Effects of the Bushen Ningxin Chinese herb-containing serum on the adherence of human monocytes to endothelial cells

AIM: To study effect of the Bushen Ningxin decoction, a Chinese medicine, on the adherence of monocytes to endothelial cells and its mechanism. METHODS: Using cultured human umbilical vein endothelial cells (HUVECs) as target cells, oxidized low density lipoprotein (ox-LDL) was added to the endothelial cell culture to prepare the model of human endothelial cell injury. The serum of rabbits having been treated with Bushen Ningxin decoction was added to trial architecture, the adherence of monocyte-like cell line U937 to HUVECs was analyzed using Rose Bengal staining. In addition, the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1(VCAM-1) and E-selectin in HUVECs was measured by flow cytometry. RESULTS: Treatment of HUVEC with ox-LDL (100 mg/L) for 24 hours significantly increased adhesion of U937 to HUVECs. If serum of the animal treated with Bushen Ningxin decoction was added to trial architecture, the adhesion decreased significantly. The flow cytometry analysis showed that ox-LDL could induce the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs. Serum of the animal treated with Bushen Ningxin decoction significantly decreased the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs. CONCLUSION: The Bushen Ningxin Chinese herb-containing serum has an inhibitory effect on the adherence of monocytes to endothelial cells, probably by way of down-regulating the expression of ICAM-1, VCAM-1 and E -selectin in endothelial cells.     

he effects of constant magnetic field on apoptosis,adhesion molecule expression in endothelial cells and their adhesion rates with monocytes

AIM: To investigate the effects of constant magnetic field on apoptosis, secretion and expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVEC), and their adhesion rates with THP-1 monocytes induced by angiotensin Ⅱ (AngⅡ).METHODS: The third passage of cultured HUVEC was used.There were six groups: control group, Ang Ⅱ (10^-6 mol/L) group, Ang Ⅱ with 1, 5, 10 or 20 gausses of constant magnetic field group.Samples were collected 24 h after incubation with or without magnetic field.Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and propidinm iodide staining with flow cytometry.Secretion and expression of ICAM-1 and VCAM-1 were detected by ELISA and immunocytochemistry, respectively.Adhesion rate between HUVEC and THP-1 was measured by counting method.RESULTS: Ang Ⅱ at concentration of 10^-6mol/L induced apoptosis in HUVECs (P<0.05 vs control), whereas in 1, 5, 10 and 20 gausses group, apoptosis of HUVECs was significantly lower than that in Ang Ⅱ group (P<0.05).Ang Ⅱ at concentration of 10-6 mol/L significantly increased secretion and expression of ICAM-1 and VCAM-1 (P<0.05 vs control), whereas secretion and expression of ICAM-1 and VCAM-1 in 1, 5, 10 and 20 gausses group significantly decreased, compared with Ang Ⅱ group (P<0.05).The adhesion rates between HUVEC and THP-1 significantly increased 24 h after incubation of HUVEC with Ang Ⅱ (P<0.05 vs control), in contrast, the adhesion rates between HUVEC and THP-1 in 1, 5, 10 and 20 gausses group significantly decreased, compaed with Ang Ⅱ group (P<0.05).CONCLUSIONS: One gauss to 20 gausses of constant magnetic field antagonizes the effects of Ang Ⅱ on HUVEC, decreases apoptosis and expression of ICAM-1 and VCAM-1 in HUVEC, and also decreases the adhesion rates between HUVEC and monocytes induced by Ang Ⅱ.     

Effect of water extract propolis on expression of vascular endothelial cell adhesion molecules

