首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM: To observe the change of subunit of NADPH oxidation enzyme complex nox-1 protein in cardiocyte hypoxia-reoxygenation injury and the role of cardiotrophin-1.METHODS: Cardiomyocytes from the hearts of 1-3 d old neonatal rats were prepared by a modified method. Five groups were included in the study: control; hypoxia/reoxygenation; hypoxia/reoxygenation+CT-1; CT-1+hypoxia/reoxygenation+LY294002 (PIK3/Akt inhibitor); CT-1+hypoxia/reoxygenation+PD98059 (ERK inhibitor); CT-1+hypoxia/reoxygenation+DMSO. The concentration of CT-1 was 10 μg/L. The survival rate of myocytes was evaluated by MTS method. Apoptosis, mitochondrial permeability transition pore (Δψm) and reactive oxygen species (ROS) were detected by flow cytometry. Nox-1 protein was determined by Western blotting.RESULTS: Apoptosis of cardiomyocytes and the level of ROS (19.7%±1.4% vs 2.1%±0.5%, 14.07%±1.25% vs 3.54%±0.86%, P<0.05) increased markedly after hypoxia/reoxygenation, but cardiomyocyte survival rate and the level of Δψm (40.55%±4.25% vs 86.28%±7.15%, P<0.01) decreased significantly. The expression of nox-1 protein was upregulated markedly. With CT-1 intervention, cardiomyocyte survival rate increased markedly, apoptosis, both ROS and expression of nox-1 protein reduced significantly. The level of Δψm increased obviously. The effect of CT-1 was inhibited by LY294002. No significant effect was observed on cells survival in DMSO group, which confirmed that LY294002 was specifically involved in blocking the protective effect of CT-1.CONCLUSION: The expression of subunit of NADPH oxidation enzyme complex nox-1 protein is upregulated markedly in cardiocyte hypoxia-reoxygenation injury. CT-1 protects cardiac cells against hypoxia-reoxygenation injury by downregulating the expression of nox-1 protein to decrease the level of ROS.  相似文献   

2.
AIM:To observe the effects of high hydrostatic pressure on asymmetric NG, NG-dimethyl-L-arginine (ADMA) metabolism of human vascular endothelial cells (HUVECs), and the role of renin-angiotensin system (RAS). METHODS:Cultured HUVECs of 3-6th passage were exposed to atmosphere (0 mmHg, APC), 120 mmHg (MPC), 180 mmHg (HPC). There were three groups in each pressure condition, one as control, the other two were interfered with captopril （Cap, 10 μmol/L or 100 μmol/L） or irbesartan （Irb, 10 μmol/L or 100 μmol/L） respectively. Cell proliferation was quantified by determining hexosaminidase activity at 12 h. Concentration of ADMA in conditioned medium was measured by high performance liquid chromatography (HPLC) at 12 h. RESULTS:Compared with APC group, ADMA concentration increased prominently in MPC and HPC (4.69±0.37 and 4.48±0.39 vs 0.75±0.05，P<0.01), but no difference was found between MPC and HPC group. ADMA concentration was not influenced by Cap and Irb in APC, but obviously reduced in MPC and HPC in a dose-dependent manner. CONCLUSION:ADMA is upregulated by high hydrostatic pressure and RAS is involved.  相似文献   

