共查询到20条相似文献，搜索用时 656 毫秒
1.
AIM: To investigate whether or not short-term high pressure proliferates human umbilical vein endothelial cells (HUVECs), and the role of pp60c-src in cell proliferation. METHODS: Cultured HUVECs of 3-6th passage were exposed to atmosphere 0 mmHg (AP), 120 mmHg (MP), 180 mmHg (HP) and interfered with captopril(Cap, 10 μmol/L)or irbesartan(Irb, 10 μmol/L). Cell proliferation was quantified by measuring hexosaminidase activity. The content of pp60c-src in cells was investigated by Western blotting. RESULTS:① Hexosaminidase activities which reflected cell number increased significantly at 4 h in MP and HP(0.145±0.018 and 0.144±0.019 vs 0.118±0.003,P＜0.01). Correspondingly, the expression of pp60c-src of 2 h in MP or HP groups was higher than that in AP which increased slowly to reach the level in MP and HP groups at 4 h. ② Cap and Irb had no effect on cell proliferation at each time points in AP group , but increased the hexosaminidase activities in MP and HP groups at 12 h. The contents of pp60c-src in groups with or without intervention of Cap or Irb were similar at each time points. CONCLUSION: High hydrostatic pressure induces early cell proliferation. The expression of pp60c-src occurs before cell proliferation in different pressure groups, which suggests that pp60c-src is involved in signal transmission pathway of pressure-induced cell proliferation. This process is not regulated mainly by renin-angiotensin system (RAS). 相似文献
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XIA Zi-rong LI Ju-xiang ZHOU Rui-hong YAN Su-juan LUO Wei CHENG Xiao-shu WU Qing-hua SU Hai WU Yan-qing 《园艺学报》2008,24(1):89-92
AIM: To investigated the role of CT-1 in the hypertensive ventricular remodeling. METHODS: The cardiac fibroblasts in 3-4 passages were cultured in vitro, and divided into eight groups according to the different intervention factors: group C (control); group DM: dimethyl sulphoxide (DMSO); group P: cultured under high hydrostatic pressure (160 mmHg); group ASODN: interfered with CT-1 antisense oligodeoxynucleotides (10 μmol/L); group SODN: incubated with CT-1 sense oligodeoxynucleotides (10 μmol/L); group AG: interfered with AG490 (25 μmol/L); group PD: interfered with PD98059 (20 μmol/L); group LY: interfered with LY 294002 (10 μmol/L). Western blotting was employed to assess the expression of STAT3, ERK1/2 and PI3-K respectively at protein level. Cell proliferation was quantified by MTT. RESULTS: High hydrostatic pressure stimulated the proliferation of cardiac fibroblasts, upregulated the expression of CT-1. CT-1ASODN inhibited the proliferation of cardiac fibroblasts (0.132±0.013 vs 0.154±0.011, P<0.05). ASODN extensively inhibited the expression of STAT3, ERK1/2 and PI3-k respectively at protein level (2.09±0.25 vs 2.47±0.28, P<0.05), (1.13±0.19 vs 1.61±0.22, P<0.05), (1.25±0.23 vs1.71±0.25, P<0.05). AG490, a JAK-STAT3 inhibitor, reversed the increase in the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure and the expression of ERK1 phosphorylation (0.118±0.018 vs 0.155±0.010, P<0.05). PD98059, a MAPK-ERK1/2 inhibitor, increased the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.185±0.011 vs 0.155±0.010, P<0.05) and the expression of STAT3 phosphorylation (1.83±0.23 vs 1.58±0.22, P<0.05). LY294002, a PI3-K inhibitor, had no effect on the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.157±0.015 vs 0.155±0.010, P>0.05). No difference of the expression of the above factors was observed in SOND (0.151±0.010 vs 0.154±0.011, P>0.05) and DMSO (0.141±0.017 vs 0.155±0.010, P>0.05) groups as compared with the control group. CONCLUSION: Under high hydrostatic pressure, the proliferation of cardiac fibroblasts is essentially mediated by STAT3, independent of PI3-K and the action is negatively regulated by ERK1/2 via inhibiting STAT3.The interaction between STAT3 and ERK1/2 may assist CT-1 in developing adequate cardiac fibroblast proliferation. 相似文献
