共查询到20条相似文献，搜索用时 31 毫秒
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AIM: To establish the THP-1-derived foam cell formation and to evaluate the effects of angiotensin-(1-7) and MDL (an inhibitor of adenylate cyclase) on the expression of ATP-binding cassete transporter A1(ABCA1) and the content of cholesterol. METHODS: THP-1-derived macrophages were treated with oxidized low-density lipoprotein(ox-LDL) to develop into foam cells. The foam cells were divided into 4 groups: control group, MDL group, Ang-(1-7) group and MDL+Ang-(1-7) group. At 24 h after treatment, the content of cAMP was measured by ELISA. The mRNA and protein levels of ABCA1 were determined by real-time RT-PCR and Western blotting, respectively. The content of cholesterol was detected by high performance liquid chromatography. RESULTS: The cAMP, the mRNA and protein levels of ABCA1 in Ang-(1-7) group were significantly higher, and the content of cholesterol was significantly lower than those in control group (P<0.05). On the contrary, the cAMP, the mRNA and protein levels of ABCA1 in MDL group were significantly lower and the content of cholesterol was significantly higher than those in control group (P<0.05). The results in MDL+Ang-(1-7) group were between Ang-(1-7) group and control group. CONCLUSION: Ang-(1-7) inhibits the formation of foam cells by promoting the expression of ABCA1 and decreasing the content of cholesterol. MDL partly antagonizes the effect of Ang-(1-7) by inhibiting the adenylate cyclase and decreasing the content of cAMP. 相似文献
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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. 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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ZHANG Na-na LI Mao-lian BIAN Yun-fei GAO Fen YANG Zhi-ming YANG Hui-yu XIAO Chuan-shi 《园艺学报》2011,27(8):1485-1489
AIM: To observe the effects of angiotensinⅡ (AngⅡ) and angiotensin-(1-7) on the expression of (pro)renin receptor in rat vascular smooth muscle cells.METHODS: The cultured VMSCs were randomly divided into control group, AngⅡ group, Ang-(1-7) group, AngⅡ+losartan (an AT1 receptor antagonist) group, AngⅡ+PD123319(an AT2 receptor antagonist) group and CGP42112A (an AT2 receptor agonist)group. The expression of (P)RR at protein and mRNA levels was detected by Western blotting and real-time PCR,respectively.RESULTS: Compared with control group, AngⅡ distinctly increased and Ang-(1-7) decreased the expression of (P)RR mRNA and protein in VMSCs in a dose-dependent manner (P<0.01). Compared with AngⅡ group, losartan did not inhibit the expression of (P)RR mRNA and protein in VMSCs induced by AngⅡ (P>0.05), but PD123319 did (P<0.01). CGP42112A also induced the expression of (P)RR protein and mRNA in VMSCs (P<0.01).CONCLUSION: AngⅡ induces the expression of (P)RR in VMSCs by AT2. However, Ang-(1-7) inhibits the expression of (P)RR in VMSCs. 相似文献
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AIM To explore the effects of nicotinic acid (NA) on lysosomal free cholesterol efflux in macrophages and its underlying mechanism. METHODS Macrophages induced from human monocytic leukemia cell line THP-1 by phorbol myristate acetate served as the cell model. Laser scanning confocal microscopy was applied to observe the effects of NA on lysosomal free cholesterol efflux in macrophages loaded with oxidized low-density lipoprotein (oxLDL). The influences of nicotinic acid adenine dinucleotide phosphate (NAADP) antagonist Ned-19, Ca2+ chelator BAPTA, liver X receptor α (LXRα ) siRNA and Niemann-Pick C1 protein (NPC1 ) siRNA on NA effects were also evaluated. RT-qPCR and Western blot were conducted to evaluate the influence of NA, Ned-19 and BAPTA on LXRα mRNA and NPC1 protein expression. RESULTS NA dose-dependently promoted lysosomal free cholesterol efflux in macrophages. This effect was markedly inhibited by Ned-19 and BAPTA. NA increased NPC1 protein and LXRα mRNA expression. These effects were also attenuated by Ned-19 and BAPTA remarkably. LXRα siRNA significantly inhibited the promoting effect of NA on NPC1 protein expression. Silencing of LXRα and NPC1 with siRNA remarkably abolished the effect of NA on lysosomal free cholesterol efflux. CONCLUSION NA promotes lysosomal free cholesterol efflux in macrophages. This effect may be mediated by the increased production of NAADP, which subsequently promotes Ca2+ release through lysosomal transient receptor potential mucolipin 1 (TRPML1) channel and finally up-regulates NPC1 protein expression via LXRα. 相似文献
