Effect of corilagin on cholesterol metabolism in macrophages and its mechanism北大核心CSCD

Aim To elucidate the effect of corilagin (Cor) on cholesterol metabolism in macrophages and the underlying mechanism. Methods Molecular docking was applied to predict the protein target of Cor on cellular cholesterol metabolism. The RAW264.7 macrophage foam model induced by 80 mg • L-1 oxidized low density lipoprotein (ox-LDL) was established to evaluate the activity of Cor on lowering-cholesterol. The expression of genes and proteins related with cholesterol metabolism were detected by q-PCR and Western blotting,respectively. Then the activity of Cor on lipid metabolism was validated in ApoE mice fed with high-fat-diet. Results Cor and Class A Scavenger receptor (SRA), CD36, peroxisome proliferator-activated receptor γ (PPAR-γ), ATP binding cassette transporter Gl(ABCGl), which associated with cholesterol metabolism, could form hydrogen bonds and hydrophobic interactions. Cell experiments showed that Cor (60,120 and 240 μmol • L-1) significantly decreased TC content in macrophages, Cor could down-regulate SRA and CD36 gene expression, SRA protein expression, up-regulate the expression of ABCA1 and ABCG1 genes. Animal experiments demonstrated that Cor (15,30 and 60 mg • k g - 1 ) could decrease the serum TMAO content, the plaque area and formation of foam cells in the aortic root,the expression levels of CD36 and SRA fluorescent proteins in aortic root plaques. Conclusions Cor could inhibit the formation of macrophage foam cells through the regulation of cholesterol metabolism mediated by CD36,SRA, ABCA1 and ABCG1 to cure the AS. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

Oxidized LDL upregulated ATP binding cassette transporter-1 in THP-1 macrophages

INTRODUCTIONOxidized lipid signaling in macrophages is centralto the pathogenesis of atherosclerosis[1]. Exposure ofmacrophages and other vascular cells to oxidized low-density lipoprotein (ox-LDL) leads to complex changesin gene expression that are collectively thought to influ-ence the development of the atherosclerotic lesion[2].Using two-dimensional gel electrophoresis, the overallprotein map in U937 control cells and U937 foam cellswas obtained. Compared with U937 cells, 37 spots…     

肝X受体激动剂对RAW 264.7细胞ABCA1蛋白表达和TNF-α、IL-6产生和分泌的影响

目的:研究肝X受体激动剂3β-羟基-5α,6α-环氧胆烷酸甲酯和(MHEC)T-0901317对小鼠巨噬细胞株RAW264.7细胞三磷酸腺苷结合盒转运体A1(ABCA1)蛋白表达和TNF-α、IL-6产生和分泌的影响.方法:应用免疫细胞化学染色法检测RAW264.7细胞ABCA1蛋白表达的影响;应用夹心法ELISA检测细胞培养上清液中TNF-α和IL-6的浓度,分析肝X受体激动剂对氧化低密度脂蛋白(ox-LDL)诱导的巨噬细胞TNF-α、IL-6产生和分泌的影响.结果:3β-羟基-5α,6α-环氧胆烷酸甲酯和T-0901317均可显著促进RAW264.7细胞ABCA1蛋白的表达;与维甲酸X受体激动剂9-顺式视黄酸联合作用时,ABCA1蛋白表达增加更为显著.氧化低密度脂蛋白可促进RAW264.7细胞TNF-α、IL-6的产生和分泌,而这一促进作用可部分地被3β-羟基-5α,6α-环氧胆烷酸甲酯和T-0901317所抑制.结论:肝X受体激动剂MHEC和T-0901317均可上调RAW264.7细胞ABCA1蛋白表达,并可减少氧化低密度脂蛋白诱导的巨噬细胞中TNF-α、IL-6的产生和分泌.     