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AIM: To investigate the role of mitochondrial calcium uniporter (MCU) in the cardioprotection by hypoxic preconditioning (HPC) and its relationship to mitochondrial permeability transition pore (MPTP). METHODS: Intraventricular balloon technique was employed to measure the left ventricular developed pressure (LVDP), the maximum rise/fall rate of left ventricular pressure (±dp/dtmax), and the left ventricular end-diastolic pressure (LVEDP) in Langendorff isolated rat heart. The hypoxia was achieved by ligation of left anterior coronary artery for 30 min followed by release of ligation for 120 min as reoxygenation. Hypoxic preconditioning was set as two episodes of 5 min global hypoxia and 5 min reoxygenation. RESULTS: Both HPC and treatment with ruthenium red (5 μmol/L) during the first 10 min reoxygenation improved recovery of LVDP, ±dp/dtmax and decreased LVEDP, which was associated with reduced infarct size and lactate dyhydrogenase release. These protective effects were attenuated by treatment with spermine (20 μmol/L) during the first 10 min reoxygenation. Administration of cyclosporin A (0.2 μmol/L) during the last 5 min of hypoxia period and first 15 min of reoxygenation period reduced the injury effect by spermine. CONCLUSION: These results indicate that inhibition of MCU is involved in the cardioprotection of HPC via inhibiting MPTP. 相似文献
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AIM: To observe the effects of oxidized free radical (OFR) on dimethylarginine dimethylaminohydrolase (DDAH) activity and concentration in human umbilical vein endothelial cells (HUVECs), and to investigate the metabolic mechanism of endogenous NOS inhibitor and the role of carvedilol. METHODS: HUVECs of 3-6th passage, cultured with modified Jaffes method, were divided into three groups: (1) cells cultured with equivalent DMEM medium as control; (2) OFR intervention groups, 0.01 mmol/L, or 0.1 mmol/L OFR was added respectively; (3) drug intervention groups: 0.1 mmol/L OFR plus 10 μmol/L carvedilol. ADMA, nitric oxide (NO), endothim (ET), L-citrulline concentrations and the activity of NOS in conditioned medium were measured after 24 h exposure. ADMA concentration in the conditioned medium was determined by high-performance liquid chromatography. Western blotting was performed to evaluate DDAH expression. RESULTS: Compared with control group, ADMA and ET concentrations were increased, while the level of NO and the activity of NOS decreased and relevant to the concentrations of OFR. We assayed DDAH activity by determining L-citrulline formation from ADMA. The concentration of L-citrulline was decreased, while the DDAH expression had no obvious change. With the role of carvedilol, ADMA, ET concentrations were decreased, while the level of NO, L-citrulline and the activity of NOS increased. CONCLUSION: Endothelial dysfunction induced by OFR is associated with the increase in ADMA concentration and reduction of DDAH activity, but not DDAH expression. Carvedilol promotes the degradation of ADMA through increasing activity of DDAH and improving endothelium function. 相似文献
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AIM: To observe the effects of rosiglitazone on the oxidative stress injury in endothelial outgrowth cells (EOCs), which caused by asymmetric dimethylarginine(ADMA). METHODS: The mononuclear cells were harvested from umbilical cord blood by density gradient centrifugation, and induced into EOCs and expanded in vitro. The endothelial characteristics of EOCs were identified by immunostaining and fluorescent staining. The second generation of EOCs was treated with 10 μmol/L ADMA and different concentrations of rosiglitazone (0, 1, 5, 10 μmol/L) for 72 h. Then the cells were harvested and the apoptosis rate, reproductive activity and vasculogenesis activity were measured by flow cytometry, MTT assay and Matrix gel vasculogenisis assay, respectively. The endothelial nitric oxide synthase gene expression was assayed by RT-PCR. RESULTS: EOCs possessed many endothelial characteristics. Immunostaining showed that the surface antigen factor VIII, CD34 and Flk-1 were positive. The fluorescent staining experiment revealed that EOCs both bound to FITC-UEA-1 