3.
AIM: The purpose of the present study was to investigate the effect of interleukin-10 (IL-10) on the proliferation and calcineurin (CaN) activity in cultured cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP).METHODS: The CFs of left ventricle in neonatal Sprague-Dawley rats were isolated and cultured by trypsin digestion and selective plating technique. Then the proliferation rates of cells were determined by using the MTT ［3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide］ assay (A490 value). Cell cycle distribution was determined with flowcytometry technique. The CaN activity was measured by ultra-violet spectrophotography.RESULTS: (1) MTT colorimetry showed that 10-7 mol/L AVP significantly increased A490 value of CFs in comparison with control group (P<0.01). IL-10 attenuated the A490 value of AVP group in a concentration dependent manner. The A490 value of the 10-8, 10-7, 10-6, 10-5 g/L IL-10+10-7 mol/L AVP groups was 0.201±0.007, 0.187±0.006, 0.173±0.010 and 0.157±0.029 respectively, all data significantly lower than those in the presence of AVP alone (P<0.05 or P<0.01). (2) The percentage of the cells in S stage and proliferation index were markedly increased in 10-7mol/L AVP group compared with the control (P<0.01, respectively). In the 10-6 g/L IL-10+10-7 mol/L AVP group, the percentage cells in S stage and proliferation index were significantly lower than those in AVP group (P<0.01, respectively). IL-10 itself had no effect on fibroblast proliferation, but reduced AVP-induced fibroblast proliferation. (3) There was a significantly increase in CaN activity in AVP group compared with control (P<0.01). In the 10-8, 10-7, 10-6 and 10-5 g/L IL-10＋10-7 mol/L AVP groups, the CaN activity was 3.22±0.04, 3.06±0.06, 2.53±0.04 and 2.22±0.04, respectively. IL-10 dose-dependently down-regulated the CaN activity induced by AVP (P<0.01, respectively). However, the CaN activity was still higher in IL-10+AVP group than that in control group (P<0.05 or P<0.01).CONCLUSION: Our data indicate that IL-10 regulates the CaN activity of CFs in the cell proliferation induced by AVP, suggesting that IL-10 plays a role in the regression of cardiac remodeling.  相似文献   

4.
AIM: To explore the anticancer function of Shp2 in lung adenocarcinoma A549 cells and the related molecular mechanisms. METHODS: The viability and proliferation of A549 cells treated with Shp2 specific inhibitor Phps-1 or cisplatin (DDP) were measured by CCK-8 assay and EdU assay. Annexin V-FITC/PI double staining was applied to detect apoptotic rate of A549 cells with different interventions. The protein levels of caspase-3-17p, Bcl-2, Bax, p-STAT3/STAT3 and p-ERK/ERK were determined by Western blot. RESULTS: Compared with control group, Phps-1 at the concentration of 20 μmol/L significantly increased the viability of A549 cells after 24 h of treatment (P<0.05). Meanwhile, the proliferation rate of A549 cells in Phps-1 20 μmol/L group was significant increased compared with control group (P<0.05). The apoptotic rate of A549 cells in DDP treatment group decreased from 13.01%±2.62% to 3.67%±0.93% after adding Phps-1 (P<0.05). Phps-1 down-regulated the protein levels of caspase-3-17p, Bax and p-ERK, but up-regulated p-STAT3.CONCLUSION: Shp2 is a tumor suppressor in A549 cells, which may be associated with the activation of STAT3 signal pathway.  相似文献   

5.
  相似文献   

6.
AIM: To determine whether chronic hypercholesterolemia affects ionic currents on cardiac ventricular myocytes of rats. METHODS: Whole-cell patch-clamp technique was used to record the ionic currents in single cardiac myocytes isolated from normal cholesterolemia and hypercholesterolemia rats. RESULTS: In the hypercholesterol group (group Ⅱ), serum total-cholesterol level was significantly higher than that of normal group (group Ⅰ) ［(3.10±0.62)mmol·L-1 vs (1.18±0.37)mmol·L-1, P<0.01, n=20］. The serum triglyceride content of group II was remarkably higher than that of group Ⅰ ［(1.51±0.30)mmol·L-1 vs (0.43±0.15)mmol·L-1, P<0.01, n=20］. In ventricular myocytes of rats, 50% repolarization of action potential duration (APD50) prolonged from (70.86±8.12)ms (group Ⅰ) to (116.16±6.90)ms (group Ⅱ) (n=10 in each group, P<0.01); APD90 prolonged from (95.10±7.27)ms (group Ⅰ) to (144.04±7.39)ms (group Ⅱ) (n=10 in each group, P<0.01); at the test potential of -120 mV, Ik1 increased from (-16.98±4.54) pA/pF(group Ⅰ) to (-19.92±4.08) pA/pF (group Ⅱ) (n=12 in each group, P<0.05); at the test potential of 0 mV, ICa-L decreased from (-8.56±1.29) pA/pF (group Ⅰ) to (-5.24±0.90) pA/pF (group Ⅱ) (n=10 in each group, P<0.01); at the test potential of +60 mV, Ito decreased from (13.20±1.97) pA/pF (group Ⅰ) to (10.30±1.97) pA/pF (group Ⅱ) (n=8 in each group, P<0.05). CONCLUSION: Hypercholesterolemia affects the ionic currents on cardiomyocytes of rats greatly, which may be the ionic mechanism of cardiac toxicity induced by hypercholesterolemia.  相似文献   