Effects of stilbenes on glucose and lipid metabolism in insulin resistant HepG2 cells北大核心CSCD

Aim To explore the effect of four stilbenes including rhaponticin, desoxyrhaponticin, rhapontigenin and resveratrol on glucose and lipid metabolism in insulin-resistant HepG2 cells induced by high glucose and high fat. Methods The model of insulin resistance was established by incubating HepG2 cells with a complex of glucose and oleic acid. MTT assay was used to detect cell viability. The intracellular triglyceride (TG) and glucose levels were measured by the kit method. The lipid production was observed by oil red O staining, and the cell morphology and uptake of 2-NBDG were observed by confocal microscope. The PPAR signaling pathway and PI3K/Akt insulin signaling pathway related proteins were determined by Western blot to evaluate the effect of stilbenes on glycolipid metabolism in IR-HepG2 cells. Results The complex containing 50 mmol • L-1 glucose and 0.5 mmol • L-1 oleic acid induced a successful insulin resistance model in HepG2 cells for 48 hours. Compared with the model group, all the four compounds could reduce the content of TG and lipid accumulation, and increase the ability of glucose uptake. These compounds could significantly inhibit the expression level of peroxisome proliferatorsactivated receptor (PPAR-) lipid metabolism-related proteins, and up-regulate the expression of phosphoinositide 3 -kinase (PI3 K) glycometabolism-related proteins, among which rhaponticin and resveratrol had the most significant effect. Conclusions The four stilbenes may alleviate insulin resistance in HepG2 cells by regulation of glucose and lipid metabolism disorder, especially rhaponticin and resveratrol. The mechanism may be related to the regulation of PPAR signaling pathway and the activation of PI3 K/AKT/mTORl pathway to reduce lipid production and promote glucose uptake. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

Baicalin prevents LPS-induced activation of TLR4/NF-κB p65 pathway and inflammation in mice via inhibiting the expression of CD14

Previous studies have shown that baicalin,an active ingredient of the Chinese traditional medicine Huangqin,attenuates LPS-induced inflammation by inhibiting the activation of TLR4/NF-κBp65 pathway,but how it affects this pathway is unknown.It has been shown that CD14 binds directly to LPS and plays an important role in sensitizing the cells to minute quantities of LPS via chaperoning LPS molecules to the TLR4/MD-2 signaling complex.In the present study we investigated the role of CD14 in the anti-inflammatory effects of baicalin in vitro and in vivo.Exposure to LPS(1μg/mL)induced inflammatory responses in RAW264.7 cells,evidenced by marked increases in the expression of MHC II molecules and the secretion of NO and IL-6,and by activation of MyD88/NF-κB p65 signaling pathway,as well as the expression of CD14 and TLR4.These changes were dose-dependently attenuated by pretreatment baicalin(12.5–50μM),but not by baicalin post-treatment.In RAW264.7 cells without LPS stimulation,baicalin dose-dependently inhibit the protein and mRNA expression of CD14,but not TLR4.In RAW264.7 cells with CD14 knockdown,baicalin pretreatment did not prevent inflammatory responses and activation of MyD88/NF-κB p65 pathway induced by high concentrations(1000μg/mL)of LPS.Furthermore,baicalin pretreatment also inhibited the expression of CD14 and activation of MyD88/NF-κB p65 pathway in LPS-induced hepatocyte-derived HepG2 cells and intestinal epithelial-derived HT-29 cells.In mice with intraperitoneal injection of LPS and in DSS-induced UC mice,oral administration of baicalin exerted protective effects by inhibition of CD14 expression and inflammation.Taken together,we demonstrate that baicalin pretreatment prevents LPS-induced inflammation in RAW264.7 cells in CD14-dependent manner.This study supports the therapeutic use of baicalin in preventing the progression of LPS-induced inflammatory diseases.     

P2X7 receptor inhibitor suppressed extracellular ATP/LPS-primed human hepatic stellate cells activation via downregulating NLRP3 inflammasome

OBJECTIVE To investigate the effect of P2X7receptor(P2X7r)inhibition,using a specific inhibitor(A438079)to prevent the development of liver fibrosis on human hepatic stellate cells,LX-2.METHODS The supernatant from lipopolysaccharide(LPS)-stimulated RAW264.7 mouse macrophages was supplemented to LX-2 cells for 24 h.LX-2cells were primed with LPS for 4h and subsequently stimulated for 30 min with 3mmol·L-1 of adenosine 5′-triphosphate(ATP).A438079(10μmol·L-1)was supplemented to LX-2 cells 10 min prior to ATP.RESULTS Directly treated with LPS on LX-2 cells,mRNA expressions of IL-1β,IL-18 and IL-6 were increased,as well as P2X7 r.And caspase-1,ASC and NLRP3 mRNA expressions were increased with LPS stimulation.LPS stimulation also increasedα-SMA and collagenⅠ mRNA expressions.Interestingly treatment of LX-2cells with mediums from LPS-primed RAW264.7mouse macrophages exhibited greater increase of mRNA expressions of above genes than those in LX-2directly treated with LPS.Pretreatment of directly or indirectly LPS-stimulated LX-2 cells with A438079 both suppressed IL-1βmRNA expression.In addition treatment of LPS-primed LX-2 cells with 3mmol·L-1 ATP induced the significant increase of IL-1β,IL-6,caspase-1,pannexin-1,α-SMA and collagenⅠ mRNA expression,the increasing ofα-SMA protein expression and cleavage of IL-1β.These events were significantly suppressed by pretreatment with P2X7 rantagonist A438079.P2X7 rblockade also significantly reduced the protein expression ofα-SMA.CONCLUSION Our results suggest that the involvement of the P2X7r-NLRP3 inflammasome pathway in the secretion of IL-1βfrom extracellular ATP/LPS-stimulated human hepatic stellate cells.This study demonstrated that repression of the P2X7 rrepresents a novel potential therapeutic approach to control liver fibrosis.     