and up-took DiI-ac-LDL. Incubation of EOCs with ADMA increased the apoptosis rate and inhibited the reproductive activity and vasculogenesis activity in the cells. Rosiglitazone at concentrations of 1 and 5 μmol/L counteracted such inhibition and stimulated reproductive activity in EOCs (P<0.01), while such protective effects were attenuated or abolished at concentration of 10 μmol/L. In addition, the vasculogenesis activity was inhibited by 10 μmol/L rosiglitazone cooperated with ADMA. RT-PCR assay revealed that eNOS gene expression in 5 μmol/L group was up-regulated and that in 10 μmol/L group was down-regulated. CONCLUSION: Rosiglitazone at lower concentration (<10 μmol/L) protects EOCs from the oxidative stress injury caused by ADMA, and stimulates reproductive activity of EOCs. Such protective effects are partially achieved through the up-regulation of eNOS gene expression. 相似文献
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2,3,5,4’-Tetrahydroxystilbene-2-O-β-D-glucoside protects against LPC-induced endothelial cell injury
AIM: To observe the protective effect of 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside (TSG) on lysophosphatidylcholine (LPC)-induced vascular endothelial cell injury. METHODS: The 3rd and 4th generations of human umbilical vein endothelial cells (HUVECs) were cultured in vitro and propagated. The cells were randomly divided into 3 groups: control group, model group (LPC) and experimental group (TSG+LPC). The cells in control group were not treated with any reagent. To establish endothelial cell injury model, LPC was administered to HUVECs at concentration of 10 mg/L and incubated with the cells for 24 h. In TSG+LPC group, TSG was administered to HUVECs at concentrations of 10.0, 1.0 and 0.1 μmol/L 1 h before administration of LPC, and then the cells were incubated for 24 h. The cell viability, the content of asymmetric dimethyl arginine (ADMA) and NO, and apoptotic rate were detected. RESULTS: Compared with control group, ADMA content in the cell culture supernatants and apoptotic rate of the HUVECs in LPC group were significantly increased, while the NO content and cell viability were notably decreased. Compared with LPC group, ADMA content and apoptotic rate in TSG+LPC group was significantly decreased, while the NO content and cell viability were notably increased. CONCLUSION: TSG may protect LPC-injured vascular endothelial cells by attenuating the expression of ADMA and enhancing the production of NO, thus inhibiting apoptosis and increasing cell survival rate. 相似文献
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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. 相似文献
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XIA Xue ZHANG Huai-qin JIA Hong-mei LIN Yi-nuo HUANG Wei-jian YE Sheng SHAO Xiao-lin 《园艺学报》2010,26(6):1052-1058
AIM: To investigate the effects of asymmetric dimethylarginine (ADMA) on apoptosis, adhesion ability and phosphorylation of p38 mitogen-activated protein kinase in endothelial outgrowth cells (EOCs). METHODS: The mononuclear cells were harvested from umbilical cord blood by Ficoll density gradient centrifugation, and induced into EOCs and then expanded in vitro. The endothelial characteristics of EOCs were identified by immunostaining and fluorescent staining. The EOCs were treated with different concentrations of ADMA (0, 1, 5, 10, 30 μmol/L) for 48 h. Apoptotic incidences of EOCs were quantitatively determined by flow cytometry. The morphologic changes of the apoptotic cells were visualized by DAPI staining and Annexin-V/PI staining. Adhesion ability of EOCs was measured by replacing the cells on dishes and adherent cells were counted under the inverted microscopy. The p38MAPK activity was evaluated by immunoblotting technique with phospho-p38MAPK antibody. RESULTS: EOCs possessed many endothelial characteristics. Immunostaining showed that the surface antigen factor VIII, CD34 and Flk-1 were positive. The fluorescent staining revealed that EOCs were double positive for Dil-ac-LDL-uptaking and FITC-UEA-I-lectin binding. ADMA (1-30 μmol/L) induced apoptosis of EOCs in a dose-dependent manner (P<0.01). Obvious change of apoptotic morphology in EOCs incubated with ADMA was observed with DAPI staining and Annexin-V/PI staining. ADMA (5-30 μmol/L) inhibited the adhesion ability of EOCs, whereas ADMA at concentration of 1 μmol/L had no effect. ADMA (5-30 μmol/L) induced phosphorylation of p38MAPK in a dose-dependent manner (P<0.01). CONCLUSION: ADMA induces apoptosis and inhibits adhesion ability in EOCs. Activated p38MAPK might be involved in the course of apoptotic effects of ADMA. 相似文献