7.
AIM: To observe the inhibition effects of 10-23 deoxyribozyme (DNAzyme) specific to human proliferating cell nuclear antigen (PCNA) gene on the proliferation of human umbilical artery smooth muscle cells (HUASMC) in vitro. METHODS: Using lipofectamine (Lip)-mediated method, the DNAzyme specific to PCNA was introduced into HUASMC. ［3H］-TdR incorporation was determined. The cell proliferation was examined by MTT assay and cell cycle was detected by flow cytometry. RESULTS: ［3H］-TdR incorporation in 1.0 μmol/L DNAzyme group was lower than that in control group (P<0.05) at 2 days after transfection. Compared with control group, the A value of MTT cholorimetric analysis decreased in 1.0 μmol/L DNAzyme group and antisense oligodeoxynucleotide (ASODN) group, at 2, 3 and 5 days after transfection significantly (P<0.01). The decrease in A value showed a dose-dependent manner within the experimental range at 5 days. After 2 days, the percentage of quiescence cells (G0/G1) was 73.8%, 54.7% and 41.1% in DNAzyme, ASODN and control groups, respectively. CONCLUSION: The DNAzyme specific to PCNA suppresses the proliferation of HUASMC effectively in vitro.  相似文献   

8.
AIM: To investigate the effects of cardiotrophin 1 (CT-1) on differentiation of swine bone marrow mesenchymal stem cells (MSCs) into cardiomyocyte-like cells in vitro.METHODS: MSCs were isolated and proliferated from Tibet miniswine. Adipogenic and osteogenic potentials were identified. MSCs were divided into 4 groups for induction: untreated group, 5-azacytidine (5-Aza) group,CT-1 group and 5-Aza combined with CT-1 group. After induction for 4 weeks, the expression of cardiac cell markers including α-actin and cardiac troponin-T (cTnT) was estimated by immunofluorescence staining. Finally, the rates of red fluorescence positive-staining cells were calculated. RESULTS: The expression of α-actin in the 4 groups by red fluorescence staining was as follows: the differentiation rate of cardiomyocyte-like cells in combination group was 29.90%±4.76%, significantly higher than that in 5-Aza group (17.73%±2.34%, P<0.01), CT-1 group (6.63%±0.55%, P<0.01) and untreated group (1.62%±0.09%, P<0.01). The differentiation rate in 5-Aza group was significantly higher than that in CT-1 group (P<0.01) and untreated group (P<0.05). The differentiation rate in CT-1 group was significantly higher than that in untreated group (P<0.01). The expression of cTnT in the 4 groups was as follows: the differentiation rate of cardiomyocyte-like cells in combination group was 36.50%±4.09%, significantly higher than that in 5-Aza group (14.37%±1.65%, P<0.01), CT-1 group (7.50%±0.61%, P<0.01) and untreated group (1.12%±0.23%, P<0.01). The differentiation rate in 5-Aza group was significantly higher than that in CT-1 group (P<0.01) and untreated group (P<0.01). The differentiation rate in CT-1 group was significantly higher than that in untreated group (P<0.01).CONCLUSION: Appropriate concentrations of 5-Aza (10 μmol/L) and CT-1 (0.1 μg/L) induce swine bone marrow MSCs to differentiate into cardiomyocyte-like cells in vitro. CT-1 combined with 5-Aza significantly increases the differentiation rate.  相似文献   

