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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. 相似文献
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AIM: To study the senescence of human umbilical vein endothelial cells (HUVECs) and Bcl-2, Bax gene expression associated with apoptosis induced by angiotensinⅡ (AngⅡ).METHODS: HUVECs were cultured in vitro and the cell viability was observed by methyl thiazolyl tetrazolium (MTT). HUVECs were intervened by AngⅡ and valsartan (AngⅡ type 1 receptor blocking) and divided into 3 groups: the control group, AngⅡ group (stimulated with AngⅡ10-6mol/L for 48 h), valsartan group (valsartan was added to cells 1 h before 10-6mol/L AngⅡ treatment). β-gal staining and cell cycle analysis were used to identify the cell aging status. Morphologic changes and percentage of apoptosis were assayed with Hoechst33258 under fluorescent microscope. The expressions of Bcl-2 and Bax, and the apoptosis-associated genes were detected by immunocytochemical staining, RT-PCR and Western blotting. RESULTS: The cell viability by AngⅡ-induced cells was (81.9%±4.1)%, the positive cell number of β-gal staining was significantly higher in AngⅡ-induced cells (80.10%±6.81)% than that in the control cells. The cell cycle was at G0-G1(91.36%±6.45)%, the apoptotic cells significantly increased (31.84±2.86)% under fluorescent microscope. In valsartan group, Bcl-2 mRNA and protein expression increased markedly (P<0.05), but Bax mRNA and protein expression decreased evidently (P<0.05) compared to those in the AngⅡ group.CONCLUSION: Cell apoptosis is possibly an important factor for endothelial cell senescence and vascular aging induced by AngⅡ. One of its molecular mechanisms might be associated with decreasing the expression level of Bcl-2 and increasing that of Bax, which regulate the imbalance between mRNA and protein expression of Bcl-2 and Bax. Valsartan improves endothelial cell aging. 相似文献
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AIM: The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS: Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 μmol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L, 1 h); PMA+AngⅡ+PDTC group (10 μmol/L, 30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-κB p65, and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS: Compared to control group, the expression of MMP-9 (1.06±0.11, P<0.05) and phosphorylation of NF-κB p65 (1.02±0.10, P<0.05) in THP-1 macrophages were expressed when treated with AngⅡ (10-7mol/L); and the expression of MMP-9 mRNA were upregulated (1.22±0.08, P<0.05). However, NF-κB inhibitor PDTC reduced the NF-κB p65 (0.99±0.12, P<0.01) and MMP-9 (1.04±0.14, P<0.01) expressions and decreased the expression of MMP-9 mRNA (0.90±0.06,P<0.01). CONCLUSION: NF-κB signaling pathway contributes to the expression of MMP-9 in THP-1 macrophage induced by AngⅡ. 相似文献
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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 (rTNFα) 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. 相似文献
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AIM:To investigate the effect of angiotensin 1-7 (Ang1-7) on the human glomerular endothelial cells (HGECs) injury induced by angiotensin Ⅱ (Ang Ⅱ) and its possible mechanism. METHODS:Cultured HGECs were divided into 6 groups randomly:control group, Ang Ⅱ group, Ang1-7 group, Ang Ⅱ +Ang1-7 group, Ang Ⅱ +Ang1-7+A779 (an inhibitor of Mas receptor) group and A779 group. The apoptotic rate and reactive oxygen species (ROS) of HGECs were analyzed by flow cytometry and photographed by fluorescence microscopy. The levels of lactate dehydrogenase (LDH), nitric oxide (NO), endothelin-1 (ET-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) in the supernatant of cell cultures were measured. RESULTS:Compared with the control group, the apoptotic rate and the average fluorescence intensity of ROS were increased in the Ang Ⅱ group, IL-6, TNF-α, TGF-β, ICAM-1 and MCP-1 in cell