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WEN Zhong-yuan LIU Yong-ming WANG Teng ZHANG Ping-an CHEN Xiao-lin LI Geng-shan 《园艺学报》2005,21(6):1081-1084
AIM: To study the effect of rosiglitazone (RSG) to improve insulin sensitivity on myocardial energy substrate utilization as well as the cardiac function in a rat model of type 2 diabetes mellitus. METHODS: Sprague-Dawley rats were conducted into three groups: chow-fed rats were fed with normal chow (12% of calories as fat); fat-fed/STZ rats were fed with high-fat diet (40% of calories as fat) for 4 weeks and then injected with streptozotocin 35 mg/kg intraperitoneal; fat-fed/STZ/RSG rats were fat-fed/STZ rats treated with rosiglitazone (3 mg·kg-1·d-1) for 2 weeks. A cannula connected to a passive transducer was inserted the heart for the measurement of the cardiac function including heart rate (HR), left ventricular end-diastolic pressure (EDP) and ±dp/dtmax. Then the isolated hearts were mounted onto a Langendorff perfusion apparatus to perfuse with Krebs-Henseleit buffer in the presence of 5 mmol/L glucose and 0.4 mmol/L ［3H］ labelled palmitate. Glucose uptake and ［3H2O］ collection were measured to evaluate the rate of carbohydrate and fatty acid oxidation. RESULTS: Compared with the chow-fed rats, fat-fed/STZ rats had a significantly depression of glucose uptake in the hearts ［(54.7±6.2 vs 69.0±5.7) μmol·g-1 dry weight, P<0.01］ after 30 min perfusion. The oxidation of glucose and palmitate were 18% and 82%, respectively. Paralleling the reduction was a change of EDP ［(14.3±1.8 vs 10.5±1.1) mmHg, P<0.05］ and -dp/dt ［(550±57 vs 650±42) mmHg/s, P<0.01］, indicating a impaired left ventricular diastolic function. In the hearts subjected to fat-fed/STZ group, rosiglitazone treated for 2 weeks resulted in a elevated level of glucose uptake ［(63.5±6.4 vs 54.7±6.2) μmol·g-1 dry weight, P<0.05］. A protective role of the ventricular function ［EDP decreased from （14.8±1.9） to （11.0±0.8） mmHg/s and -dp/dtmax increased from （558±60） to （629±51） mmHg/s, P<0.05］ were observed. CONCLUSIONS: Our study indicates that there is a depression of glucose oxidation and at increase in fatty acid oxidation in type 2 diabetic hearts. Elevation of insulin sensitivity using rosiglitazone increases the myocardial glucose metabolism and shows a benefitial result to heart functions. 相似文献
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AIM:To study the effect of activated protein C (APC) at different concentrations on apoptosis of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS).METHODS:The HUVECs were induced by LPS (1.0 mg/L) as apoptotic model that was administered by different concentration of APC (10 μg/L or 50 μg/L). Meanwhile, the control group and induced apoptosis group induced by LPS (1.0 mg/L) stimulation were also set up. The changes of cellular ultrastructures were observed under electron microscope. The DNA ladder and TUNEL fluorescent staining were measured in cells. Annexin-Ⅴ/PI double staining was used to measure the cell apoptosis rate by flow cytometry. Cell survival rate was measured by MTT assay. The proliferating cell nuclear antigen (PCNA) expression levels in cells were also measured by Western blotting to reflect the proliferation of the cells.RESULTS:There were significant apoptotic changes in the cells induced by LPS, but the apoptotic changes were reduced and apoptosis rates were decreased in the cells treated with APC. Meanwhile, cell survival rate and the protein levels of PCNA were increased after APC treatment, particularly at the concentration of 50 μg/L, which showed difference when compared with those induced apoptosis group by LPS (P<0.05).CONCLUSION:APC can inhibit HUVECs apoptosis induced by LPS and promote cell proliferation, thus protect the cells from injury. 相似文献
