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 glycated serum albumin on expression of MCP-1 in cultured human umbilical vein endothelial cells

AIM: To investigate the effects of glycated serum albumin (GSA) on the expression of monocyte chemoattratant protein-1 (MCP-1) in endothelial cells.METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured with GSA at different concentrations in the presence or absence of glycosylation-product inhibitor aminoguanidine (AG) and anti-oxidant N-acetylcysteine (NAC). The expression of MCP-1 was evaluated by the methods of immunocytochemistry and sandwich ELISA.Malondialdehyde(MDA) content and superoxide dismutase(SOD) activity were determined by the technique of thiobarbituric acid(TBA) and xanthine oxidase(XOD),respectively. RESULTS: GSA stimulated HUVECs to produce and release MCP-1. After HUVECs were treated with 50 mg/L GSA, the expression of MCP-1 at 4 h, 8 h and 12 h was 1.3, 1.9 and 2.8 folds higher than that in control group (P<0.01), respectiuely.The significant difference among the experiment groups (P<0.01) was observed, indicating that GSA took effect in a concentration-dependent manner. The release of MCP-1 in cultured supernatants in the experiment groups with 3 different concentrations of GSA was 1.6, 2.4 and 3.0 folds as much as that in control group (P<0.01), and the significant difference among the experiment groups (P<0.01) was also observed. GSA decreased the activity of SOD (P<0.05) and increased the content of MDA (P<0.01). AG and NAC obviously inhibited the upregulation of MCP-1 expression in HUVECs by GSA (P<0.01). NAC also inhibited the effect of GSA on SOD activity and MDA content in HUVECs (P<0.05). CONCLUSION: GSA stimulates the expression of MCP-1 by inducing oxidative stress in endothelial cells.     

Effect of peroxisome proliferator activated receptor δ on mRNA expression of MCP-1 induced by homocysteine in cultured human umbilical vein endothelial cells

AIM: To investigate the effects of peroxisome proliferator activated receptor δ (PPARδ) on the mRNA expression of monocyte chemoattractant protein 1 (MCP-1) induced by homocysteine (Hcy) in human umbilical vein endothelial cells (HUVECs). METHODS: Collagenase was used to isolate endothelial cells from human umbilical vein, and the cells were cultured in vitro . The HUVECs were divided into blank control group, Hcy group, GW0742 (a specific agonist of PPARδ) group and diphenyleneiodonium (DPI,a specific inhibitor of NADPH oxidase) group. RT-PCR was used to examine the mRNA expression of MCP-1 and PPARδ. The protein level of PPARδ was detected by Western blotting.2',7'-Dichlorofluorescin diacetate(DCFH-DA) was added to monitor intracellular production of reactive oxygen species (ROS). RESULTS: Compared with control group, Hcy promoted the mRNA expression of MCP-1 in a concentration-dependent manner, and decreased the mRNA expression of PPARδ in HUVECs. The mRNA expression of MCP-1 was significantly elevated by Hcy at the concentration of 10^-5 mol/L, and the mRNA expression of PPARδ was decreased remarkably (P<0.01). GW0742 decreased the mRNA expression of MCP-1 compared with Hcy group (P<0.01). Hcy remarkably increased the production of ROS compared with control group. Hcy-induced production of ROS was also significantly attenuated by GW0742. CONCLUSION: The activation of PPARδ decreases the Hcy-induced mRNA expression of MCP-1 by suppressing Hcy-stimulated production of ROS.     

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).     

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.     

Effect of angiotensin-(1-7) on angiotensin II-induced rat renal interstitial fibroblast activation

AIM: To explore the influence of angiotensin-(1-7) on angiotension II (Ang II)-induced activation and extracellular matrix secretion in rat renal interstitial fibroblasts (NRK-49F cells). METHODS: The NRK-49F cells were maintained and sub-cultured, then the cells were divided into control group, Ang II group, Ang-(1-7) group and Ang II+Ang-(1-7) group. The expression of α-smooth muscle actin(α-SMA),transforming growth factor β₁ (TGF-β₁) and insulin-like growth factor I(IGF-I) was detected by the method of immunocytochemistry when the cells were cultured for 72 h. The content of TGF-β₁, IGF-I and collagen type I(Col I) in the cultured supernatants were measured by ELISA. RESULTS: In control group and Ang-(1-7) group, only basic expression of α-SMA and almost no expression of TGF-β₁, IGF-I and Col I were observed. Compared with control group, the expression of α-SMA, TGF-β₁, IGF-I and Col I was increased in Ang II group. Compared with Ang II group, the expression of α-SMA, TGF-β₁, IGF-I and Col I was significantly decreased in Ang II+Ang-(1-7) group.CONCLUSION: Ang-(1-7) inhibits the activation of renal interstitial fibroblasts and decreases the Ang II induced secretion of Col I by suppressing TGF-β₁ and IGF-I expression.     