supernatants were also increased in the Ang Ⅱ group (P<0.05). Compared with the Ang Ⅱ group, the apoptotic rate, ROS level, and the above inflammatory factors were decreased in Ang Ⅱ +Ang1-7 group (P<0.05). Compared with the Ang Ⅱ +Ang1-7 group, adding A779 increased the cell apoptotic rate, ROS production and the releases of the above inflammatory factors in cell supernatants (P<0.05). Compared with the Ang Ⅱ group, adding Ang1-7 inhibited the LDH leakage, ET-1 secretion and promoted the release of NO in a dose-dependent manner (P<0.05). CONCLUSION:Ang1-7 attenuates the HGECs injury induced by Ang Ⅱ by inhibiting the Mas receptor. 相似文献
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AIM:To study the influence of angiotensin Ⅱ (AngⅡ) on ATP-binding cassette transporter A1 in THP-1 derived foam cells. The variance of the expression of ABCA1, the content and the effluent rate of cholesterol were also investigated. METHODS:The regulatory effect of AngⅡ on the expression of ABCA1 mRNA and protein in THP-1 derived form cells were measured by RT-PCR and Western blotting. The effect of variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer, cholesterol effluent was measured by liquid scintillator. RESULTS:A positive facilitative effect of Ang Ⅱon form cells was observed. Total cholesterol content were increased significantly by Ang Ⅱ treatment (P<0.05). The mRNA and protein of ABCA1 were down-regulated significantly by Ang Ⅱ stimulation (P<0.05). Irbesartan reduced the total cholesterol content significantly (P<0.05). Meanwhile, the increase in the effluent rate of cholesterol and the expression of ABCA1 were observed (P<0.05). CONCLUSION:The effects of Ang Ⅱ on the formation of foam cells and atherosclerosis may be correlated to the activation of AT1 receptor and down-regulation of ABCA1. 相似文献
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AIM:To investigate the effect of platelet inhibitor from Agkistrodon halys venom (AHV-PI) on lipopolysaccharide (LPS) induced human umbilical vein endothelial cells (HUVECs) injury in vitro, and to explore its mechanism. METHODS:Cultured HUVECs were induced inflammatory injury by LPS (1 mg/L). The experiment was divided into blank control group, LPS group, AHV-PI group and AHV-PI+LPS group. The viability of HUVECs was measured by MTT assay. The morphological changes of HUVECs were observed under inverted microscope. The optimum concentration of AHV-PI at 5 mg/L was selected. Flow cytometry was used to detect apoptosis of HUVECs. Immunohistochemical method was used to observe the expression of tissue type plasminogen activator (t-PA) and plasminogen activator indhibitor-1 (PAI-1) of HUVECs. ELISA was used to detect the concentrations of intercellular adhesion molecule-1 (ICAM-1) and tissue factor (TF) in the supernatant. The activation and translocation of NF-κB subunit p65 were observed by immunofluorescence staining. RESULTS:The HUVECs were spindle shaped, the ratio of length to width was increased, the cells were fibroblast-like, and granular substance appeared in the cytoplasm in LPS group. The viability and morphological changes of HUVECs were not significantly affected as treated with AHV-PI at concentration of 0~5 mg/L, but the viability of HUVECs induced by LPS was inhibited and the morphological changes were alleviated. Compared with the blank control group, the levels of TF and ICAM-1 in the supernatant increased, and the expression of t-PA and PAI-1 in the HUVECs was decreased in LPS group. Compared with the LPS group, the contents of TF and ICAM-1 in the supernatant were significantly decreased, the expression of t-PA and PAI-1 in the HUVECs was increased and the expression of nucleus NF-κB p65 was decreased in AHV-PI+LPS group (P<0.05). CONCLUSION:AHV-PI reduces HUVECs damage. The protective mechanism is related to the inhibition of cytokine secretion and NF-κB activation. 相似文献
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ZHANG Yan ZHANG Hai-nan XU Jing L&# Yi-zhen ZHANG Jin PENG Jing LI Pan QIAO Xi LIU Qing-hua 《园艺学报》2018,34(7):1183-1188