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AIM: To detect the effect of sepsis on hepatic,renal functions and corresponding enzymes in intestine of mice,and to explore the role of leptin in acute inflammation.METHODS: A mice model of sepsis was made by cecum ligation and perforation,and 96-well spectrophotometry was used to detecte the levels of alanine aminotransferase (ALT),uric acid (UA) and activities of myeloperoxidase (MPO),glutathin-S-transferase (GST),xanthine oxidase (XOD),superoxide dismutase (SOD) in serum and intestinal homogenized fluids,respectively.Hematoxylin-eosin staining was used simultaneously to check the histopathologic changes of intestine.RESULTS: Compared with sham group (330.12 μmol/L±94.15 μmol/L),serum UA level (521.92 μmol/L±91.86 μmol/L) at 6 h after sepsis was significantly higher.12 h after sepsis,both serum ALT (83.55 U/L±40.44 U/L) and UA (474.03 μmol/L±75.22 μmol/L) were significantly higher than those in sham group (66.23 U/L±16.80 U/L and 320.95 μmol/L±99.14 μmol/L,respectively).12 h after leptin injection (0.1 mg/kg,ip) or indomethacin injection (2 mg/kg,ip),the serum ALT and UA levels significantly decreased (vs sepsis group,P<0.05).Moreover,the activities of MPO,GST,XOD and SOD in intestine were changed at different degrees.CONCLUSION: During the process of sepsis,trace dose of leptin injected peritoneally significantly improves and stabilizes the hepatic and renal functions.The mechanisms may be related with those intestinal enzymes associated with metabolism of free radicals,mercapto group and purine.Indomethacin exerts a similar role as leptin though at much higher dose. 相似文献
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AIM: To investigate the synergistic effect of decitabine (DCA) and valproic acid (VPA) on apoptosis and cell cycle arrest at G0/G1 phase in gastric cancer MGC-803 cells. METHODS: Gastric cancer MGC-803 cells were used in the study and divided into the following groups according to the treatment with different drugs for 72 h: DCA 1.5 μmol/L,DCA 3.0 μmol/L, VPA 1.5 mmol/L, DCA 1.5 μmol/L+VPA 1.5 mmol/L and DCA 3.0 μmol/L+VPA 1.5 mmol/L. The early and late apoptotic rates were detected by annexin V and PI staining. The cell cycle was also determined by flow cytometry. The relative nm23-H1 mRNA expression level was measured by real-time quantitative PCR. RESULTS: The apoptotic rates in VPA 1.5 mmol/L+DCA 1.5 μmol/L group (early: 33.58%±3.88%; late: 31.52%±4.20%) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (early: 42.61%±4.23%; late: 38.01%±3.86%), the percentages of the cells in G0/G1 phase in VPA 1.5 mmol/L+DCA 1.5 μmol/L group (61.55%±2.38%) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (66.75%±2.48%), and the relative nm23-H1 mRNA expression levels in VPA 1.5 mmol/L +DCA 1.5 μmol/L group (1.84±0.46) and VPA 1.5 mmol/L+DCA 3.0 μmol/L group (3.02±0.36) were all significantly higher than those in the corresponding concentrations of single drug treatment groups (P<0.01). CONCLUSION: Synergistic effect of VPA and DCA on apoptosis and cell cycle arrest in gastric cancer MGC-803 cells is possibly via inactivation of nm23-H1 gene expression. 相似文献
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AIM: To investigate the effects of resveratrol on the L-type calcium current in isolated guinea pig ventricular myocytes. METHODS: The whole cell patch clamp method was used. RESULTS: （1）Resveratrol (1, 50, 100 μmol/L) reduced the ICa-L by 18.31%±3.15%, 56.20%±2.50% and 84.51%±4.01% in a concentration-dependent manner (n=5, P<0.05). But it has no change on I-V shape of ICa-L. (2) 8Br-cGMP (100 μmol/L), an activator of protein kinase G(PKG), deduced the density of ICa-L by 10.50%±1.11%. Applying resveratrol and 8Br-cGMP simultaneously decreased the ICa-L significantly by 87.58%±3.49％ (n=6, P<0.05). (3) 5 μmol/L H8, a PKG inhibitor, inhibited the decrease in ICa-L caused by resveratrol. CONCLUSION: Resveratrol inhibits ICa-L in guinea pig ventricular myocytes, and this inhibitory effect involves the PKG pathway. 相似文献
