Effect of mininally modified low density lipoprotein on the adhesive function of vascular endothelial cell and its mechanism

AIM: To observe the effect of MM-LDL (minimally modified LDL) on the interaction between human umbilical vein endothelial cell (HUVEC) and U937 monocyte-like cell line and the exporession of vascular cell adhesion-1 (VCAM-1), intercellular adhesion molecule-1(ICAM-1), P-selectin.METHODS:The adhesive percentage between HUVEC treated with MM-LDL and U937 was determined by counting and the expression of VCAM-1, ICAM-1, P-selectin were examined by ELISA. RESULTS: Treatment of HUVEC with MM-LDL (75 mg/L) for 4 hours significantly increased adhesion of U937 to HUVEC ( P <0.01) and did not induce the surface expression of VCAM-1, ICAM-1, P-selectin . Recombination tumor necrosis factor-alpha (rTNF_α) 5.0 μg/L, as a positive control, induced the expression of these adhesion molecules ( P <0.05). Prolonged (18 h) exposure to MM-LDL resulted in the expression of P-selectin, but not VCAM-1.CONCLUSION: the adhesion of monocytes to endothelial cells induced by MM-LDL is not mediated by VCAM-1, ICAM-1. P-selectin induction may be partly involved in the process.     

Role of MEK1/2 in ICAM-1 over expression induced by lipopolysaccharide in human umbilical vein endothelial cells

AIM: To investigate the role of MEK1/2, a subfamily of mitogen activated protein kinase-kinase (MAPKK), in expression of intercellular adhesion molecule-1 (ICAM-1) induced by lipopolysaccharide (LPS) in human umbilical vein endothelial cells (HUVECs). METHODS: Expression levels of ICAM-1 mRNA and its protein were assayed using RT-PCR and Western blotting, respectively, in HUVECs pretreated with different concentrations of LPS for different times with or without PD98059, a specific inhibitor of MEK1/2. RESULTS: LPS up-regulated the expression of ICAM-1 mRNA and its protein in HUVECs in a concentration- and time-dependent manners. The expression levels of ICAM-1 mRNA and its protein began to elevate at 2 h after LPS treatment, and reached nearly a peak value at 6 h after LPS (100 μg·L-1) treatment. PD98059 (10 μg·L-1) significantly inhibited LPS-induced expression of ICAM-1 mRNA and protein, the expression inhibitory rates of which were 54.4% and 44.9%, respectively (P<0.01). CONCLUSION: Modulation of MEK1/2 signaling pathway might be a new and useful strategy for the prevention and treatment of vascular endothelial injury induced by LPS.     

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 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 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.     

Change of ICAM-1 expression in intestine tissue of mice induced by LPS and role of p38 MAPK in its expression

AIM: To study the change of intercellular adhesion molecule-1(ICAM-1) expression in intestine tissues of mice induced by LPS and regulatory effect of p38 mitogen-activated protein kinase(p38 MAPK) on ICAM-1 expression. METHODS: Protein and mRNA of ICAM-1 were measured using Western blotting and RT-PCR respectively in intestine tissue of BALB/c mice treated by lipopolysaccharide(LPS) or LPS plus SB203580, a specific inhibitor of p38 MAPK. RESULTS: Compared with control group, the expression of ICAM-1 protein and mRNA was increased significantly by LPS stimulation in dose- and time-dependent manner. ICAM-1 expression reached peak value at 12-36 h after LPS stimulation. 20.0 mg/kg of LPS could induce the maximum of ICAM-1 expression. Pretreatment of mice with SB203580 for 30 min could inhibit significantly LPS-induced expression of ICAM-1 protein and mRNA expression in mouse intestine tissues. CONCLUSIONS: These data highlight that LPS could up-regulate ICAM-1 protein and mRNA expression in intestine tissue of mice in dose- and time-dependent manner, and p38 MAPK signal pathway plays an important role in ICAM-1 expression induced by LPS. It suggests that inhibition of p38 MAPK might be a useful principle for the prevention and treatment of intestine damage of endotoxic shock.     

