg/L) was obvious lower in patients with ACS than controls(81.5±23.9 ng/L,26.3±10.5 μg/L)(both P><0.01).Furthermore,the PPARδ mRNA expression level was negatively correlated to IL-1β level(r=-0.437,P><0.05) and positively related to TGF-β1 level(r=0.598,P><0.05). Conclusion The PPARδ might play a critical role in the pathogenesis of ACS.

Abstract:Aim To investigate the relation between the polymorphisms of angiotensinogen(AGT) genetpye M235T and angiotensin-converting enzyme(ACE) genetpye I/D and coronary atherosclerosis. Methods The study population was consisted of 151 patients with coronary heart disease(CHD),the healthy control group was consisted of 127 without CHD.Patients with CHD were compared with those persons in the healthy control group.AGT gene polymorphisms was tested with polymerase chain reaction and restriction fragment length polymorphism(PCR-RFLP) technology and ACE gene polymorphisms was tested with PCR. Results The ratio of AGT-TT and ACE-DD genetype in CHD group was separately 76.26% and 35.10%,which was significantly higher than the control group(44.10% and 14.96%).There was significant difference of the AGT-TT genetype between the CHD group and the control group P><0.01;so was ACE-DD genetype between the two group(P><0.01). Conclusion In the population of Chinese miao nationality,the gene polymorphisms of genetype AGT-TT and genetype ACE-DD are two risk factors of CHD morbidity and they are both independent of each other but also mutually coordinated.

Abstract:Aim To assess effect of different lipid levels on coronary lesion progression. Methods Patients were studied who successfully underwent PCI and were received coronary angiography again after three months to one year(average 7.4±2.2 months).95 patients had coronary lesion progression. 307 cases had no restenosis and lesion progression.Total cholesterol(TC),triglyceride(TG),high density lipoprotein cholesterol(HDLC) and low density lipoprotein-cholesterol(LDLC) were determined before perscutaneous coronary intervention(PCI) and re-angiography.Non high density lipoprotein-cholesterol(non-HDLC)=TC-HDLC. Results The levels of TC,LDLC and non-HDLC with follow-up angiography in lesion progression group were higher than those in control group(TC: 4.62±1.14 mmol/L vs 4.26±1.01 mmol/L,LDLC: 2.51±0.93 mmol/L vs 2.25±0.75 mmol/L,non-HDLC: 3.52±1.12 mmol/L vs 3.20±0.98 mmol/L,respectively,P><0.05).Logistic regression showed that the risk of lesion progression was markedly associated with concentrations of TC,LDLC and non-HDLC. Conclusion The levels of TC,LDLC and non-HDLC are the important risk factors for coronary lesion progression.Secondary prevention should be long-term emphasized and strengthened and non HDLC level should be controlled for patients with coronary artery disease.

Abstract:Visfatin is a novel pro-inflammatory adipokine which was predominantly produced and secreted in visceral fat,involved in regulating glucose and lipid metabolism,inflammation,and so on.In clinical study,serum visfatin was obviously elevated in patients with obesity,type 2 diabetes and metabolic syndrome,especially higher among patients with atherosclerosis.The results suggest that visfatin is closely correlated to macrovascular complications in diabetes mellitus.This paper will review the biological effects of visfatin and its influence on macrovascular complications in diabetes mellitus.

Abstract:Asymmetric dimethylarginine(ADMA) is an endogenous inhibitor of NO synthase(NOS) and can decrease the production of NO via inhibition of NOS competitively.ADMA is reported to be implicated in the pathophysiological processes of several diseases such as atherosclerosis,hypertension,chronic kidney disease,stroke,diabetes and cancer,and is regarded as a novel cardiovascular risk factor.Dimethylarginine dimethylaminohydrolases(DDAH) are enzymes responsible for inactivation of ADMA.A decrease in DDAH activity may lead to ADMA accumulation and thus promotes the development of ADMA-related diseases.Recent development in tissue distribution,biological function,regulation of DDAH,and implication of DDAH in human diseases are reviewed presently.