AIM: To explore the mechanism of propolis on the inhibition of atherosclerosis and thrombosis in injured human umbilical vascular endothelial cells (HUVECs) induced by tumor necrosis factor alpha (TNF-α)in vitro.METHODS: TNF-α at the concentration of 50 μg/L was used to induce the injury of HUVECs. The injured HUVECs were treated with water extract propolis (WEP) at the concentrations of 50, 100 and 200 mg/L for 6 h, 12 h and 24 h. The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was examined by flow cytometry.RESULTS: The expression of ICAM-1 and VCAM-1 was significantly higher in injured HUVECs (P<0.01) than that in the control cells. The expression of ICAM-1 and VCAM-1 was downregulated by WEP treatment in a dose-dependent manner. Between the groups of 100 and 200 mg/L WEP, the difference was significant. In the injured HUVECs treated with 50 mg/L WEP, the inhibitory effect on the expression of ICAM-1 and VCAM-1 was presented in a time-dependent manner. Compared to the single administration, the use of WEP combined with fluvastatin showed better inhibitory effect on the expression of ICAM-1 and VCAM-1 in the injured HUVECs induced by TNF-α (P<0.01).CONCLUSION: WEP may be helpful for the protection of vascular endothelial cells by inhibiting the expression of ICAM-1 and VCAM-1 in a time-and dose-dependent manner. The protective effect of WEP on endothelial cells may be synergic with the inhibitor of HMG-CoA reductase such as fluvastatin sodium.     

Effect of N,N-dimethylsphingosine on the expression of adhesion molecules in human umbilical vein endothelial cell line EA.hy926

AIM: To investigate whether and how N, N-dimethylsphingosine (DMS) plays a role in modulating the adhesion of monocytes to vascular endothelial cells, and identify whether human umbilical vein endothelial cell line EA.hy926 take place of the vascular endothelial cells.METHODS: Adhesion ratio was measured by flow cytometry, and immunohistochemistry was used to detect the expression of ICAM-1 and P-selectin in HUVEC: EA.hy926 cells after the effect of DMS. RESULTS: DMS inhibited the adhesion of monocytes to HUVEC: EA.hy926 cells in a time-dependent and concentration-dependent manner by reducing the expression of ICAM-1 and P-selectin. CONCLUSIONS: DMS reduced adhesion molecule expression in vascular endothelial cells. DMS may be an important contributor to reduce adhesion ratio, suggesting that DMS plays a negative role in proinflammatory and immune functions of the modified vascular endothelial cells during atherosclerosis and restenosis.     

Effects of Astragalus polysacharin on fibroblast proliferation and adhesion between HUVECs and white cells

AIM: To investigate the effects of Astragalus polysacharin(APS) on human fibroblast and human umbilical vein endothelia cell (HUVEC) proliferation, as well as its acts on adhesion between white cells and HUVECs. METHODS: Human fibroblasts from distal and proximal skin away the ulcer were cultured as normal fibroblasts(NF) and wounded fibroblasts(WF). MTT assay was used for detecting cell proliferation, Rose Bengal staining and fluorescence immunohistology assay were used for examining the adhesion of human polymorpho-nuclear cell(PMN) and TPH-1 to HUVECs. RESULTS: 2.44-156 mg/L APS promoted WF proliferation, and 2.44-39 mg/L APS also promoted NF proliferation, but it did not show any proliferating effect on HUVECs. APS inhibited the adhesion of PMN or TPH-1 to HUVECs induced by tumor necrosis factor(TNF). At 25-100 mg/L, it also inhibited both VCAM-1 and ICAM-1 expression in HUVECs induced by TNF. Treatment with APS for 12 h also inhibited CD44 expression in HUVECs. CONCLUSION: APS shows mitogenic activity on both human normal and wounded fibroblasts. It also exerts anti-inflammation effects by inhibiting adhesion molecule expression and adhesion of white cells to HUVECs.     

Inhibiting role of polydatin to expression of intercellular adhesion molecule-1 induced by lipopolysaccharide on vascular endothelial cells

AIM and METHODS:To investigate expression of intercellular adhesion molecule-1(ICAM-1) on human umbilical vein endothelial cells (HUVEC) induced by lipopolysaccharide (LPS) , and inhibiting role of polydatin by cellular immune fluorescent staining and laser confocal microscope scanning technology. RESULTS: Compared with basic expression of ICAM-1 on HUVEC, the ICAM-1 expression was enhanced significantly after stimulated by LPS from 8 h to 36 h, dose-dependent relation appeared between expression of ICAM-1 and LPS. ICAM-1 expression on endothelial cells treated only by polydatin had no abvious change,but inducing role of LPS to expression of ICAM-1 was inhibited significantly by polydatin pretreating endothelial cells. CONCLUSION:The expression of ICAM-1 on endothelial cells can be promoted by LPS , and polydatin can inhibit LPS-induced ICAM-1 expression.     