Effects of oxidized HDL on the levels of MCP-1, ICAM-1 and free calcium in cultured human umbilical venous endothelial cells

AIM:To study the effects of oxidized high-density lipoprotein (oxHDL) on the expression of monocyte chemoattractant protein-1(MCP-1) and intercellular adhesion molecule-1(ICAM-1) and intracellular free calcium concentration ([Ca²⁺]i) level in cultured human umbilical venous endothelial cells(HUVECs). METHODS:The MCP-1 protein content in the medium of conditioned HUVEC was measured by ELISA, and the ICAM-1 on HUVECs was detected by indirect immunofluorescence, and [Ca²⁺]i was determined by Fluo-3/AM, the injury of cells was observed by scanning electron microscopy (SEM).RESULTS:oxHDL could induce the expression of MCP-1 and ICAM-1 in HUVECs. In oxHDL group (HUVECs were incubated with 100 mg protein/L oxHDL for 24 h), the levels of MCP-1, ICAM-1 and [Ca²⁺]i increased by 160%, 60% and 70% respectively compared with the control group (P＜0.01). When HUVECs were incubated with 300 mg protein/L oxHDL for 24 h, cells were injured obviously. CONCLUSION:By inducing the expression of ICAM-1 and MCP-1 in endothelial cells, oxHDL may promote monocyte-endothelium adhesion and monocyte migration to intima, it may promote atherosclerosis as oxidized low-density lipoprotein (oxLDL).     

Influence of the serum of Radix Ophiopogonison the apoptosis related gene expression and intracellular Ca2+ in vascular endothelial cells treated with LPS

AIM:To explore the molecular mechanism of Radix Ophioponis against vascular endothelial cell (VEC) apoptosis induced by LPS.METHODS:The apoptosis of human umbilical vascular endothelial cells(HUVEC) was induced by lipopolysaccharide(LPS). The influence of Radix Ophiopogonis on the expression of bcl-2 and intracellular Ca²⁺ was detected by flow cytometry and laser confocal microscope.RESULTS:The serum containing Radix Ophiopogonis suppressed the increase in bcl-2 expression and overloading of Ca²⁺ induced by LPS in HUVEC.CONCLUSION:The mechanism of Radix Ophiopogonis against HUVEC apotosis may be related with its regulatory effect on bcl-2 expression and remission of Ca²⁺ overloading.     

Activation of vascular endothelial cells improves the homing of hematopoietic stem cells

AIM: To study the effect of endothelial cell activation on the homing of hematopoietic stem cells (HUHSC) during transplantation. METHODS: Human umbilical vein endothelial cells (HUVEC) were cultured to single layer and activated by vascular endothelial growth factor (EVGF), granulocyte colony stimulating factor (G-CSF) and lipopolysaccharide (LPS), respectively. The HUHSC, enriched by eliminating red blood cells, granulocytes, monocytes and lymphocytes from cord blood, were cocultured with activated HUVEC to make adhesion. The adhesive ability of activated HUVEC to C-Kit⁺ HUHSC was assayed by ELISA. Anti-VCAM-1 monoclonal antibody was used to detect the effect of activation on HUVEC and HUHSC interactions. RESULTS: Resting HUVEC had a little adhesive ability to HUHSC. A great enhancement of adhesive ability was showed when HUVEC was activated by VEGF, G-CSF and LPS. In the presence of anti-VCAM-1, the adhesive ability of activated HUVEC was decreased remarkablely. CONCLUSION: HUHSC homing may be related to the activation of endothelial cells and adhesion molecules.     

Effects of Ginsenosides on LPS-induced TF and PAI-1 expression in vascular endothelial cells

