Abstract:Aim To understand the monocyte chemoattractantprotein-1 (MCP-1 ) expression by the cells in dietaryatherosclerotic lesions in rabbits. .Methods The male 4～6 week old Japanese 1p rab-bits were fed on cholesterol to develop a hyperlipidemiaand atherosclerosis model. The MCP-1 mRNA ex-pression in the plaques was examined by dot blot anal-ysis using a probe of P-end-labeled 35-mer oligonu-cleotide of MCP-1. Meanwhile, the MCP-1 in themedia conditioned by cultured SMCs from theatherosclerotic lesions was determined by using sand-wich ELISA. Immunohistochemically, the expres-sion of MCP-1 in various cells in the plaques was ex-amined using a rabbit anti-MCP-1 polyclonal antibody,and to recognize the cells in the plaques, several anti-bodies including factor Ⅶ　related antigen, a1-antit-rypsin and a-smooth muscle actin were used.Results Dot blot analysis showed that after hybridiza-tion of the RNA with the probe, the integral opticaldensity value (4. 1 5 ) of the autoradiographic pictures ofthe dots from the atherosclerotic lesions was 10. 7times the controls(0. 38). The MCP-1 content in themedia conditioned by cultured SMCs from theatherosclerotic lesions , asthe ELISA showed,was significantly higher than thatof the normal SMC conditioned media (7. 0±0. 7 g/L) and unconditioned medium (6.4 ±0. 7 g/L) (P<0. 01 ). Immunohistochemically, endothelial cells,macrophage derived foam cells and SMCs in theplaques were positively stained with anti-MCP-1 anti-body in varying degrees. Of the three cell types, themacrophage derived foam cells showed the strongestimmunostaining.Conclusion Under hyperlipidemic condition, theartery wall cells which participate in the developmentof atherosclerotic plaques were in full activity, andproduced and secreted MCP-1 in different degrees.The production of MCP-1 mainly by macrophages sug-gests that they play an important role in the recruit-ment of additional monocytes to the atheroscleroticplaques.

Abstract:Aim The effects of macrophage colony stimulatingfactor (0CSF) on the antioxidative capacity and foamcell formation of murine peritoneal macrophages wereobserved.Methods MCSF was in the conditional cultural liquidsof L929 cell line. Superoxide dismutase(SOD) activi-ty was detected by Pyroyallol method, and seleniumdependent glutathione peroxidase (SeGSHPx) activitywas detected by DTNB method, the survival numberof murine macrophages was detected by MTT method.Results MCSF could enhance SeGSHPx and SOD ac-tivities , moreover , it could prevent foam cell formationcaused by active oxygen and elevate the survival num-ber of murine macrophages.Conclusion The enhancement of antioxidase activitiesby MCSF may be one of the reasons that MCSF canprevents foam cell formation and retard the progressionof atherosclerosis.

Abstract:Aim To investigate the intracellular signalling relatedto the migration promoted by platelet-derived growthfactor (PDGF) .Methods Cultured smooth muscle cells(SMC) derivedfrom rats (A7r5) were used. Modified Byoden cham-ber technique was employed for migration accessment.Intracellular free calcium ion concentration was measured using Fure-2. Results PDGF-BB promoted migration of SMC andcaused an increase in of SMC, with peak re-sponse at concentration of PDGF 5 g/L. The migra-tion and increase in induced by PDGF weremarkedly inhibited by 1 00 mol/L BAPTA 1 97 ±30 vs 1 7.7± 6 nmol/L , P < 0.01 ) , a calciumchelator, and 50 mol/L genestein, a tyrosine kinaseinhibitor.Conclusion The increase in plasmic ionic calcium isone of early intracellular signalling after interaction ofPDGF and SMC. The migration of SMC induced byPDGF is either calcium dependent or tyrosine kinasedependent.