9.
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   

10.
AIM: To compare the evaluations for the structure and function of the hypertrophic hearts induced by volume overload or pressure overload in rats. METHODS: Volume overload-induced cardiac hypertrophy was established by abdominal aortacaval fistula (ACF) and pressure overload-induced cardiac hypertrophy was developed by constriction of aorta (CA). The cardiac structure and function were analyzed by echocardiography, hemodynamic determination, heart weight measurement and histological examination. RESULTS: Heart weight of rats in all the operated groups was increased compared to the sham-operated groups. In 1-week ACF group, the internal diameter ［(0.67±0.03)cm vs (0.60±0.02)cm, P<0.01］ and volume of left ventricle increased ［(0.69±0.10)mL vs (0.50±0.04)mL, P<0.01］，relative wall thickness (RWT) decreased (0.46±0.05 vs 0.55±0.05, P<0.01), compared with the sham-operated group. In 1-week CA group, interventricular septal thickness ［(0.20±0.03)cm vs (0.16±0.02)cm, P<0.05］, left ventricular posterior wall thickness ［(0.20±0.03)cm vs (0.16±0.02)cm, P<0.01］, RWT (0.71±0.17 vs 0.56±0.12, P<0.05) and +dp/dtmax (4 886±1 304 vs 3 674±325, P<0.05) were all increased compared with the sham-operated group. In 2-week-groups, these parameters changed more significiantly. CONCLUSION: Cardiac structure and function could be evaluated by echocardiography and hemodynamic determination. RWT is a sensitive index for the cardiac hypertrophy induced by both volume overload and pressure overload.  相似文献   

11.
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   

12.
AIM: To investigate the effect of mycophenolic acid (MPA) alone or in combination with anti B7-1 mAb on proliferation of T lymphocytes and the possible mechanisms. METHODS: The proliferation of T lymphocytes was detected by BrdU incorporation method. The expressions of IL-2, IFN-γ and IL-10 in mRNA and protein levels were detected by RT-PCR and ELISA, respectively. RESULTS: (1) MPA markedly inhibited the T lymphocyte proliferation as compared with control (P<0.01). (2) MPA significantly inhibited the levels of IL-2 and IFN-γ (42.73 ng/L±14.64 ng/L vs 99.70 ng/L±9.15 ng/L, P<0.01; 7.87 ng/L±4.22 ng/L vs 82.42 ng/L±25.55 ng/L, P<0.05), and significantly increased content of IL-10 compared with control (770.95 ng/L±126.85 ng/L vs 545.71 ng/L±22.45 ng/L, P<0.05). MPA in combination with anti B7-1 mAb obviously enhanced the content of IL-10 compared with MPA alone (941.90 ng/L±56.61 ng/L vs 770.95 ng/L±126.85 ng/L, P<0.05). (3) The expression levels of IL-2 and IFN-γ mRNA in the MPA group were obviously lower than those in control (0.74±0.10 vs 1.17±0.15, 0.52±0.05 vs 0.75±0.12, P<0.01). MPA in combination with anti-B7-1 mAb showed a statistically significant increase in IL-10 mRNA expression (1.28±0.06 vs 0.84±0.09, P<0.01) as compared with MPA alone. CONCLUSION: MPA induces the changes of cytokine expressive spectrum and the Th1 and Th2 shift might be involved in the immunosuppressive effect. The combination of MPA with anti B7-1 mAb might have a synergic effect.  相似文献   

13.
AIM: To investigate the effect of Jagged1 expression in endothelial cells (EC) on platelet derived growth factor (PDGF) induced proliferation and migration of vascular smooth muscle cells (VSMC) in rat.METHODS: Rat aorta EC was inoculated in the lower chamber and VSMC were in the upper chamber of the cell coculture system. Three groups were divided: control, sicontrol and siJagged1. The EC Jagged1 protein expression was assayed by Western blotting to evaluate small RNA interfering (RNAi) efficiency. After the cells were cocultured with PDGF for 24 h, the proliferation and migration of VSMC were respectively evaluated by ［3H］-TdR incorporation and migrating cells counting. Protein expression of α-SM-actin in VSMC was assayed by Western blotting. RESULTS: The Jagged1 protein expression in EC was significantly lower in siJagged1 group than that in control group (0.26±0.02 vs 0.67±0.02, P<0.05), and no statistic significance was observed between control and sicontrol groups. The VSMC ［3H］-TdR incorporation and migration were higher in PDGF +siJagged1 group than those in PDGF group {［3H］-TdR incorporation (23 074±2 702) counts·min-1·well-1 vs (16 442±1 803)counts·min-1·well-1, n=5, P<0.05; migration (27±4) cells/field vs (15±3)cells/field, n=5, P<0.05}. The α-SM-actin protein in VSMC was lower in PDGF + siJagged1 group than that in PDGF group (0.25±0.06 vs 0.49±0.04, n=3, P<0.05).CONCLUSION: Jagged1 knock down in rat EC accelerates PDGF induced proliferation and migration of VSMC. These results suggest that Jagged1 expression in EC plays an important role in maintaining VSMC contract phenotype and inhibiting VSMC overgrowth after arterial injury.  相似文献   