AIM: To study the effect of ginsenosides on lipopolysaccharide-induced expression of tissue factor (TF) and plasminogen activator inhibitor type-1 (PAI-1) in vascular endothelial cells (EC), and to investigate the mechanism of ginsenosides in the healthy protection and treatment of cardiovascular diseases. METHODS: Human umbilical vein endothelial cells (HUVEC) were cultured by trypsin digestion method. PAI-1 was measured in the conditioned medium of HUVEC by a specific enzyme-linked immunosorbent assay (ELISA), whereas TF activity was measured in the lysates of these cells by a single step clotting assay. Specific mRNA expressions were determined by Northern blotting. RESULTS: Treatment of HUVEC with LPS resulted in a significant increase in PAI-1 antigen and TF activity. Ginsenosides inhibited this LPS-induced upregulation of PAI-1 protein and TF activity in HUVEC. These effects were also confirmed on the level of specific PAI-1 and TF mRNA expression by Northern blotting. CONCLUSION: Ginsenosides counteract endothelial cell activation by inhibition LPS-induced PAI-1 and TF expression in these cells. This ability of ginsenosides might explain its efficacy in the healthy protection and the treatment of cardiovascular diseases.     

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.     

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.     

Chlamydia pneumoniae enhanced the expression of ICAM-1 in cultured human umbilical vein endothelial cells

AIM: To investigated the effects of Chlamydia pneumoniae (C.pneumoniae) infection on the expression of intercellular adhesion molecule-1 (ICAM-1) in cultured human umbilical vein endothelial cells (HUVECs). METHODS: After propagated in HEP-2 cells, C. pneumoniae organisms were infected to HUVECs. The infection was assessed by ectromicroscope and PCR. The expression of ICAM-1 on HUVECs was detected by flow cytometry before infection and 12 h, 24 h, 48 h, 72 h after infection. RT-PCR was used to detect the ICAM-1 mRNA expression. RESULTS: C.pneumoniae was able to infect cultured HUVECs. After infection, the expression of ICAM-1 on the surface of cultured HUVECs was increased,, the peak was at the time of about 24-48 h; The light quantative RT-PCR analysis demonstrated that the infection also enhanced the ICAM-1 mRNA expression. CONCLUSION: The ability of C.pneumoniae to grow in HUVECs and to stimulate the expression of ICAM-1 protein and mRNA suggests that C.pneumoniae may playa role in atheriosclerosis.     

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.     

Effects of lipopolysaccharide on aquaporin-1 expression and function in rat lung microvessel endothelial cells

AIM: To determine if aquaporin-1 (AQP-1) expression and function is influenced after lipopolysaccharide (LPS) stimulation in rat lung microvessel endothelial cells and to investigate the mechanisms of lung fluid abnormal metabolism in acute lung injury. METHODS: LPS at different concentrations (100 μg/L, 1 mg/L or 10 mg/L) was used to stimulate cultivated rat lung microvessel endothelial cells in vitro at different stimulatory times (4 h, 12 h or 24 h), respectively. Tritium water permeation was conducted for determining the intracellular signal intensity in rat lung microvessel endothelial cells. The RT-PCR technique was applied for the assay of the expression of AQP-1 mRNA. RESULTS: The signal intensity of intracellular tritium water in the LPS stimulation group was less than that in normal control significantly. Compared with the normal control group (P<0.01), there was obvious decrease in the expression of AQP-1 mRNA in LPS stimulation groups. CONCLUSION: The decreased expression of AQP-1 mRNA and the weaken function of transporting water suggest that AQP-1 may play a major role in abnormal fluid transportation in acute injured lung.     

Antagonistic effect of captopril on activation and injury of vascular endothelial cells induced by lipopolysaccharide

AIM: To investigate the antagonistic action of Captopril (Cap) on the activation and injury of human umbilical vascular endothelial cells (HUVECs) induced by lipopolysaccharide(LPS) and the possible mechanisms. METHODS: After 18 h exposure of the cultured HUVECs to LPS (1 mg/L), or LPS (1 mg/L) plus Cap at the concentration of 10^-7mol/L, 10^-5mol/L and 10^-3mol/L, the expression of vWF protein in the conditioned media was tested by enzyme-linked immunosorbent assay (ELISA), the expression of ICAM-1 protein in HUVECs was determined by indirect immunofluorescence technique with flow cytometry as well. In addition, the expression of TNFα mRNA was determined by in situ hybridization. RESULTS: The results of ELISA and indirect immunofluorescence technique showed that exposure to LPS at a concentration of 1 mg/L led to a significant increase in the vWF and ICAM-1 expression in HUVECs as compared to the control (P＜0. 05), whereas they were somewhat decreased when exposed to Cap at three increasing concentrations mentioned above, especially in the Cap (10^-3mol/L) plus LPS group (P＜0.05). Cap inhibited vWF secretion and ICAM-1 expression of HUVECs caused by LPS in a concentration-dependent manner. In situ hybridization revealed that the expression of TNFα mRNA was inhibited by Cap both in a concentration of 10^-3mol/L, and in a lower concentration of 10^-5mol/L. CONCLUSION: Cap antagonizes the activation and injury of HUVECs induced by LPS, which may be related to the decrease in TNFα mRNA expression.     