Abstract:Aim To investigate whether basic fibroblast growthfactor (bFGF) , epidermal growth factor (EGF) , tu-mor necrosis factor-a (TNF-a ), and granulocyte-macrophage colony stimulating factor (GM-CSF) haveeffect on the binding of scavenger receptor of vascularsmooth muscle cells(VSMC) and oxidized low densitylipoprotein (ox-LDL) .Methods Antibody against ox-LDL was prepared us-ing immunizing guinea pig with ox-LDL which wasmade by means of copper oxidization. Smooth musclecells were collected from the culture of calf aorta medi-a. The binding activity between scavenger receptorand ox-LDL was analyzed using cell BA-ELSA.Results The binding activity of scavenger receptorand ox-LDL was 4. 8 ±4. 0 g/L. The activity in-creased 3～3. 5 fold by adding bFGF , EGF , TNF-a (P<0. 05) ; Adding GM-CSF had no significant effect onthe binding.Conclusion bFGF, EGF, and TNF may play role inregulation of scavenger receptor activity of SMCs.

Abstract:Aim To investigate the effects and mechanism oframiprilat on c-myc expression induced by oxidized lowdensity lipoprotein (x-LDL) in vascular endothelialcells.Method After endothelial cells incubated with ox-LDL (250 mg/L) , ox-LDL+ramiprilat (20 mol/L) ,ox-LDL+ ramiprilat (40 mol/L) + N-Arg (1 00 mol/L ) , ox-LDL+N-Arg for 4 h in vitro. Reverse tran-scription PCR technique was employed to measure c-myc mRNA of cultured human umbilical vein endothe-lial cells (HUVEC). Nitric oxide (NO) and cGMPwere assayed by means of Griess reaction and radioim-munoassy respectively.Results in response to ox-LDL (250 mg/L) for 4 h,c-myc mRNA transcription of endothelial cells signifi-cantly increase (P<0. 05). In contrast , NO releaseand cGMP contents markedly decreased (P< 0. 05).Ramiprilat ( 20, 40 mol/L ) inhibited ox-LDL-in-duced c-myc expression and increased NO ,cGMP levelsof HUVEC. The effects of ramiprilat was partlyabolished by nitro-L-Arginine, a compeptitive in-hibitor of NO synthetase.Conclution Ramiprilat suppresses OLDL-induced c-myc overexpresion of endothelial cells by enhencingNO release.

Abstract:Aim The serum lipids and apolipoproteins betweenthe hyperlipidemic and healthy residents in Beijing andGuangzhou were studied in order to find out the clue ofhigher incidence of cardiovascular diseases in Beijingthan that in the Guangzhou area.Methods Serum samples of 336 males (168 hyper-lipidemic cases and 168 healthy controls ) from Beijingsurvey field and 388 male subjects ( 194 hyperlipidemicand 194 healthy controls) from Guangzhou field werecollected respectively for the assays of total cholestetol(TC ), triglycerides (TG ) , high density lipoproteincholesterol (HDLC ) , HDL3-C, low density lipoproteincholesterol (LDLC) (by enzyme methods ) , apolipopro-teins B, AI (by immunoturbidimetric assay) and A Ⅵ(by ELISA).Results Most of the hyperlipidemic cases were hy-pertriglyceridemia in both areas. TC, apolipoprotein A Ⅵ were higher, but HDLC, mainly HDL₂C weremarkedly lower in cases of the hyperlipidemic than thatof the healthy control groups. There was no differ-ence seen about the apolipoprotein AI level betweenthe hyperlipidemic and control groups , anyhow, on theother hand, the TC, apolipoprotein B, HDLC andapolipoprotein AⅠ of the hyperlipidemic subjects weresignificantly lower in Beijing than that in Guangzhou ,and similar results were obtained in the healthy controlgroups in both areas.Conclusion High triglycerides and low HDL levelpredominated in the serum lipids of the hyperlipidemicsubjects in both Beijing and Guangzhou areas. Theimportant point is that the serum HDL and apolipopro-tein AⅠ levels were significantly lower in the residentsof Beijing which may contribute to the higher incidenceof coronary heart disease in Beijing than in theGuangzhou area.