AIM:To investigate the effect of inwardly rectifying potassium channel (IK1) agonist zacopride (Zac) on angiotensin Ⅱ (Ang Ⅱ)-induced viability and apoptosis of cardiac fibroblasts (CFb) and to explore the underlying anti-fibrosis mechanism.METHODS:The ventricular fibroblasts from neonatal SD rats were isolated and cultured by tissue digestion and differential adherence methods. The model of rat cardiac fibroblast activation induced by angiotensin Ⅱ was established. The CFb were randomly divided into control group, Ang Ⅱ model group, Ang Ⅱ+Zac group, Ang Ⅱ+Zac+BaCl2 group, AngⅡ+Zac+chloroquine group and Ang Ⅱ+captopril group. CCK-8 assay was used to detect the effect of Zac on the viability of CFb. The amount of collagen I and collagen Ⅲ secreted by CFb was determined by ELISA. The apoptosis of the CFb was analyzed by flow cytometry. The protein expression of Kir2.1 was determined by Western blot. RESULTS:Compared with the control group, the viability and collagen synthesis of the CFb were significantly increased, along with decreased Kir2.1 expression (P<0.05). Compared with the Ang Ⅱ model group, Zac treatment inhibited the viability and collagen synthesis of the CFb, induced apoptosis and up-regulated Kir2.1 expression (P<0.05). IK1 blockers BaCl2 and chloroquine reversed the effect of Zac. CONCLUSION:By enhancing IK1 (Kir2.1) expression, Zac attenuates Ang Ⅱ-induced ventricular fibrosis, in response to the inhibition of cell viability and induction of apoptosis. 相似文献
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AIM:To observe the role of ox-LDL in rabbit endothelium/circulating monocyte adhesion in vitro and the effect of vitamin E.METHODS:Cultured rabbit's endothelial cells were incubated with different concentrations of ox-LDL, then incubated with rabbit's monocytes to observe cell's adhesion. With Northern blotting, endothelial VCAM-1 mRNA expression was measured. By using vitamin E incubation before ox-LDL, above steps were repeated to observe the effect of vitamin E.RESULTS:When ox-LDL concentrations were 2.5 mg/L,5 mg/L,10 mg/L,monocytes adhesive to endothelium per microscope field were 132.8±20.2,350.0±37.2,502.6±78.8,respectively They were al significantly higher than that of control group(51.2±7.7,P<0.01)Addition of vitamin Eat comcentration of 10 mol/L,20 mol/L,40 mol/L respect ively before ox-LDL incubation yield fewer adhesive monocytes as follow:422.3±32.2,296.0±21.7,205.2±36.6,respectively,but only the last two concentrations had significant effects(P<0.01)Endothelial VCAM-1 mRNA expression in ox-LDL group was higher than that in vitamin E group(0.49±0.09 vs 0,33±0.10,P<0.05).CONCLUSIONS:ox-LDL directly enhances rabbit's endothelium/monocyte adhesion by inducing expression of VCAM-1 in endothelium. Vitamin E inhibites these effects of ox-LDL. 相似文献
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SUN Jian-ping LI Fu-ping XU Zhao-juan BAI Jian-ying YANG Jiang-xia ZHANG Xiu-fen LI Cui-qing ZHAO Dong 《园艺学报》2017,33(12):2139-2142
AIM: To investigate the effects of vinpocetine on inflammation of brain in intracerebral hemorrhage (ICH) rats and to explore the underlying mechanisms. METHODS: All rats were randomly divided into sham group, ICH group, ICH with low dose of vinpocetine treatment group, ICH with medium dose of vinpocetine treatment group, and ICH with high dose of vinpocetine treatment group. Except sham group, the rats in other groups were injected with type VⅡ collagenase to establish ICH model, and then the rats in vinpocetine treatment groups were received vinpocetine at 0.5, 1.0 or 1.5 mg/kg by intraperitoneal injection once a day for 7 days. After corresponding treatment, the impairment of neurological function in the rats was scored and the water content of the brain tissues was measured. Moreover, the activity of myeloperoxidase (MPO) was determined by ELISA, and the protein expression of Toll-like receptors 4 (TLR4), nuclear