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AIMTo investigate the role of soluble Klotho protein in THP-1-derived foam cell formation. METHODSTHP-1 monocytes were induced into macrophages by treatment with 160 nmol/L phorbol myristate acetate for 48 h, and then were divided into 6 groups: negative control group (THP-1-derived macrophages), positive control group [THP-1-derived foam cells induced by oxidized low-density lipoprotein (ox-LDL) for 48 h], and 25, 50, 100 and 200 μg/L soluble Klotho protein groups (THP-1-derived macrophages pretreated with soluble Klotho protein at the indicat?ed concentraions for 2 h and then induced by ox-LDL for 48 h). Lipid droplets in cytoplasm were observed by oil red O staining. The cholesterol outflow rate was detected by scintillation counting technique. The content of intracellular total cholesterol, free cholesterol and cholesterol ester was detected by enzyme fluorescence analysis. The expression of acyl-coenzyme A:cholesterol acyltransferase 1 （ACAT1） and ATP-binding cassette transport?er A1 (ABCA1) at mRNA and protein levels was determined by RT-qPCR and Western blot, respectively. RESULTSOil red O staining and lipid mass quantification showed that THP-1-derived foam cell formation was dose-dependently suppressed by soluble Klotho protein. The cholesterol efflux rate of THP-1-derived foam cells was increased by soluble Klotho protein in a dose-dependent manner (P <0.05). In addition, soluble Klotho protein decreased the expression of ACAT1 and increased the expression of ABCA1 in a dose-dependent manner (P <0.05). CONCLUSION The soluble Klotho protein inhibits THP-1-derived foam cell formation in a dose-dependent manner by down-regulating the expression of ACAT1 and up-regulating the expression of ABCA1. 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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HAO Xiao LI Shu-ren MENG Tian-tian GAO Qing DANG Yi XUN Li-ying YUAN Ke-xin ZHANG Qian-hui HAO Qing-qing QI Xiao-yong 《园艺学报》2016,32(3):554
AIM: To investigate the different dose of perindopril on cardiac function in the rabbits with ischemic cardiac dysfunction. METHODS: Male rabbits weighing 2.5~3.0 kg(n=30) were randomly divided into 3 groups(n=10):high dose perindopril group(HD group), low dose perindopril group(LD group) and cardiac dysfunction group(CD group). The Left anterior descending coronary artery of the rabbits was ligatured for model preparation. In HD group, the rabbits were treated with perindopril split normal saline solution(1 g/L)2 mL·kg-1·d-1. In LD group, the rabbits were treated with perindopril split normal saline solution(0.33 g/L)2 mL·kg-1·d-1. In CD group, the rabbits were treated with normal saline solution 2 mL·kg-1·d-1. Four weeks after treatment, the cardiac function was measured via echocardiography, the mRNA expression of angiotensin-converting enzyme 2(ACE2) and angiotensin type 2 receptor(AT2R) was analyzed by real-time PCR, serum angiotensin(Ang)-(1-9) and Ang-(1-7) levels were detected by ELISA. RESULTS: Compared with CD group, the cardiac function of the 2 groups treated with perindopril was significantly improved(P<0.01), and more improvement in HD group was observed than LD group(P<0.05). The serum angiotensin(Ang)-(1-9) and Ang-(1-7) level and the mRNA expression of ACE2 and AT2R in the 2 groups treated with perindopril were significantly improved(P<0.01). Compared with LD group, the mRNA expression of ACE2 and AT2R and the serum levels of Ang-(1-9) in HD group were significant improved(P<0.05), while no difference of serum Ang-(1-7) level was observed. Correlation analysis revealed that the improvement of the cardiac function was associated with serum Ang-(1-9) level, mRNA expression of ACE2 and AT2R(P<0.01), but has no significant correlation with serum Ang-(1-7) level. CONCLUSION: High dose of perindopril may improve more cardiac function in ischemic cardiac dysfunction model in rabbits. The mechanism may relate to increasing serum Ang-(1-7) level to activate AT2R. 相似文献