Abstract:Aim Antisense c-myc retrovirus vector was con-structed and was introduced into smooth muscle cell(SMC) by Lipofection. The effect of antisence c-mycRNA on c-myc mRNA and c-myc protein expression inSMC was investigated , exploring the new strategy forgene therapy for diseases of c-myc overexpression.Methods 1. 53 kb c-myc fragment including a partof the first intron, the second exon and first 8 bp ofthe second intron was placed under 5'LTR downstreamof in inverted orientation. Antisense c-myc retrovirus vector was introduced into PA317 packagingcells by Lipofection and selected by G418. SMC wereinfected with this recombinant retrovirus. Northernblot, and Western blot hybridizations were performedin SMC transfected by antisense c-myc retrovirus vec-tor to observe whether it was integrated into SMC ge-nomic DNA, whether antisense c-mycRNA expressedin SMC and whether the expression of antisense c-mycRNA reduced c-myc mRNA expressed in SMC andwhether the expression of antisense c-myc RNA re-duced c-myc mRNA and c-myc protein levels.Results Southern blot analysis confirmedthe inte-gration of the antisense c-myc retrovirus vector intoSMC genomic DNA. Northern blot analysis demon-strated the expression of antisense c-myc RNA and thelatter recuced the level of c-myc mRNA. Westernblot analysis showed antisense c-myc RNA inhibitedthe translation of c-myc protein, whereas sense c-mycRNA didn't have such effect.Conclusion Antisense c-myc RNA inhibited the ex-pression of c-myc mRNA and c-myc protein in a se-quence-specific manner. Antisense c-myc RNA is anefficient tool to inhibit the expression of c-myc gene ex-pression. This investigation provides a basis for fu-ture study using antisense c-myc RNA for gene therapyfor diseases of c-myc overexpression inducing malignanttumors and some cardiovascular diseases.

Abstract:Aim To investigate if platelet-derived growth fac-tor (PDGF-BB) is a chemoattr actant factor for mono-cytes adhesing vascular endothelium.Methods Pretreated with or without inflammatorymediators (tumor necrosis factor, 50 g/L;lipopolysaccharide 100 g/L) , the 51 Cr-labeled mono-cyte adhesion to endothelial cell (EC) monolayer wasassayed.Results PDGF-BB (1 , 10, 100 g/L) do not exerta direct influence on the monocyte adhesion to ECmonolayer, but it can potentiate the augmented effectof inflammatory mediators (tumor necrosis factor, 50g/L ; lipopolysaccharide , 100 g/L) on the monocyteadhesion.Conclusion PDGF-BB is by itself not a chemoat-tractant factor for MC, but can synergize the action ofsome monocyte active factors on monocyte adhesion tothe vascular endothelium.

Abstract:Aim To determine the effects of insulin on prolifer-ation of vascular smooth muscle cells (VSMC) and ac-tivity of tissue type plasminogen activator (tPA) andplasminogen activator inhibJtor (PAI) .Methods The cell proliferation was detected by H-thymidine (³ H-TdR) incorporation. The activity oftPA and PAI were determined by spectrophotometricassay.Results Insulin increased the activity of PAI andstimulated cell proliferation. There was no activity oftPA in procine VSMC.Conclusion Hyperinsulinemia could be one of theimportant factors in causing atherosclerosis.

Abstract:Aim To better understand the inhibition of growthand induction of apoptosis in smooth muscle cells(VSMC) by nitric oxide (NO) and the mechanism inthese processes.Methods Cultured rat VSMC at passage 5 to 8 wereused for experiment. After reaching 60 % ～70 % con-fluence, VSMCs were preincubated for 24 h (at least)with serum free Dubecco's modified Eagle's medium(DMEM ) to become quiescent before the experiments.Then SNAP (0. 4 mol/L) was added to the medium.The cells were fixed with 3% paraformaldehyde after 8h. Expression of Bcl-2, Bax, P53, and Fas in VSMCwere examined by fluorescein immunocytochemistrymethods through ACAS 570.Results Expression of Bcl-2 was decreased by NO.But expression of Bax , P53 , and Fas were increased byNO.Conclusion Bcl-2, Bax, P53, and Fas may take partin the effects of NO on inhibition of growth and induc-tion of apoptosis in VSMCs.