Effect of lipid peroxidation on expression of vascular cell adhesion molecule-1 in cultured human endothelial cells

AIM:To observe the expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human umbilical vein endothelial cells (HUVEC) by lipid peroxidation injury induced by exposure to diamide.METHODS:Expression of VCAM-1 mRNA and protein in HUVEC was determined by in situ hybridization and a cell enzyme-linked immunosorbent essay (cell ELISA), respectively.RESULTS:The HPIAS-1000 image analytic system in situ hybridization detected that the mean absorbance values in experiment groups(1, 5 and 10 μmol/L diamide for 8 hours) were 0.147±0.013, 0.292±0.020 and 0.396±0.022, which were 1.91-fold, 3.79-fold and 5.14-fold as much as that of the control group (0.077±0.011), respectively. There was significant statistical difference between groups (P＜0.01). The cell ELISA showed that the mean absorbance values of VCAM-1 proteins in experiment groups were 0.158±0.008, 0.220±0.017 and 0.321±0.023, which were 1.53-fold, 2.12-fold and 3.09-fold as much as that of the control group (0.104±0.016), respectively. The analysis of variance proved the significant difference between groups (P<0.01).CONCLUSION:The results suggest that the increased expression of VCAM-1 is integral in promoting adhesion of monocytes to the vascular endothelium.     

Advanced glycation end products-modified protein up-regulates expression of adhesion molecules in human umbilical vein endothelial cells

AIM: Advanced glycation end products (AGEs)-modified proteins are found in plasma and atherosclerosis lesion of diabetes mellitus patients. The study was conducted to elucidate the effect of AGE on expression of adhesion molecules in human endothelial cells. METHODS: Human endothelial cells derived from umbilical veins (HUVECs) were coincubated in vitro with native human serum albumin (HSA) or HSA modified with advanced glycation end products (AGE-HSA). The expression of adhesion molecule intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined by immunofluorescent staining and flow cytometry analysis. RESULTS: ICAM-1 and VCAM-1 were constitutively expressed on HUVECs. AGE-HAS enhanced the expression of ICAM-1 and VCAM-1 on HUVECs in a time- and dose-dependent manner. HSA had no effect on the expression of adhesion molecules. CONCLUSIONS: AGE-HSA up-regulates the expression of adhesion molecules in human endothelial cells. AGEs may therefore promote the infiltration of monocytes in the vascular endothelium and have an important effect in the generation and progress of atherosclerosis.     

Effects of berberine on IL-1 or tumour necrosis factor induced polymorphonuclear leucocyte－endothelium adhesion

AIM:To investigate the effect of berberine on IL-1 or tumour necrosis factor (TNF) induced polymorphonuclear leucocyte(PMN)-endothelium adhesion and adhesion molecules.METHODS:Based on the model of human umbilical vein endothelial cell (HUVEC), this study adopted Rose Bengal Stain, cell ELISA, immunocyto-chemical techniques to investigate the effect of berberine on PMN-endothelium adhesion and the expression of cell adhesion molecules (CAMs).RESULTS:Berberine inhibited IL-1, TNF-induced HUVEC adhesion for PMN when pretreated HUVEC and antagonised IL-1, TNF-induced upregulation of ICAM-1 on HUVEC. Meanwhile, TNF-stimulated PMN adhesion for HUVEC and CD18 upexpression on PMN was diminished in the presence of berberine.CONCLUSION: Inhibite PMN-endothelium adhesion by downregulating the CAMs expression to inhibite PMN migration across endothelium is one of the mechanisms of antiinflammation of berberine.     