Effects of nicotine on the release of t-PA and PAI-1 in cultured human umbilical vein endothelial cells

AIM: To study the effect of nicotine on the release of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in human umbilical vein endothelial cells (HUVECs).METHODS: HUVECs were cultured in 24-well tissue-culture plates and randomly divided into control group and nicotine treatment groups. In nicotine treatment groups, HUVECs were either incubated with nicotine at the concentrations of 0.1, 1, 10 and 100 μmol/L for 12 h, or exposed to 100 μmol/L nicotine for 0 h, 4 h, 6 h, 8 h, 12 h and 24 h. The cells in control group were exposed to the same volume of PBS instead of nicotine at corresponding time points. The supernatants were collected for determining the concentrations of t-PA and PAI-1 by ELISA. RESULTS: (1) Compared with control group, the protein levels of PAI-1 in 100 μmol/L nicotine treatment group increased significantly (P<0.01). No significant difference of t-PA protein among the groups was observed (P>0.05). (2) After stimulated with 100 μmol/L nicotine for 4 h, 6 h, 8 h, 12 h and 24 h, the protein levels of PAI-1 in the cells increased over time and reached the peak at 12 h, which was significantly higher than those in the control cells (P<0.05). However, no significant difference of t-PA protein in these cells was found as compared to the controls (P>0.05).CONCLUSION: Nicotine inhibits the fibrinolytic activity in HUVECs in vitro, thereby damaging the vascular endothelial cells.     

Effect of homocysteine on the apoptosis of cultured human umbilical vein endothelial cells

AIM: To investigate the effect of homocysteine(Hcy) on the apoptosis of endothelial cells (EC). METHODS: First-passaged human umbilical vein endothelial cells (hUVEC) were cultured with M199 containing 3 mmol/L Hcy. hUVEC apoptosis was detected as follow: demonstration of nuclear changes by Hoechst 33258 staining, agarose gel electrophoresis of DNA fragments, detection of apoptotic cells by flow cytometry following Annexin V-PI doubled stain, Western blot for P53 and Bax protein detection and colorimetry detecting caspase-3 activity. RESULTS: Compared with control, homocysteine induced characteristic apoptotic changes in hUVEC. The chromosomal DNA of hUVEC appeared "DNA ladder" by agarose gel electrophoresis. Apoptotic cells were increased significantly (P<0.01, n=3). Hcy promoted the expression of protein Bax, P53 (P<0.01, n=3) and enhanced the activity of caspase 3 (P<0.05, n=3). CONCLUSION: Homocysteine induces apoptosis in cultured hUVEC.     

NF-κB site of promotor mediates nicotine-induced ICAM-1 expression in human umbilical vein endothelial cells

AIM:To study the mechanisms of nicotine-induced expression of intercellular adhesion molecule-1(ICAM-1).METHODS:Related luciferase reporter gene plasmids were constructed with molecular cloning techniques;above plasmids and intracontrol plasmid pSV-β-gal were co-transfected into human umbilical vein endothelial cells(HUVECs) with eukaryotic gene transfection techniques; the relative luciferase activities were detected in the transfected HUVECs.RESULTS:Series of luciferase reporter gene containing different sequences of human ICAM-1 promotor and site-directed mutants of NF-κB and Sp-1 in promotor were successfully constructed; Nicotine could increase the expression of luciferase reporter gene plasmid containing-579 bp(pGL3E-579/+36),-230 bp(pGL3E-230/+36) and mutated Sp-1 version(pGL3E-Sp-1-MU)(P＜0.05 vs control) of ICAM-1 promotor in the transfected HUVECs, whereas deletion derivative (pGL3E-134/+36) and mutation (pGL3E- NF-κB -MU) of downstream NF-κB site of ICAM-1 promotor prevent nicotine-induced increase in expression of luciferase reporter gene plasmid.CONCLUSION:NF-κB site of promotor mediates nicotine-induced ICAM-1 expression in human umbilical vein endothelial cells.     