factor-κB(NF-κB), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molcule-1 (VCAM-1) in the brain tissues was determined by Western blot. RESULTS: Compared with ICH group, vinpocetine treatment significantly decreased the scores of the impairment of neurological function and the water content of the brain tissues. Moreover, the activity of MPO and the protein expression of TLR4, NF-κB, ICAM-1 and VCAM-1 were also reduced after vinpocetine treatment (P<0.05). CONCLUSION: Vinpocetine improves neurological function in ICH rats via suppression of inflammation by inhibiting NF-κB signaling and expression of ICAM-1 and VCAM-1. 相似文献
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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. 相似文献
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AIM: To investigate the mechanism of protein phosphatase 2A (PP2A) activation in mesenteric arteries of angiotensinⅡ(AngⅡ)-induced hypertensive rats. METHODS: Adult male Sprague-Dawley (SD) rats were subjected to AngⅡinfusion (500 ng·kg-1·min-1) using osmotic minipump up to 14 d to established the hypertension model. The rats (n=40) were randomly divided into 4 groups:control group (n=10), AngⅡgroup (n=10), candesartan (CAN; AngⅡtype 1 receptor blocker)+AngⅡgroup (n=10) and CAN group (n=10). The rats in CAN+AngⅡgroup and CAN group were administered with candesartan ester at the dose of 10 mg·kg-1·d-1 by gavage on the first day after implantation of osmotic minipump. The rats were sacrificed on the 15th day after minipump implantation. Serum and mesenteric arteries were collected. Systolic blood pressure was measured by tail-cuff method. The serum levels of AngⅡ were measured by ELISA. The protein levels of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (Ser1177), PP2A catalytic subunit (PP2Ac), phosphorylated PP2Ac (Tyr307) and PP2A inhibitor 2 (I2PP2A) in the mesenteric arteries were determined by Western blot. The activity of PP2A in the arteries was detected using PP2A activity assay kit. RESULTS: Compared with control group, the systolic blood pressure in AngⅡgroup was significantly increased(P<0.05), while those in CAN+AngⅡgroup and CAN group were significantly decreased (P<0.05). The serum levels of AngⅡ in AngⅡ group and CAN+AngⅡ group were significantly higher than that in control group (P<0.05). Compared with control group, the phosphorylation levels of eNOS Ser1177 were decreased in AngⅡgroup (P<0.05), but the activity of PP2A was significantly increased (P<0.05), and Pearson correlation analyses showed a negative correlation between PP2A activity and eNOS S1177 phosphorylation (r=-0.842, P<0.05). Compared with AngⅡgroup, the phosphorylation levels of eNOS Ser1177 in CAN+AngⅡgroup were significantly increased (P<0.05), but the activity of PP2A was reduced (P<0.05). Compared with control group, the protein levels of phosphorylated PP2Ac (Tyr307) and I2PP2A in the mesenteric arteries were decreased in AngⅡgroup (P<0.05), but increased in CAN+AngⅡgroup (P<0.05). No significant difference in all above-mentioned measures between control group and CAN group, nor in the levels of total eNOS and PP2Ac protein expression among all the groups was observed. CONCLUSION: AngⅡmay reduce the protein levels of phosphorylated PP2Ac (Tyr307) and I2PP2A in the mesenteric arteries of AngⅡ-induced hypertensive rats through AngⅡ/AngⅡ type 1 receptor-mediated signaling pathway, resulting in the activation of PP2A, then leading to down-regulation of eNOS S1177 phosphorylation, which ultimately mediates the occurrence of vascular endothelial dysfunction. 相似文献
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DUAN Xiao-yu ZHU Hong SUN Shan HU Hong-ling BU Xiao-fen MING Xiao-yan HE Ying-xia 《园艺学报》2019,35(3):522-529