Effects of nicotine on activation of PMNs and the ICAM-1 mRNA expression of HUVEC

AIM: To investigate the effects of nicotine on activation of PMNs, adhesion of PMNs-HUVEC and expression of ICAM-1 mRNA in HUVEC. METHODS: Activation of PMNs was measured by detecting the activity of β-glucuronidase and lysozym of PMNs. Adhesion of PMNs and HUVEC was observed. Northern blot was conducted for quantitating ICAM-1 mRNA. RESULTS: Nicotine could increase the activity of β-g [(8.76± 1.01)μg/10⁷·h vs(14.87±2.00)μg/10⁷·h,P<0.05]and Lysozym [(20.0±1.5)μg/10⁷·h vs(36.5±4.4)μg/10⁷·h,P<0.05], and also could promote adhesion of PMNs-HUVEC(38.5±9.8 vs 61.0±4.4,P＜0.05). The expression of ICAM-1 mRNA was induced by nicotine in dose-dependent fashion (10^-5-10^-3mol/L).After a 2 h treatment of HUVEC with nicontine(10^-4mol/L), the level of ICAM-1 mRNA is above the control(1.23 vs 1.63) and the highest level (2.03) is at a 12 h treatment. 764-3 can obviously counteract the above effect of nicotine. CONCLUSIONS: Nicotine could activate PMNs, enhance adhesion of PMNs-HUVEC and increase the expression of ICAM-1 mRNA in HUVEC.     

Protective effect of anti-aging Klotho protein on human umbilical vein endothelial cells treated with high glucose

AIM: To study the protective effect of anti-aging Klotho protein on human umbilical vein endothelial cells (HUVECs) treated with high glucose (HG).METHODS: HUVECs were cultured in vitro, and divided into PBS control group, 5.5 mmol/L glucose group, 33.3 mmol/L glucose group, 0.1 μmol/L Klotho+33.3 mmol/L glucose group, 1 μmol/L Klotho+33.3 mmol/L glucose group, and 10 μmol/L Klotho+33.3 mmol/L glucose group. The viability of the HUVECs was measured by MTT assay. The content of malondialdehyde (MDA), and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione (GSH) in cell culture supernatants were observed. The production of reactive oxygen species (ROS) in HUVECs was analyzed by flow cytometry. The levels of nitric oxide (NO), endothelin (ET-1), intercellular adhesion molecule-1 (ICAM-1) in HUVEC culture medium were detected by ELISA. The protein expression of nuclear factor-kappa B (NF-κB) in the HUVECs was determined by Western blot. RESULTS: Compared with PBS control group, 33.3 mmol/L glucose significantly decreased the HUVEC viability, increased ROS, LDH and MDA levels, reduced the activities of SOD and GSH, decreased the NO secretion, and induced the ET-1 and ICAM-1 secretion and the protein expression of NF-κB in HUVECs. When HUVECs were treated with Klotho protein at different concentrations combined with 33.3 mmol/L glucose, the cell viability was increased significantly, the ROS, LDH and MDA levels were decreased significantly, the antioxidant SOD and GSH activities were significantly increased, the secretion of NO was increased, but ET-1 and ICAM-1 releases and protein expression of NF-κB were significantly reduced.CONCLUSION: Anti-aging Klotho protein promotes the viability of HUVECs treated with HG, reduces the oxidative damage and ROS production, and restores the normal secretory function of HUVECs, thus playing a protective role in vascular endothelial cells through reducing the protein expression of NF-κB.     

Effects of xijiao dihuang decoction on the expression of adhesion molecules in vascular endothelial cells of adrenine and hypothermia-treated rats

AIM: To study the effects of xijiao dihuang decoction, a Chinese medicine, on the expression of adhesion molecules in vascular endothelial cells (VECs) of adrenine and hypothermia-treated rats. METHODS: The expression of VCAM-1, ICAM-1, PECAM-1, iNOS and their corresponding mRNA in VECs was assayed by immunohistochemistry analysis and RT-PCR, respectively. RESULTS: Immunohistochemistry analysis showed the expression of VCAM-1, ICAM-1, PECAM-1 and iNOS are higher in adrenine and hypothermia-treated rats than that in controls, xijiao dihuang decoction decreased the expression of VCAM-1, ICAM-1, PECAM-1 and iNOS in a dose-dependent manner in adrenine and hypothermia-treated rats. CONCLUSION: Xijiao dihuang decoction can down-regulate the expression of adhesion molecules in vascular endothelial cells of adrenine and hypothermia-treated rats.     

p38 MAPK/ATF-2 pathway is involved in C-relative protein-induced endothelial cell activation