Effect of lipopolysaccharide on viability and secretion function of human umbilical vein endothelial cells

AIM: To observe the direct effect of lipopolysaccharide (LPS) on secretion of endothelin-1 (ET-1) and nitric oxide by human umbilical vein endothelial cell and cell viability of the secretor. METHODS: The third passage of human umbilical vein endothelial cells were incubated with different concentrations of LPS (1 g/L, 100 mg/L, 10 mg/L, 1 mg/L, 100 μg/L, 10 μg/L, 1 μg/L) for 6 hours, and the culture supernatants were collected. The concentrations of ET-1 were determined by radioimmunoassay, the concentrations of nitric oxide were determined using Greiss's method. The viabilities of cells were measured by MTT method. RESULTS: The concentration of ET-1 (pg/L) of normal control group was 251.64±10.90. The concentrations of ET-1 (pg/L) of LPS treated groups were 220.85±19.14, 278.67±15.45, 306.40±11.60, 312.87±33.50, 324.38±17.02, 291.49±14.30, 282.11±13.38, respectively (each group compared with normal control group, P<0.05 or P<0.01). The concentration of NO_x (μmol/L) of normal control group was 629.46±13.36. The concentrations of NO_x (μmol/L) of LPS treated groups were 732.58±23.21, 669.87±9.32, 661.24±16.80, 650.33±13.24, 606.59±12.94, 626.75±9.83, 627.61±5.61, respectively (each group compared with normal control group, P<0.05 or P<0.01). The viabilities of endothelial cells of LPS treated groups were 74%, 81%, 86%, 88%,91%, 93%, 93%, respectively. CONCLUSION: LPS of lower concentrations had no significantly lethal effect on human umbilical vein endothelial cells, but enhanced secretion of ET-1 and inhibited NO production. LPS in higher concentrations showed significant lethal effect on human umbilical vein endothelial cells, inhibited secretion of ET-1 and enhanced NO production.     

Effects of angiotensin-(1-7) on calcification in vascular smooth muscle cells and its signal transduction pathway

AIM: To clarify the effects of angiotensin-(1-7) on the calcification in rat vascular smooth muscle cells(VSMCs) and its signal transduction.METHODS: Calcification of cultured rat VSMCs was prepared by incubation of VSMCs with β-glycerophosphate.Calcification was confirmed by Von Kossa staining.The cells were treated with angiotensin-(1-7).The calcium content,alkaline phosphatases activity,osteocalcin and Cbfa1 mRNA expression were also measured.RESULTS: Angiotensin-(1-7) inhibited the increases of calcium content,alkaline phosphatases activity（P>0.05）,osteocalcin concentration and Cbfa1 mRNA expression in calcified VSMCs（P<0.05）,and the effects of angiotensin II on calcium content,alkaline phosphatases activity,osteocalcin concentration and Cbfa1 mRNA expression in calcified VSMCs were also inhibited （P<0.05）.Angiotensin-(1-7) increased cAMP concentration in calcified VSMCs（P<0.05）and selective PKA inhibitor blocked the effects of angiotensin-(1-7) on calcium content,alkaline phosphatases activity,osteocalcin concentration and Cbfa1 mRNA expression（P<0.05）.CONCLUSION: Angiotensin-(1-7) can inhibit beta-glycerophosphate-induced calcification in VSMCs through cAMP-PKA-Cbfa1 pathway and antagonize the effect of angiotensin II on calcification in VSMCs.     