Effects of dehydroepiandrosterone on expression of ICAM-1 in rabbit aorta and HUVECs induced by high lipid levels

AIM: To investigate the effects of dehydroepiandrosterone (DHEA) on the expression of intercellular adhesion molecule-1 (ICAM-1) induced by high lipid levels in rabbit aorta and human umbilical venous endothelial cells (HUVECs), and the effects of all-trans retinoic acid (ATRA) in this process.METHODS: For in vitro experiments, the cultured HUVEC were divided into control group, oxidized low-density lipoprotein (ox-LDL) group, ox-LDL+DHEA group, ox-LDL+DHEA+ATRA group and DHEA group. The HUVECs in all groups were treated with the corresponding reagents for 24 h. The expression of ICAM-1 at mRNA and protein levels in all groups were determined by RT-PCR and ELISA, respectively. For in vivo experiments, the rabbits were divided into control group, high lipid group, high lipid+DHEA group, high lipid+DHEA+ATRA group and DHEA group. The rabbits in all groups were fed with the corresponding diets for 10 weeks. The expression of ICAM-1 in the rabbit aorta at mRNA and protein levels was determined by RT-PCR and immunohistochemistry. RESULTS: The expression of ICAM-1 in the HUVECs in ox-LDL group was significantly increased compared with control group (P<0.05). Compared with ox-LDL group, the expression of ICAM-1 in ox-LDL+DHEA group was obviously decreased (P<0.05). The expression of ICAM-1 was similar in both control group and DHEA group (P>0.05). The expression of ICAM-1 was similar in both ox-LDL+DHEA group and ox-LDL+DHEA+ATRA group (P>0.05). The expression of ICAM-1 in the rabbit aorta in high lipid group was significantly increased compared with control group (P<0.05). Compared with high lipid group, the expression of ICAM-1 in high lipid+DHEA group was obviously decreased (P<0.05). No remarkable difference in the expression of ICAM-1 between control group and DHEA group was observed (P>0.05), so did between high lipid+DHEA group and high lipid+DHEA+ATRA group (P>0.05). CONCLUSION: DHEA inhibits high lipid-induced ICAM-1 expression in rabbit aorta and HUVECs. That may be one of the mechanisms of antiatherosclerotic effect of DHEA. ATRA seems no positive effect on DHEA function.     

Expression of intercellular adhesion molecule in lung tissues of experimental acute lung injury and the effect of rhubarb

AIM:To approach the relationship between the expression of intercellular adhesion (ICAM-1 mRNA) and acute lung injury (ALI) as well as the mechanisms of rhubarb in the prevention and treatment of the lung injury. METHODS:ALI animal model was performed by Lipopolysaccharide (LPS). The rats were divided into 4 groups: LPS group, control group, rhubarb+LPS group and dexamethasone+LPS group. Histopathological examination and biological markers were measured for the lung specimens. Molecular hybridization method was used to determine the expression of ICAM-1 mRNA. RESULTS:The ICAM-1 mRNA expression in the lung tissues of LPS group significantly increased compared with control group (P＜0.01), rhubarb and dexamethasone had the action of decreasing the ICAM-1 mRNA expression (P＜0.05, P＜0.01); pathologic changes and the biological markers of ALI significantly decreased or ameliorated. CONCLUSION:The increase in the expression of ICAM-1 mRNA in the lung tissues of ALI is involved in the formation of ALI. Rhubarb and dexamethasone can ameliorate the lung damage, mechanism of which may be related to the inhibition of ICAM-1 mRNA expression.