14.
AIM: To observe the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) in the proliferation, released cytokines and expression of collagen Ⅰ and Ⅲ in rat cardiac fibroblasts induced by angiotensin Ⅱ (AngⅡ) or electrical field stimulation (EFS).METHODS: The cultured cardiac fibroblasts were isolated from the neonatal rats of 1-3 days and used in the 3rd passage. The cells were divided into 10 groups: control group, 0.1 μmol/L AngⅡ group, 0.1 μmol/L AngⅡ+0.5 μmol/L KN92 group, 0.1 μmol/L AngⅡ+0.5 μmol/L KN93 group, 0.1 μmol/L AngⅡ+0.5 μmol/L AIP group; 10V 1.0 Hz EFS group, 10 V 1.0 Hz EFS+0.5 μmol/L KN92 group, 10 V 1.0 Hz EFS+0.5 μmol/L KN93 group, 10 V 1.0 Hz EFS+0.5 μmol/L AIP group, 10 V 1.0 Hz EFS+0.1 μmol/L AngⅡ group.MTT was used to detect the proliferation of cardiac fibroblasts. The release of cytokines was measured by ELISA. The mRNA expression of TNF-α, TGF-β1 and collagen Ⅰ, Ⅲ was determined by RT-PCR.RESULTS: CaMKⅡ inhibitors (0.5 μmol/L KN93 or 0.5 μmol/L AIP) prevented the proliferation and the increase in the expression of TGF-β1 and TNF-α in cardiac fibroblasts induced by AngⅡ (0.1 μmol/L) or EFS (10 V 1.0 Hz). CaMKⅡ inhibitors (0.5 μmol/L AIP or 1.0 μmol/L AIP) also prevented the increase in mRNA expression of collagen Ⅰ and Ⅲ induced by 0.1 μmol/L AngⅡ. CONCLUSION: Inhibition of CaMKⅡ prevents the proliferation of cardiac fibroblasts induced by AngⅡ or EFS. The possible mechanism of CaMKⅡ inhibitors may be involved in preventing the mRNA expression and release of cytokines (TGF-β1 and TNF-α), and regulating collagen I and III expression.  相似文献   

15.
AIM: To investigate the effect of urotensinⅡ (UⅡ) on the proliferation of cultured rat pulmonary arterial smooth muscle cells (PASMCs), and to explore whether mitogen-activated protein kinase (MAPK) signaling pathways and early growth response factor-1 (Egr-1) involved in the regulation of the PASMCs proliferation stimulated by UⅡ. METHODS: The rat PASMCs were isolated and cultured in vitrowith explant culture technique. The proliferation of cultured PASMCs stimulated by different doses of UⅡwas detected by BrdU incorporation. The mRNA expression of extracellular signal-regulated kinase 1/2 (ERK1/2), stress-activated protein kinase (SAPK), p38 MAPK and Egr-1 in cultured PASMCs treated with UⅡ, UⅡ-specific antagonist urantide, and ERK1/2 inhibitor PD98059 was detected by real-time PCR. The protein levels of phosphorylated ERK1/2 (p-ERK1/2), p-SAPK, p-p38 and Egr-1 in cultured PASMCs were determined by Western blotting. RESULTS: UⅡ at concentrations of 1 μmol/L, 0.1 μmol/L and 0.01 μmol/L increased the proliferation of cultured PASMCs in a dose-dependent manner (P<0.01 or P<0.05), with the maximal effect at a concentration of 1 μmol/L. However, urantide inhibited the promotion effect of UⅡ on PASMC proliferation (P<0.05). UⅡ up-regulated the mRNA expression of ERK1/2, SAPK and Egr-1 (P<0.01 or P<0.05), but not the p38 MAPK. However, the up-regulatory effect of UⅡ on ERK1/2 and Egr-1 expression was inhibited by PD98059 and/or urantide (P<0.01 or P<0.05). UⅡ also increased the protein levels of p-ERK1/2, p-SAPK and Egr-1 (P<0.01 or P<0.05), but the promotion effect was also inhibited by PD98059 and/or urantide (P<0.01 or P<0.05).CONCLUSION: UⅡ increases the proliferation of PASMCs, and U Ⅱand Egr-1 participates in UⅡ-mediated proliferation of cultured PASMCs through activation of ERK1/2 signal pathway.  相似文献   