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AIM：To investigate the therapeutic effect and the mechanism of neuregulin-1β (NRG-1β) on the rat model of myocardial hypertrophy induced by pressure overload．METHODS：Eight weeks after coarctation of abdominal aorta, the Wistar rats were randomly divided into 4 groups: myocardial hypertrophy (model) group, sham operation (sham) group, NRG-1β treatment group (intravenous injection of NRG-1β at dose of 10 μg/kg daily for 7 d) and NRG-1β+Herceptin (HERCE) treatment group ［intravenous injection of NRG-1β (10 μg/kg) plus HERCE (10 μg/kg) daily for 7 d］. The characteristics of heart functions were evaluated by the methods of hemodynamics and echocardiography. Masson staining was employed to observe the pathological changes of myocardial tissues. The concentration of angiotensin II (Ang II) in myocardial tissues was measured by radioimmunoassay. The level of tumor necrosis factor α (TNF-α) in myocardial tissues was detected by ELISA. The mRNA expression of B-cell lymphoma/leukemia-2 (bcl-2) and bcl-2-associated X protein (bax) in the myocardium was determined by RT-PCR. RESULTS：The left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were higher, while the left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) were smaller in NRG-1β group than those in model group. The left ventricular end-systolic pressure (LVESP) and maximal rate of increase/decrease in left ventricular pressure (±dp/dtmax) were higher, and left ventricular end-diastolic pressure (LVEDP) was significantly lower in NRG-1β group than those in model group. Compared with model group, treatment with NRG-1β decreased collagen volume fraction (CVF), reduced the Ang II and TNF-α, increased bcl-2 mRNA expression, and decreased bax mRNA expression in myocardial tissues. No difference of the above parameters between model group and NRG-1β+HERCE treatment group was observed. CONCLUSION：NRG-1 reduces the expression of Ang II and TNF-α in myocardial tissues in pressure-overload rats, thus reducing Ang II and TNF-α mediated myocardial interstitial remodeling. Increase in the mRNA expression of bcl-2 and decrease in the mRNA expression of bax by NRG-1 inhibit myocardial cell apoptosis, which is responsible for its role of improving cardiac function of myocardial hypertrophy induced by pressure overload. 相似文献
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AIM: To investigate the protective effect of astragaloside IV (ASIV) on angiotensin II (Ang II)- induced apoptosis of H9c2 cardiomyocytes. METHODS: H9c2 cardiomyocytes were treated with different concentrations of Ang II and ASIV. The effects of Ang II and ASIV on the viability of H9c2 cells was measured by CCK-8 assay. The optimum concentration of Ang II was 1 μmol/L and the concentrations of ASIV were 25, 50 and 100 μmol/L. The H9c2 cells was divided into 6 groups:control group, ASIV group, Ang II group, Ang II+ASIV (25 μmol/L) group, Ang II+ASIV 50 (μmol/L) group and Ang II+ASIV (100 μmol/L) group. The morphological changes of the H9c2 cells were observed under inverted phase-contrast microscope. Apoptosis was detected by TUNEL assay. The generation of reactive oxygen species (ROS) was detected by DCFH-DA staining. The protein expression of Bax, Bcl-2, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was determined by Western blot. H9c2 cardiomyocytes were transfected with negative control shRNA (NC) or Nrf2-shRNA (shRNA), and the cells were divided into 8 groups:NC+control group, NC+AngⅡgroup, NC+ASIV group, NC+AngⅡ+ASIV group, shRNA+control group, shRNA+AngⅡgroup, shRNA+ASIV group and shRNA+AngⅡ+ASIV group. ROS level was detected by ROS detection kit. The protein expression of Nrf2 and HO-1 was determined by Western blot. RESULTS: Ang II decreased the viability of H9c2 cells in a concentration-dependent manner (P<0.05). ASIV reversed the effect of Ang II on the viability of H9c2 cells in a concentration-dependent manner (P<0.05). Compared with control group, the apoptotic rate, the level of ROS and the protein expression of Bax in Ang II group were increased significantly, while the protein expression of Bcl-2, Nrf2 and HO-1 was decreased significantly (P<0.05). Compared with Ang II group, ASIV reversed the increase in apoptotic rate of H9c2 cells induced by Ang II in a concentration-dependent manner, reduced ROS level, down-regulated the protein expression of Bax and up-regulated the protein expression of Bcl-2, Nrf2 and HO-1 (P<0.05). After shRNA transfection, the effects of ASIV decreasing ROS production induced by Ang II and up-regulating the expression of Nrf2 and HO-1 were eliminated. CONCLUSION: ASIV protects H9c2 cardiomyocytes from apoptosis induced by Ang II, which may be related to reducing ROS generation and mediating the Nrf2/HO-1 signaling pathway. 相似文献