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LIU Lu-yu WANG Yan-ping WANG Lin-xi LIU Xiao-ying TANG Li LIU Xiao-hong LIU Li-bin 《园艺学报》2010,26(8):1540-1544
AIM: To investigate the effects of oxidative damage on the expression of endoplasmic reticulum stress-related proteins in human umbilical vein endothelial cells (HUVECs) exposed to tert-butylhydroperoxide (t-BHP). METHODS: HUVECs were cultured in DMEM medium with 10％FBS and induced by t-BHP at concentrations ranging from 25 to 400 μmol/L for 1-24 h. MTT assay was used to measure the cell viability after treatment with t-BHP. The apoptotic rate was evaluated by fluorescence microscopic analysis with Hoechst/PI staining. The endoplasmic reticulum stress-related proteins were detected by Western blotting.RESULTS: Under the conditions of exposure to t-BHP at concentrations ranging from 25 to 400 μmol/L for l-24 h, the viabilities of HUVECs were gradually reduced in dose-dependent and time-dependent manners. The results of Hoechst/PI staining showed that the ratio of apoptotic cells was increased gradually under the conditions of exposure to t-BHP at concentrations of >25 μmol/L for 8 h. The upregulations of several ER stress-related proteins, including inositol requiring enzyme 1α (IRE1α), an ER transmembrane protein kinase/endoribonuclease, and phospho-c-Jun NH2-terminal kinase (p-JNK), a downstream effector protein of ER stress, and subsequently, caspase-3 were observed by Western blotting. CONCLUSION: The results suggest that oxidative stress mediates apoptosis in HUVECs, which might be correlated to the expression of endoplasmic reticulum stress-related proteins. 相似文献
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AIM: To observe the effects of oxygen free radical (OFR) and captopril on the level of asymmetric NG, NG-dimethyl-L-arginine (ADMA) in human vascular endothelial cells (HUVECs).METHODS: HUVECs of 3-6 th passage, cultured with modified Jaffes’ method, were used in the experiment and divided into three groups: (1)Cells cultured with equivalence of DMEM medium as control; (2)OFR intervention groups, OFR at concentrations of 0.01 mmol/L, or 0.1 mmol/L, respectively, were added to the cell culture; (3)Drug intervention groups: the cell culture was treated with 0.1 mmol/L of OFR combined with 50 mg/L or 100 mg/L of captopril, respectively. Concentrations of ADMA, L-arginine, nitric oxide(NO), endothelin(ET) and the activity of angiotensin-converting enzyme(ACE) in conditioned medium were measured after 24 h exposure. RESULTS: Concentrations of ADMA, ET and the activity of ACE were increased, while the amount of NO decreased in OFR intervention groups compared with control group. After treatment with captopril, ADMA, ET concentrations and the activity of ACE were decreased, while the amount of NO increased, but the level of L-arginine had no obvious change. CONCLUSIONS: OFR induces endothelial dysfunction through increasing ADMA concentration, while captopril relieves endothelial dysfunction induced by ox-LDL through decreasing ADMA concentration. 相似文献
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YANG Jin-xia MA Yue MU Shi LIU De-qing LIANG Chun-hong XU Chang-qing ZHNAG Zhuo-ran 《园艺学报》2009,25(10):1903-1906
AIM: To study the effects of exogenous spermine on human umbilical veins endotheliocytes (HUVECs) and to explore its possible mechanism. METHODS: The serial subculture of HUVECs was used to investigate the effect of exogenous spermine with different concentrations (50 μmol/L-5 mmol/L) on HUVECs in different times (2 h, 4 h). The morphological changes of HUVECs (by inverted microscope and electron microscope), the cell viability, the level of MDA and activity of SOD were observed. RESULTS: Compared to normal control group, no change of all index detected in the group with spermine (50 μmol/L) was observed (P>0.05). Spermine injured HUVECs in a concentration-dependent manner. After adding spermine for 2 h and 4 h, it was observed that cellular injury in 4 h group was more serious than that in 2 h group. The injury of HUVECs caused by exogenous spermine was characterized by decrease in cellular viability and activity of SOD, ultrastructural injury, increase in MDA level. CONCLUSION: Exogenous spermine induces the injury of HUVECs in concentration and time-dependent manners. Its mechanisms may be related to lipid peroxidation induced by increase in the production of oxygen free radical. 相似文献