Lectin-like oxidized low density lipoprotein receptor-1 mediates expression of MCP-1 induced by ox-LDL in cultured human vascular endothelial cells

AIM: To investigate the effects of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) on the expression of MCP-1 in the cultured human unbilical vein endothelial cells (HUVECs). METHODS: Cultured HUVECs was incubated with ox-LDL, or preincubated with carrageenan and polyinosinic acid. LOX-1 and MCP-1 mRNA and protein were determined by RT-PCR and Western blot. RESULTS: Incubation of HUVECs with ox-LDL (from 0-100 mg/L) for 24 h markedly increased the expression of LOX-1 and MCP-1 (mRNA and protien) in a concentration-dependent fashion. Preincubation of HUVECs with carrageenan and polyinosinic acid, the chemical inhibitors of LOX-1, for 2 h, ox-LDL-mediated upregulation of LOX-1 and MCP-1 was suppressed (P<0.05). CONCLUSION: These findings indicate that ox-LDL upregulates MCP-1 and its own endothelial receptor, and ox-LDL-induced MCP-1 is mediated by the action of LOX-1. LOX-1 plays a critical role in the pathogenesis of atherosclerosis.     

Effect of activated protein C on apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide

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.     

Proliferation and apoptosis of human umbilical vein endothelial cells induced by oxidized low density lipoprotein

AIM:To investigate proliferation and apoptosis of cultured endothelial cell (ECV-304 cell line) induced by varied concentrations of oxidized low density lipoprotein (ox-LDL). METHODS:Cell morphology, Typan blue test, MTT test, LDH release test, flow cytometry and micro-molecular weight DNA fragment gel electrophoresis of apoptosis were used for the detection of the cytotoxic effects of ox-LDL on ECV-304 cell line.RESULTS:0.1, 1, 10 mg/L ox-LDL could promote proliferation of ECV-304 cells. When the concentration of ox-LDL reached up to 100 mg/L and above, the distinct cytotoxic effect appeared. Further study showed that the apoptosis rate of endothelial cells, induced by ox-LDL of 150 mg/L and 200 mg/L for 12 hours, are 15.86% and 21.89%, respectively. 18 h and above hours after incubation, the apoptosis rate began to decrease and rate of necrosis increased. CONCLUSION:ox-LDL has strong cytotoxic effects on endothelial cells and could give rise to different pathologic process, such as proliferation, apoptosis prophase, apoptosis and necrosis.     

Effect of oxidized LDL on expression of connexin43 in cultured human umbilical vein endothelial cells

AIM: To investigate the effect of oxidized LDL (ox-LDL) on the expression of gap junction protein connexin43 in cultured human umbilical vein endothelial cells (HUVECs) in vitro. METHODS: Human umbilical vein endothelial cells cultured in normal condition were divided into blank control group, 50 mg/L,100 mg/L and 200 mg/L ox-LDL intervention groups. The mRNA expression of connexin43 in cultured HUVECs was detected with RT-PCR method; while the protein level of connexin43 was determined by the method of immunocytochemistry in the control and 100 mg/L ox-LDL intervention groups 24 h after ox-LDL was given. RESULTS: Different concentrations (50 mg/L, 100 mg/L, 200 mg/L) of ox-LDL up-regulated mRNA expression of connexin43 in cultured HUVECs after 24 h intervention (P<0.01). The protein level of connexin43 in cultured HUVECs intervened with 100 mg/L Ox-LDL for 24 h was up-regulated as compared to the control cells (P<0.01).CONCLUSION: Ox-LDL may up-regulate the expression of connexin43 at mRNA and protein levels in cultured human umbilical vein endothelial cells within short time, indicating that connexin43 plays an important role in the pro-atherosclerotic effect of Ox-LDL.     

Effects of She Xiang Bao Xin Wan (SXBXW) on the proliferation of primary cultured human umbilical artery vascular smooth muscle cells induced by endothelin-1