AIM: To investigate the role of p38 MAPK/ATF-2 pathway in C-relative protein (CRP)-induced endothelial cell activation. METHODS: Human coronary artery endothelial cells (HCAEC) were cultured and were used between passages 3 and 7. CRP served as a stimulus for endothelial cell activation. Western blotting was performed to determine the expression and phosphorylation of eNOS, p38 and ATF2. ELISA was carried out to detect the levels of ICAM-1, VCAM-1 and MCP-1 released from HCAEC. Pharmacological p38 inhibitors SB203580 and SB202190 were used to determine the effect of p38/ATF-2 pathway. RESULTS: CRP reduced the p-eNOS level in a concentration-dependent manner and induced the release of ICAM-1, VCAM-1 and MCP-1. The p38/ATF-2 pathway was activated by CRP treatment. SB203580 and SB202190 partially rescued p-eNOS level and suppressed the secretion of ICAM-1, VCAM-1 and MCP-1. CONCLUSION: p38MAPK/ATF-2 pathway participates in CRP-induced endothelial activation.     

Effects of Xijiao Dihuang and Yinqiao San decoction on ICAM-1 and VCAM-1 expression in mouse lung tissues and rat pulmonary microvascular endothelial cells infected with influenza virus

AIM：To investigate the effects of Xijiao Dihuang and Yinqiao San decoction (XDY) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in mouse lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) infected with influenza virus, and to explore its mechanism for treatment of viral pneumonia. METHODS：Fifty-four male BALB/c mice were randomly divided into normal group, model group and XDY group (n=18 in each group). The viral pneumonia model was established by intranasally dripping influenza A (H1N1) virus into the mice. The mice in XDY group were treated with XDY 1 h after dripping the virus. The expression of ICAM-1 and VCAM-1 in lung tissues was examined by immunohistochemical staining 2, 4 and 6 d after infection. On the other hand, RPMVECs were obtained from male Wistar rats and primarily cultured. The cells were randomly divided into control group, virus group, virus+XDY group, tumor necrosis factor α (TNF-α) group and TNF-α+XDY group. The mRNA and protein expression of ICAM-1 and VCAM-1 was evaluated by real-time PCR and flow cytometry 24 h after infection. RESULTS：Virus exposure increased ICAM-1 and VCAM-1 expression in mouse lung tissues (P<0.01), and XDY treatment attenuated this effect (P<0.01). Virus and TNF-α both led to the increases in mRNA and protein expression of ICAM-1 and VCAM-1 in RPMVECs (P<0.01), which were also reduced by treatment with XDY (P<0.01). CONCLUSION：Treatment with XDY decreases virus-induced ICAM-1 and VCAM-1 expression, suggesting an important role of XDY in treatment of viral pneumonia.     

Influence of different flow pattern on VCAM-1, NF-κB expression in vascular endothelial cells

AIM:The objective of this study was to examine the influence of different flow pattern, particularly low shear stress flow regimens, on VCAM-1 and NF-κB in vascular endothelial cells. METHODS:HUVEC covered sheets were placed within rectangular parallel plate flow chambers. Cells were subjected to 4, 18 h of either laminar or oscillatory shear stress. The expression of VCAM-1 and NF-κB activity were analyzed by immunohistochemistry. VCAM-1 mRNA was also detected using in situ hybridization. RESULTS:VCAM-1 mRNA and VCAM-1 expression were not upregulated by laminar shear stress. However, oscillatory shear stress significantly upregulated VCAM-1 mRNA and VCAM-1 expression. Translocation of NF-κB P65 was remarkably increased.CONCLUSION:In same low shear stress, the different expression of VCAM-1 mRNA and VCAM-1 were induced by HUVEC exposed to laminar or oscillatory flow patterns.     

Inhibition of ICAM-1 expression on endothelial cells in hypoxia/reoxygenation by antisense oligodeoxynucleotides

AIM: To investigate the effect of antisense oligodeoxynucleotides (AS-ODN) on the intercellsular adhesion molecule-1(ICAM-1) expression on endothelial cells in hypoxia/reoxygenation(H/R). METHODS: With cultured glomerular vascular endothelial cell in H/R, the positive percentage of ICAM-1 expression was measured by flow cytometry before and after giving AS-ODN. RESULTS: The ICAM-1 expression did not increase on glomerular vascular endothelial cell in 10 hours hypoxia compared to control group, it increased in 6 hours reoxygenation, and decreased by 40.6% after giving AS-OND. CONCLUSION: AS-ODN may decrease the expression of ICAM-1 on endothelial cells in H/R.     