The anti-tumor properties of two tumstatin peptide fragments in human gastric carcinoma

Aim： The aim was to study the anti-tumor activities and mechanisms of two synthetic peptide fragments of tumstatin （alpha3 （iV） NCl domain） in human gastric carcinoma cells in vitro and in vivo. Methods： MTr assay and cell cycle assay were used to study the anti-tumor and anti-angiogenic activities of two peptide fragments in vitro. Apoptosis induced by the two peptide fragments was demonstrated by TUNEL assay and morphological observation. The orthotopic tumor model was established to investigate the activities of two peptide fragments in vivo. Intratumor vascularization and the expressions of VEGF, bFGF, Fas, FasL, Bax, Bcl-2, and caspase 3 were determined using immunohistochemistry and Western blot analysis. Results： Peptide 19 inhibited SGC-7901 proliferation and induced apoptosis both in vitro and in vivo. Notably, peptide 21 suppressed the proliferation of HUVEC-12 cells in vitro. Each peptide arrested both cell lines at the G0/G1 phase of the cell cycle, and they also synergistically suppressed in vitro and in vivo tumor growth. Immunohistochemistry and Western blot analysis revealed the strong expression of Fas, FasL and caspase 3 in orthotopic tumor tissues treated with peptide 19 alone or in combination with peptide 21. Decreased expressions of VEGF and bFGF and decreased microvessel density （MVD） in orthotopic tumor tissues were seen in mice treated with peptide 21 alone or in combination with peptide 19. Conclusion： Two tumstatin peptide fragments facilitate two unique antitumor activities. Thus, they are drug candidates in the treatment of gastric carcinoma.     

Ginsenoside Rg1 attenuates palmitate-induced HMCs fibrosis by inhibiting NOX4/MAPK pathways北大核心CSCD

Aim To investigate the inhibitory effect of ginsenoside Rg1 on sodium palmitate induced fibrosis in human glomerullar mesangial cells (HMCs) and its mechanism. Methods (1) HMCs were treated with different concentrations of PA for 24 h, the intracellular lipid accumulation was observed by oil red staining, and the intracellular ROS production was detected by H2DCFDA kit; (2) HMCs were divided into control, PA (160 μmol·L -1), HG (25 mmol·L -1) and PA + HG groups, then the changes in cell morphology were detected by live cell imaging technique for 24 h; (3) HMCs were divided into control, PA (160 μmol ·L -1), PA + Rg1 (5 μmol·L -1), PA + Rg1 (10 μmol· L -1), PA + Apocynin (50 μmol · L -1) groups, the expression of Col4 was observed using immunofluorescence, and the mRNA expressions of Col4, TGF-β and FN were detected by Real-time PCR; Western blot was used to determine the expression of TGF-β, FN, NOX4 and MAPK related proteins. Results Different concentrations of PA exposure could dose-dependently increase intracellular lipid deposition and ROS generation in HMCs. Both PA and PA + HG groups could lead to abnormal changes in HMCs. Apocynin and ginsenoside Rg1 (5, 10 μmol·L -1) could inhibit PA-induced intracellular lipid accumulation, ROS increase, and Col4, TGF-β and FN mRNA over-expression, and significantly downregulated the expression of TGF-β, FN, NOX4 and MAPK related proteins. Conclusions Ginsenoside Rg1 could significantly inhibit PA-induced fibrosis in HMCs, and its mechanism may be related to reducing lipid deposition, inhibiting NOX4/MAPK pathways. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

反义寡脱氧核苷酸抑制U937泡沫细胞血管内皮生长因子的表达(英文)