16.
AIM: To investigate the roles of intermedin1-53 (IMD1-53) and exteracellular signal-regulated kinase (ERK) signal pathway in the proliferation of rat cardiac fibroblasts (CFBs).METHODS: Isolated and cultured CFBs from new born SD rats were randomly divided into control group, aldosterone (ALD) groups (at different concentrations) and ALD+IMD groups (IMD at different concentrations). The viability of CFBs was determined by MTT assay. Western blotting was used to observe the effect of IMD on ALD-induced ERK phosphorylation.RESULTS: IMD1-53 had no significant effect on the proliferation of CFBs in basal state, but inhibited the CFBs growth stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner. IMD1-53 also inhibited ERK phosphorylation stimulated by ALD in a concentration (10-9~10-7 mol/L)-dependent manner.CONCLUSION: IMD1-53 inhibits the proliferation of CFBs by ERK signal pathway.  相似文献   

17.
AIM: To test the effect of ERK1/2 on ischemic preconditioning (IPC) in diabetic rat hearts. METHODS: The diabetic rat model was made with alloxan. After eight weeks, 24 rats were divided into 4 groups: non-diabetic IPC rats (group A); non-diabetic non-IPC rats (group B); diabetic IPC rats (group C); diabetic non-IPC rats (group D). ECGⅡ lead, left ventricular development pressure (LVDP), and first derivative of LVDP (±dp/dtmax) were recorded. Myocardial phosphorylation of extracellular signal regulated kinases1/2 (ERK1/2) was detected by Western-blotting. RESULTS: (1) The ventricular arrythmia score was significantly lower in group A than that in group C (P<0.01). (2) LVDP and +dp/dtmax % were significantly higher in group A than those in group B and group C (P<0.01). -dp/dtmax% was significantly higher in group A than that in group B. (3) Phosphorylation of myocardial ERK1/2 was significantly higher in group A than those in group B and group C. CONCLUSIONS: IPC reduced the severity of ischemia/rerperfusion- induced arrhythmias, improved cardiac function in non-diabetic rats. However, such beneficial effects of IPC were not observed in diabetic rats. The attenuation of cardioprotection by IPC in diabetic animals may be due to the decrease in the activation of myocardial ERK1/2.  相似文献   

18.
  相似文献   

19.
  相似文献   

20.
AIM: To investigate the potential role of Src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) in the proliferation of cardiac fibroblasts induced by angiotensin Ⅱ (Ang Ⅱ). METHODS: The neonatal rat cardiac fibroblasts were separated by trypsin digestion. The cardiac fibroblasts were identified by vimentin of immunochemical staining. The proliferation of the cardiac fibroblasts with or without Ang Ⅱ stimulation was measured by MTT assay. Adenoviruses containing SHP-2 gene were transfected into cardiac fibroblasts to overexpress SHP-2. SHP-2 was inhibited by its inhibitor NSC-87877. RESULTS: The proliferation of the cardiac fibroblasts was increased in a dose-dependent manner by the stimulation of Ang Ⅱ and the maximum concentration of Ang II for cell proliferation was 10-7 mol/L. SHP-2 promoted the proliferation of cardiac fibroblasts under the stimulation of Ang Ⅱ. The proliferation rate in mutant group was higher than that in wild-type group (P<0.01). Inhibition of SHP-2 by NSC-87877 attenuated the proliferation. CONCLUSION: The growth promoting effect of Ang Ⅱ on cardiac fibroblasts is regulated by SHP-2.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号