Influences of bypass-activated complement and TNF-α on endothelial cells to express ICAM-1 and PMN-EC adhesion

AIM:To investigate the influences of bypass-activated complement and TNF-α on intercellular adhesion molecule 1(ICAM-1) expression in endothelial cells, and polymorphonuclear neutrophil-endothelial cell (PMN-EC) adhesion.METHODS:In vitro, zymosan-activated human serum(ZAHS)and/or TNF-Adirectly stim-ulated the HUVECS monolayers.PMN-EC adhesion percentage was measured, and modified whole-cell ELISA was used for measurement of ICAM-1.RESULTS:ZAHS alone resulted in no significant change in the degree of PMN adhesion and the level of ICAM-1. Activation of HUVECS with TNF-α followed by ZAHS stimulation resulted in greater increase in PMN-EC adhesion and ICAM-1 expression, as compared with the activation with TNF-α alone.CONCLUSION:Bypass-activated complement can promote ICAM-1 expression and neutrophil -endothelium adhesion induced by TNF-α, and so it is effective for promoting inflammation.     

Inhibitory effect of catalpol on inflammation and expression of RAGE in EA.hy926 cells induced by advanced glycation end products

AIM: To investigate the inhibitory effect of catalpol on inflammation in EA.hy926 cells induced by advanced glycation end products(AGEs) and to explore its antioxidant mechanisms.METHODS: Human endothelial cell line EA.hy926 was cultured and randomly divided into control group, catalpol(0.5 mmol/L) group, AGEs group, high-dose(0.5 mmol/L) catalpol+AGEs group, middle-dose(0.25 mmol/L) catalpol+AGEs group and low-dose(0.05 mmol/L) catalpol+AGEs group. Intracellular reative oxygen species(ROS) production was detected by laser scanning confocal microscopy. The levels of monocyte chemotactic protein-1(MCP-1), tumor necrosis factor-α(TNF-α) and vascular cell adhesion molecule-1(VCAM-1) in culture supernatant were detected by commercial ELISA kits. The expression of MCP-1, TNF-α, VCAM-1 and receptor for advanced glycation end products(RAGE) in the EA.hy926 cells were detected by Western blot.RESULTS: In high-dose catalpol+AGEs and middle-dose catalpol+AGEs groups, the generation of ROS was decreased significantly. The levels of MCP-1, TNF-α and VCAM-1, and protein expression of MCP-1, TNF-α and VCAM-1 were significantly lower. The expression of RAGE protein in EA.hy926 cells were significantly inhibited(P<0.05).CONCLUSION: Catalpol effectively inhibits the AGEs-induced oxidative stress and inflammation in EA.hy926 cells, which may be associated with a decrease in the expression of RAGE.     

Effects of cytomegalovirus on the adhesion of bone marrow stromal cells

AIM:To investigate the effect of cytomegalovirus (CMV) on the expression of ICAM-1 and VCAM-1 in bone marrow stromal cells and on the adhesion of bone marrow stromal cells to hematopoietic cells.METHODS:Flow cytometry was used to detect the expression of adhesion molecules ICAM-1 and VCAM-1 in bone marrow stromal cells, MTT method was used to perform the adhesion assay of bone marrow stromal cells to normal hematopoietic cells. RESULTS:Bone marrow stromal cells could be infected by the CMV used in this experiment; CMV below the dose of 100TCID₅₀ could not destroy bone marrow stromal cells apparently; The expression of ICAM-1 increased at the early stage(18 h) of CMV infection, the expression of ICAM-1 decreased at the late stage (120 h) of CMV infection. Inactived CMV could also increase the expression of ICAM-1 as alive CMV; The adhesion rate of bone marrow stromal cells to hematopoietic cells increased at the early stage of CMV infection. CMV had no significant effects on the expression of VCAM-1 in bone marrow stromal cells. CONCLUSION:The adhesion capacity of bone marrow stromal cells to hematopoietic cells increased at the early stage of CMV infection, while the adhesion capacity of bone marrow stromal cells to hematopoietic cells decreased at the late stage of CMV infection.