AIM:To study the expression of vascular endothelial growth factor (VEGF) induced by oxidized low density liprotein (ox-LDL) and the inhibitory effects of antisense oligodeoxynucleotide (asODN) on the levels of VEGF protein and mRNA in the U937 foam cells. METHODS: U937 cells were incubated with ox-LDL 80 mg/L for 48h, then ,the foam cells were treated with asODN (0,5,10, and 20μmol/L). The VEGF concentration in the media was determined by ELISA. The VEGF protein expression level in cells was measured by immuohistochemistry; the positive ratio detected by a morphometrical analysis system was used as the amount of the VEGF expression level. The VEGF mRNA level was examined by Northern blotting. RESULTS: After U937 cells were incubated with ox-LDL, VEGF expression level increased greatly both in the cells and in the media. asODN markeldy inhibited the increase of VEGF. After treatment with asODN 20μmol/L, the VEGF protein concentration in the media decreased by 45.0%, the VEGF positive ratio detected by immuohistochemistry in cells decreased by 64.9%, and the VEGF mRNA level decreased by 47.1%. CONCLUSION: The expression of VEGF in U937 foam cells was strong. asODN inhibited VEGF expression significantly in U937 foam cells in vitro.     

抗多药耐药基因肽核酸与反义寡脱氧核苷酸增强K562／ADM细胞的敏感性和促进凋亡

AIM: To investigate the reversal effect and apoptosis enhancement of peptide nucleic acid (PNA) and antisenseoligodeoxyribonucleotide (ASODN) targeted to multidrug resistance gene (mdrl) on human multidrug resistantleukemia K562/ADM cells. METHODS: A 15-mer PNA and the same sequence of ASODN, complementary to the5' end of the AUG initiator codon-containing region of mdrl messenger RNA (MDR1-PNA, MDR1-ASODN), weredesigned and synthesized. Proliferation and sensitivity to adriamycin of K562/ADM cells treated with MDRI-PNAand MDR1-ASODN were analyzed with a MTT colorimetric assay. Apoptotic morphologies, P-glycoprotein (P-gp)expression, intracellular adriamycin accumulation, and cell cycle were measured. RESULTS: MDRI-PNA 1 to 10μmol/L and MDR1-ASODN 2 to 20 μmol/L alone had no inhibitory effects on the proliferation of K562/ADM cells,but significantly inhibited the growth of K562/ADM cells cultured in adriamycin-containing medium. After treatment with MDRI-PNA and MDRI-ASODN, intracellular adriamycin accumulation in K562/ADM cells increasedgreatly and P-gp synthesis was strikingly reduced. The resistance to adriamycin of the drug-resistant cells waspartly reversed and the cells were induced to apoptosis by adriamycin. The reversal efficacy of MDR1-PNA was3.1-fold higher than that of the same sequence of MDR-ASODN, but neither MDRI-PNA nor MDRI-ASODNcould completely block the mdrllP-gp expression. CONCLUSION: Sequence-special PNA targeted to mdr1 genemore effectively than the same sequence of MDR1-ASODN inhibited the expression of P-glycoprotein to overcomethe drug-resistance.     

RIP3 overexpression sensitizes human breast cancer cells to parthenolide in vitro via intracellular ROS accumulation

Aim： Receptor-interacting protein 3 （RIP3） is involved in tumor necrosis factor receptor signaling, and results in NF-KB-mediated prosurvival signaling and programmed cell death. The aim of this study was to determine whether overexpression of the RIP3 gene could sensitize human breast cancer cells to parthenolide in vitro. Methods： The expression of RIP3 mRNA in human breast cancer cell lines （MCF-7, MDA-MB-231, MDA-MB-435 and T47D） was detected using RT-PCR. Both MDA-MB-231 and MCF-7 cells were transfected with RIP3 expression or blank vectors via lentivirus. Cell viability was measured with MTT assay; intracellular ROS level and cell apoptosis were analyzed using flow cytometry. Results： RIP3 mRNA expression was not detected in the four human breast cancer cell lines tested. However, the transfection induced higher levels of RIP3 protein in MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of RIP3 decreased the IC50 values of parthenolide from 17.6 to 12.6 μmol/L in MCF-7 cells, and from 16.6 to 9.9 μmol/L in MDA-MB-231 cells. Moreover, overexpression of RIP3 significantly increased parthenolide-induced apoptosis and ROS accumulation in MCF-7 and MDA-MB-231 cells. Pretreatment with N-acetyl-cysteine abrogated the increased sensitivity of RIP3-transfected MCF-7 and MDA-MB-231 cells to parthenolide. Conclusion： Overexpression of RIP3 sensitizes MCF-7 and MDA-MB-231 breast cancer cells to parthenolide in vitro via intracellular ROS accumulation.     