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AIM: To probe into the role of 1, 4, 5-trisphosphate inositol (IP3) and survivin protein in apoptosis of HepG2 cells induced by genistein. METHODS: HepG2 cells were treated with 60 μmol/L genistein for 12 h, 24 h, 48 h and 72 h. IP3, survivin and apoptosis rate were assayed by IP3-［3H］ Birtrak assay, Western blotting and flow cytometry, respectively. RESULTS: IP3 in groups incubated for 12 h, 24 h, 48 h and 72 h with 60 μmol/L genistein were significantly lower than that in control (P<0.01) ［(12.0±1.4) pmol/106cells, (7.5±0.8) pmol/106 cells, (5.6±0.5) pmol/106cells, (3.3±0.6) pmol/106 cells， vs (29.2±0.6) pmol/106 cells］. V-survivin/ V-β-actin, which was the gray degree multiply area of survivin/the gray degree multiply area of β-actin in groups incubated for 12 h, 24 h, 48 h and 72 h with 60 μmol/L genistein, were significantly lower than that in control (P<0.01) ［（0.36±0.13, 0.33±0.03, 0.23±0.04, 0.18±0.04）， vs 0.63±0.06］. The apoptosis rate in groups incubated with 60 μmol/L genistein for 24 h, 48 h and 72 h was significantly higher than that in control （P<0.01） ［(7.4%±0.5%, 20.5%±2.0%, 30.7%±1.6%) vs 2.6%±0.1%］. CONCLUSION: Genistein induces apoptosis in HepG2 cells by reducing IP3 production and survivin protein expression. 相似文献
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AIMTo investigate the roles of protein phosphatase 4 (PP4) in down-regulation of endothelial nitric oxide synthase (eNOS) Ser633 phosphorylation induced by palmitic acid (PA). METHODSHuman umbilical vein endothelial cells (HUVECs) were treated with PA at 25 μmol/L, 50 μmol/L, 100 μmol/L and 200μmol/L for 36 h, or treated with PA at 100 μmol/L for 12 h, 24 h, 36 h and 48 h. Protein phosphatase 2A (PP2A) family inhibitor fostriecin (FST, 20 nmol/L) or okadaic acid (OA, 5 nmol/L) was selected to pretreat the HUVECs for 30 min. Protein phosphatase 4 catalytic subunit (PP4c) siRNA or protein phosphatase 2A catalytic subunit (PP2Ac) siRNA was transfected into the HUVECs. The protein expression levels of of eNOS, PP4c and PP2Ac, as well as the level of eNOS Ser633 phosphorylation, were detected by Western blot. The intracellular nitric oxide (NO) content was measured by DAF-FM DA. RESULTS(1) Compared with control group, the levels of eNOS Ser633 phosphorylation were decreased in PA groups in which the HUVECs were treated with 25 μmol/L, 50 μmol/L, 100 μmol/L and 200 μmol/L PA for 36 h (P< 0.05) and 100 μmol/L PA for 24 h, 36 h and 48 h (P< 0.05). No significant difference in the level of total eNOS protein expression among all the groups was observed. (2) Compared with control group, both FST and OA pretreatment reversed the reduction of eNOS Ser633 phosphorylation (P< 0.05) and the decrease in intracellular NO content (P< 0.05) induced by PA. No significant difference in the level of total eNOS protein expression among all the groups was observed. (3) Compared with si-Control group, the PP4c protein expression was significantly reduced (P< 0.05), while the level of eNOS Ser633 phosphorylation was significantly increased in si-PP4c group (P< 0.05). Although the levels of PP2Ac protein expression declined significantly (P< 0.05), the level of eNOS Ser633 phosphorylation remained unchanged in si-PP2Ac group. No significant differencein the level of total eNOS protein expression among all the groups was found. CONCLUSION PA significantly reduces the level of eNOS Ser633 phosphorylation and the content of NO in the HUVECs, which may be due to PA inducing the activation of the PP2A family member PP4 rather than PP2A. 相似文献