Abstract:Aim Using cultured porcine endothelial cells withsensitive quantitative methods, this study aims to in-vestigate the regulating effect of neuropeptide Y (NPY)and vasoactive intestinal peptide (VIP) on endothelialfunctions. The work should be optional for betterunderstanding the possible role of neurocrine factors inatherogenesis.Methods A specific and sensitive diazotization assayand radioimmunoreactive analysis were used respec-tively to measure the release of nitric oxide (NO) andendothelin (ET) from porcine aorta endothelial cellsgrown in culture.Results NPY and VIP could affect the release of NO and ET from cultured endothelial cells. Underthe influence of NPY, the content of NO2 and ET inendothelium-conditioned medium were increased with NPY concentration (P<0. 053 , but the increase of ETwas larger than NO in NPY group. In VIP group,the content of ET in endothelium-conditioned medium was decreased with VIP concentration (P<0. 05 ).Conclusion The first , NPY may stimulate culturedporcine aorta endothelial cells to release the NO and ET, but the increase of ET is more than NO. Thesecond, VIP may inhibit the secretion of ET from cul-tured endothelial cells.

Abstract:im To determine the effect of endothelin on highblood pressure and myocardiac hypertrophy.Methods We observed endothelin levels in plasma,and endothelin levels, gene expressions of endothelinand endothelin A receptor in left ventricle (LV) of 5,14, 26 week-old spontaneously hypertensive rats(SHR) and age-matched normotensive Wistar Kyoto(WKY) rats with radioimmunoassay and Northern blothybridization.Results Plasma endothelin levels were not significant-ly different between SHR and WKY rats. LV en-dothelin concentration, endothelin, endothelin A re-ceptor gene expressions increased only in 26 week-oldSHR.Conclusion Endothelin does not play an etiologic rolein myocardiac hypertrophy in SHR, but may play arole in the development of hypertension and the inifia-tion of its complications.

Abstract:im To compare the efficacy between injection As-tragali ,injection Salvia Militiorrhiza compound and in-jection Ahalysantinfarctasum and injection cerebrolysinin treating ischemic cerebrum vascular disorders(ICVD) .Methods 75 ICVD patients ,who were diagnosed byclinical data, were observated. 44 cases were treatedby Supplementing Qi and remove stasis with injectionAstragali and injection Salvia Miltiorrhiza compound.31 cases were treated by Anti-blood viscosity of in-jection Ahalysantinfarctasum and injection Cere-brolysin. The course of treatment of both the twogroups were 4 weeks.Results For the 44 cases group, the results were12 of recovery , 21 of effectual , 8 of active and 3 of in-effective. The total effective rate was 93. 2% . Forthe 31 cases group,the results were 10 of recovery, 10of effectual, 9 of active and 2 of ineffective. The to-tal effective rate was 93. 5% . Both the two groupshave a same effecicy (P>0. 05).Conclusion The efficacies of injection Astragali andInjection Salvia Miltiorrhiza compound are expendingblood vessel , accelerating blood flow, anoxia-resistingand protecting cerebrum.

Abstract:im The protective effects of human urinarykallidinogenase (SK-827 3 on myocardial ischemia/reperfusion (I/R) injury were investigated in the isolat-ed rabbit hearts.Methods Coronary effluent myoglubin (Mg) andlactate dehydrogenase (LDH ) content, myocardialmalondialdehyde (MDA ) andATP level were assayedby biochemical technique.Results in SK-827 group ,coronary flow increased ,cellular Mg and LDH leakage decreased, myocardialMDA content decreased and ATP content increased ascompared with I/R group.Conclusion SK-827 has an appliance in clinical my-ocardial I/R injury therapy.

Abstract:o investigate atherosclerosis in patients with border-line hypertension, 48 borderline hypertensive subjectswithout complications were compared with 38 healthycontrols. The results showed that the carotid thick-ness of tunica intima and media , and atherosclerotic in-dex in patients were significantly higher than that ofcontrols. The analysis of regression revealed thatcarotid atherosclerosis was closely associated with age ,body weight index, smoking, HDL cholesterol, totalcholesterol , oxidized LDL cholesterol and the status ofhypertension. This suggests that borderline hyper-tension could be a important risk factor for atheroscle-rosis and should be treated as early as possible.