The expression of efflux and uptake transporters are regulated by statins in Caco-2 and HepG2 cells

Aim： Statin disposition and response are greatly determined by the activities of drug metabolizing enzymes and efflux/uptake transporters. There is little information on the regulation of these proteins in human cells after statin therapy. In this study, the effects of atorvastatin and simvastatin on mRNA expression of efflux （ABCB1, ABCG2 and ABCC2） and uptake （SLCO1B1, SLCO2B1 and SLC22A1） drug transporters in Caco-2 and HepG2 cells were investigated.
Methods： Quantitative real-time PCR was used to measure mRNA levels after exposure of HepG2 and Caco-2 cells to statins. Results： Differences in mRNA basal levels of the transporters were as follows： ABCC2〉ABCG2〉ABCB1〉SLCO1B1〉〉〉SLC22A1〉SLCO2B1 for HepG2 ceils, and SLCO2B1〉〉ABCC2〉ABCB1〉ABCG2〉〉〉SLC22A1 for Caco-2 cells. While for HepG2 cells, ABCC2, ABOG2 and SLCO2B1 mRNA levels were significantly up-regulated at 1, 10 and 20 pmol/L after 12 or 24 h treatment, in Caco-2 cells, only the efflux transporter ABCB1 was significantly down-regulated by two-fold following a 12 h treatment with atorvastatin. Interestingly, whereas treatment with simvastatin had no effect on mRNA levels of the transporters in HepG2 cells, in Caco-2 cells the statin significantly down-regulated ABCB1, ABCC2, SLC22A1, and SLCO2B1 mRNA levels after 12 or 24 h treatment.
Conclusion： These findings reveal that statins exhibits differential effects on mRNA expression of drug transporters, and this effect depends on the cell type. Furthermore, alterations in the expression levels of drug transporters in the liver and/or intestine may con- tribute to the variability in oral disposition of statins.     

Compound FLZ inhibits lipopolysaccharide-induced inflammatory effects via down-regulation of the TAK-IKK and TAK-JNK/ p38MAPK pathways in RAW264.7 macrophages

Aim： The aim of this study was to investigate the effect of the squamosamide derivative FLZ （N-2-（4-hydroxy-phenyl）-ethyl-2-（Z,5-dimethoxy-phenyl）-3-（3-methoxy-4-hydroxy-phenyl）-acrylamide） on lipopolysaccharide （LPS）-induced inflam-matory mediator production and the underlying mechanism in RAW264.7 macrophages. Methods： RAW264.7 cells were preincubated with non-toxic concentrations of compound FLZ （1, 5, and 10 μmol/L） for 30 min and then stimulated with 10 μg/L LPS. The production of nitric oxide （NO）, the expression of inducible nitric oxide synthase （iNOS） and cyclooxygenase 2 （COX-2）, and the activation of nuclear factor kappa-B （NF-KB） and mitogen-activated protein kinase （MAPK） pathways were examined. Results： FLZ significantly inhibited the LPS-induced production of NO, as well as the expression of iNOS and COX-2 at both the RNA and the protein levels in RAW264.7 cells. The LPS-induced increase in the DNA binding activity of NF-KB and activator protein i （AP-1）, the nuclear translocation of NF-κB p65, the degradation of the inhibitory κBα protein （IκBα） and the phosphorylation of IκBα, IκB kinase （IKK） α/β, c-Jun NH2-terminal kinase （JNK） and p38 MAPKs were all suppressed by FLZ. However, the phosphorylation of extracellular signal-regulated kinase （ERK） was not affected. Further study revealed that FLZ inhibited the phosphorylation of transforming growth factor-β （TGF-β）-activated kinase 1（TAK1）, which is an upstream signaling molecule required for IKKα/β, JNK and p38 activation. Conclusion： FLZ inhibited the LPS-induced production of inflammatory mediators at least partly through the downregulation of the TAK-IKK and TAK-JNK/p38MAPK pathways.     