AIM: To investigate the effect of Qiliqiangxin granule on the apoptosis of renal tissues in rats with cardiorenal syndrome (CRS) and its possible mechanism. METHODS: A rat model of CRS was established by ligation of the left anterior descending coronary artery and acute renal ischemia/reperfusion injury. After operation, the rats were divided into 6 groups:2-week sham operation (2w sham) group, 2-week model (2w CRS) group, 2-week drug (2w CRS-Q) group, 4-week sham operation (4w sham) group, 4-week model (4w CRS) group and 4-week drug (4w CRS-Q) group. The rats in 2w CRS-Q group and 4w CRS-Q group were given Qiliqiangxin granule (4 g·kg-1·d-1) by gavage for 2 weeks and 4 weeks, respectively. The levels of serum cystatin C (Cys-C), plasma angiotensin Ⅱ (Ang Ⅱ), urine neutrophil gelatinase-associated lipocalin (NGAL) and urine microalbumin (UMA) were measured by ELISA. The serum level of creatinine (Cre) was detected by sarcosine oxidase method. The renal histopathological changes were observed by HE staining. The mRNA and protein expression levels of Ang Ⅱ, Bcl-2 and Bax were evaluated by RT-qPCR and Western blot, respectively. The apoptosis rate of renal cells was assessed by TUNEL staining. RESULTS: The levels of serum Cys-C, serum Cre, plasma Ang Ⅱ, urine NGAL and UMA were significantly increased in 2w CRS group and 4w CRS group compared with 2w sham group and 4w sham group after modeling (P<0.05). The mRNA and protein expression levels of Bax and Ang Ⅱ in the renal tissues of CRS rats were significantly up-regulated (P<0.05), while Bcl-2 was significantly down-regulated (P<0.05) compared with 2w sham group and 4w sham group. Compared with 2w sham group and 4w sham group, the damage of renal tissues in 2w CRS and 4w CRS group was severe, and the apoptotic rates of renal cells were significantly increased. Compared with 2w CRS group and 4w CRS group, Qiliqiangxin granule greatly decreased the levels of Cys-C, Cre, Ang Ⅱ, NGAL and UMA, down-regulated the mRNA and protein expression levels of Bax and Ang Ⅱ in the renal tissues, and up-regulated the expression of Bcl-2 at mRNA and protein levels at 2 and 4 weeks. In addition, Qiliqiangxin granule also greatly attenuated the damage and apoptosis of the renal tissues. CONCLUSION: Qiliqiangxin granule significantly inhibits the apoptosis of renal tissues and improves the renal function of CRS rats, and its mechanism may be related to the inhibition of Ang Ⅱ expression. 相似文献
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AIM: To investigate whether sinomenine(SN) can decrease TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were isolated from freshly collected umbilical cords.Positive control samples were stimulated with TNF-α, omitting SN. Negative control samples were treated in the same way, omitting TNF-α and SN. Experiment samples were co-cultured with TNF-α and SN at different concentration (0.25, 0.5, and 1.0 mol/L),or TNF-α and dexamethasone(Dex) at concentration of 1.0×10-6mol/L.Cells were harvested after cultivation with the drugs for 12 hours. VCAM-1 mRNA expression was detected by real-time quantitative PCR, and VCAM-1 expression was detected by flow cytometry (FCM).RESULTS: VCAM-1 mRNA and VCAM-1 were induced by TNF-α. Compared with the positives, the relative VCAM-1 mRNA expression decreased to varying degrees in the experiment groups (P<0.05), and SN at concentration of 0.5 mol/L and 1.0 mol/L inhibited expression of VCAM-1 (P<0.05). SN at concentration of 1.0 mol/L decreased VCAM-1 expression by 28.8%(P<0.05), and SN at concentration of 0.5 mol/L reduced VCAM-1 expression by 21.68%(P<0.05). But SN at concentration of 0.25 mol/L and Dex at concentration of 1.0×10-6mol/L didnt depress expression of VCAM-1. CONCLUSION: SN may inhibit TNF-α-induced VCAM-1 expression in HUVECs in vitro. 相似文献
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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. 相似文献
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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. 相似文献
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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. 相似文献
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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. 相似文献