AIM: To observe the effects of She Xiang Bao Xin Wan (SXBXW) of Chinese patent medicine on the proliferation of primary cultured vascular smooth muscle cells (VSMCs) from human umbilical artery and stimulated by endothelin-1 (ET-1) in vitro. METHODS: The proliferation cell models of primary cultured VSMCs were established by ET-1 stimulation. Six groups in the experiment were divided into control group; ET-1 group; ET-1+SXBXW 0.25 g/L; ET-1+SXBXW 0.5 g/L; ET-1+SXBXW 1.0 g/L and ET-1+SXBXW 2.0 g/L groups, respectively. The proliferation induced by ET-1 and the suppression mediated by SXBXW on VSMCs were measured by MTT method. The inhibitory rate and the cytotoxicity of SXBXW were detected by lactate dehydrogenase colorimetry and trypan blue exclusion tests. The effect of ET-1 and SXBXW on the cell proliferation cycle was analyzed by flow cytometry. RESULTS: Compared to control group, ET-1 significantly enhanced the proliferation of VSMCs (P<0.01). However, a certain dose of SXBXW inhibited effectively the proliferation of VSMCs induced by ET-1 in a dose-dependent manner (P<0.01). Meanwhile, SXBXW showed no influenced on both the number of living cells and the release of lactate dehydrogenase, although it inhibited the proliferation of VSMCs, indicating that SXBXW was no cytotoxicitic effect on VSMCs. ET-1 enhanced the proliferation of VSMCs by means of promoting the transition of the cell cycle from G1 phase to S phase. However SXBXW significantly inhibited the proliferation mediated by ET-1. CONCLUSION: SXBXW plays the role in suppressing VSMCs proliferation induced by ET-1. The mechanism may be involved in blocking the cell cycle from G1 phase into S phase.     

Effect of 27nt-miRNA on apoptosis of human umbilical vein endothelial cells induced by oxidized low-density lipoprotein

AIM To investigate the effect of 27nt-miRNA （27nt-miR） on apoptosis of human umbilical vein endothelial cells （HUVECs） induced by oxidized low-density lipoprotein （Ox-LDL） and its underlying mechanism. METHODS HUVECs were cultured in vitro and grouped as below： normal control group, Ox-LDL group, 27nt-miR+Ox-LDL group, anti-27nt-miR+Ox-LDL group and negative control+Ox-LDL group. The cells in Ox-LDL group were treated with Ox-LDL at 40 mg/L for 48 h, while those in normal control group were untreated but cultured normally. The cells in 27nt-miR+Ox-LDL group, anti-27nt-miR+Ox-LDL group and negative control+Ox-LDL group were transfected with their corresponding lentiviral vectors under the same procedure, followed by treatment with Ox-LDL at 40 mg/L for 48 h to induce apoptosis. The cell viability was measured by CCK-8 assay. The migration capacity was detected by scratch assay. The caspase-3 activity was measured by caspase-3 activity assay kit. The apoptotic rate was analyzed by Hoechst 33258 and flow cytometry. The mRNA and protein expression levels of Bcl-2, Bax and caspase-3 were determined by RT-qPCR and Western blot. RESUITS： Compared with negative control+Ox-LDL group, the cell viability and migration ability were significantly decreased by over-expression of 27nt-miR in the HUVECs （P<0.05）, while the activity of caspase-3 and apoptosis induced by Ox-LDL were significantly increased （P<0.05）. Furthermore, the mRNA and protein expression levels of Bax and caspase-3 were significantly up-regulated （P<0.05）, and the mRNA and protein expression level of Bcl-2 was down-regulated in 27nt-miR+Ox-LDL group （P<0.05）. Meanwhile, all the above indexes showed an opposite tendency in anti-27nt-miR+Ox-LDL group. CONCLUSION 27nt-miR promotes Ox-LDL-induced apoptosis and inhibits the viability and migration of HUVECs in vitro, possibly through regulating the expression of apoptotic/anti-apoptotic proteins such as Bax,caspase-3 and Bcl-2.     

Correlation between the effect of angiotensin-(1-7) on cardiac hypertrophy and extracellular signal-regulated kinase in pressure-overloaded rats

AIM: To investigate the effects and mechanisms of angiotensin-(1-7) on cardiac hypertrophy in pressure-overloaded rats. METHODS: Ar at model of pressure-overloaded heart was induced by constriction of abdominal aorta. Seventy-five male Sprague Dawley rats were randomized to sham-operated group, model control group and angiotensin-(1-7) treatment group. They were treated with intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour) or saline by minipump. RESULTS: Abdominal aortic banding resulted in a significant increases in LVW/BW, myocardial angiotensinⅡlevels, and p-ERK1/2 expression. Angiotensin-(1-7) had no effect on aortic banding-induced increases in myocardial angiotensinⅡlevels, but it significantly attenuated aortic banding-induced increases in LVW/BW and p-ERK1/2 expression. CONCLUSION: Angiotensin-(1-7) attenuates the development of cardiac hypertrophy in pressure-overloaded rats. It may be associated with the inhibition of p-ERK1/2 expression in cardiac tissue.