Characterization of cAMP accumulation mediated by three α1—adrenoceptor subtypes in HEK293 cells

AIM:To investigate the characterization of cAMP response mediated by α1-adrenoceptor (α1-AR) subtypes in HEK293 cells. METHODS:(1) Full-length cDNA encoding three α1-AR subtypes were transfected into HEK293 cells by the calcium phosphate precipitation method, respectively. (2) The densities of α1-AR subtypes expressed in HEK293 cells were measured by radioligand binding assay. (3)cAMP accumulation was measured by [^3H] adenine prelabeling method. RESULTS: (1)Activation of each of three subtypes resulted in an increase of cAMP accumulation in HEK293 cells in a dose-dependent manner, which was inhibited by selective α1-AR antagonist prazosin. (2) Comparing the pharmacological property, the maximal responses of α1A-AR to agonists were the most potent, while the sensitivity of α1-AR subtypes to norepinephrine(NE) was the highest. CONCLUSION: Each of three α1-AR subtypes can mediate cAMP accumulation in HEK293 cell line, and there are differences in pharmacological property.     

Oridonin induces NPM mutant protein translocation and apoptosis in NPM1c＋ acute myeloid leukemia cells in vitro

Aim： Skewed cytoplasmic accumulation of NPM mutant protein （NPM1c＋） is close related to leukemia pathogenesis. The aim of this study was to investigate whether oridonin, a diterpenoid isolated from the Chinese traditional medicine Rabdosia rubescens, was able to interfere with NPM1c＋ protein trafficking and induce apoptosis in NPM1c＋ acute myeloid leukemia cells in vitro.
Methods： OCI-AML3 cell line harboring a NPM1 gene mutation was examined. Cell growth was detected by MTT assay. Cell apoptosis was evaluated using flow cytometry and Hoechst 33258 staining. The expression and subcellular localization of relevant proteins were detected by Western blot and immunofluorescent staining. The mRNA expression was detected by RT-PCR.
Results： Oridonin （2–12 μmol/L） dose-dependently inhibited the viability of OCI-AML3 cells （the IC50 value was 3.27±0.23 μmol/L at 24 h）. Moreover, oridonin induced OCI-AML3 cell apoptosis accompanied by activation of caspase-3 and nuclear translocation of NPM1c＋ protein. Oridonin did not change the expression of Crm1 （the export receptor for nuclear export signal-containing proteins）, but induced nuclear translocation of Crm1. Oridonin markedly increased the expression of nucleoporin98 （Nup98）, which had an important role in Crm1-mediated nuclear protein export, and induced nuclear accumulation of Nup98. Furthermore, oridonin markedly increased the expression of p14arf and p53.
Conclusion： In NPM1c＋ leukemia cells, oridonin induces NPM1c＋ protein translocation into the nucleus possibly via nuclear accumulation of Crm1; the compound markedly increases p53 and p14arf expression, which may contribute to cell apoptosis.     

Dehydroepiandrosterone anti-atherogenesis effect is not via its conversion to estrogen

Aim： This study was conducted to demonstrate the anti-atherosclerotic effect of dehydroepiandrosterone （DHEA） and to investigate its possible mechanisms and whether this effect is related to its conversion to estrogen.
Methods： Forty male New Zealand White rabbits aged 3 months were divided into 5 groups （n=8 per group） and fed different diets for 10 weeks. Serum lipid levels, the area of atherosclerotic lesions and the mRNA levels of monocyte chemoattractant protein-1 （MCP-1） and vascular cell adhesion molecule-1 （VCAM-1） in aortic lesions were measured. Then cultured vascular smooth muscle cells （VSMCs） stimulated by oxidized low density lipoprotein-cholesterol （ox-LDL） were treated by DHEA. The gene and protein expression levels of MCP-1 and VCAM-1 in VSMCs was detected. The plasmid with or without the gene of cytochrome P450 aromatase （CYP19） was transient transfected into cultured VSMCs respectively. Twenty hours later, the cells were stimulated with ox-LDL and DHEA. Results： DHEA could obviously decrease the area of atherosclerotic lesions and the expressions of MCP-1 and VCAM-1 in aortic lesions. But all-trans retinoic acid （atRA） which was reported would limit restenosis after balloon angioplasty had no visible synergistic effect with DHEA. DHEA could also reduce ox-LDL-induced MCP-1 and VCAM-1 expression in untransfected or transfected VSMCs. Conclusion： The anti-atherosclerotic effect of DHEA had nothing to do with the catalysis of cytochrome P450 aromatase （CYP19）, or was not related to its conversion to estrogen.