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AIM: To explore the effect of extracellular signal-regulated kinase 1/2 (ERK1/2) on the vascular adventitial remodeling in a hypertension rat model. METHODS: The rats were randomly divided into control group, mini-pump infusion of saline group and mini-pump infusion of angiotensin II (Ang II) group as the hypertension model. The systolic pressure and vascular morphology of the rats were examined. Adventitial fibroblasts were treated with Ang II, PD98059 (ERK1/2 inhibitor) and Ang II+PD98059. The catalase (CAT) expression in the cells was detected by Western blotting. RESULTS: Compared with control group and mini-pump infusion of saline group, the systolic pressure and carotid media thickness (stained by HE) in mini-pump infusion of Ang II group were significantly increased (P<0.01). Meanwhile, artery morphology in mini-pump infusion of Ang II group had obviously changed with a significant occurrence of pathological vascular remodeling. The result of Western blotting showed that the expression of CAT in the adventitial fibroblasts treated with Ang II+PD98059 was much higher than that in the cells treated with Ang II alone (P<0.05), indicating that down-regulation of CAT induced by Ang II was restored by ERK1/2 signaling pathway. CONCLUSION: Ang II down-regulates CAT through ERK1/2 pathway and promotes cell phenotype transformation, which lead to pathological vascular remodeling. 相似文献
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DAI Pei GAO Fen GAO Hong-wei WANG Yuan FENG Gao-jie ZHANG Qin-feng BAI Rui QIN Wei-wei LI Hong SONG Xiao-su 《园艺学报》2019,35(2):212-217
AIM:To study whether homocysteine (Hcy) inhibits the expression of ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) by microRNA-33 (miRNA-33) signaling, and reduces the efficiency of reverse cholesterol transport (RCT).METHODS:RAW264.7 macrophages were induced by oxidized low-density lipoprotein (ox-LDL) to establish foam cell model. Oil red O staining was used to determine whether the model was established successfully. miRNA-33 mimics and miRNA-33 inhibitor were transfected into the cells by Lipofectamine 2000, and the cells were exposed to Hcy at concentration of 5 mmol/L for 24 h. The intracellular lipid droplets were observed by Oil red O staining. The expression of ABCA1 and ABCG1 at mRNA and protein levels was determined by real-time PCR and Western blot. The cellular cholesterol content was analyzed by HPLC, and effluent rate of cholesterol was detected by the method of liquid scintillation counting.RESULTS:Compared with blank control group, the lipid content in miRNA-33 mimics group was increased, and the expression of ABCA1 and ABCG1 at mRNA and protein levels was decreased (P<0.05). The intracellular cholesterol content was increased gradually (P<0.05), and the cellular cholesterol efflux rate was gradually decreased (P<0.05) in miRNA-33 mimics group. Compared with blank control group, the testing results in miRNA-33 inhibitor group were the opposition of those in miRNA-33 mimics group (P<0.05). No diffe-rence of the above indexes among blank control group, miRNA-33 mimics-NC group and miRNA-33 inhibitor-NC group was observed.CONCLUSION:Hcy inhibits the mRNA and protein expression of ABCA1 and ABCG1 through miRNA-33 signaling, and reduces the efficiency of RCT in RAW264.7 macrophage-derived foam cells. 相似文献
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AIM: To investigate the regulation of ghrelin on the expression of ATP-binding cassette transporter A1 and G1 (ABCA1/ABCG1)during the foam cell formation. METHODS: The human monocytic leukemia cell line (THP-1)was chosen in our study. The differentiation of THP-1 cells into macrophages was induced by using phorbol myristate acetate (PMA). Macrophages were then incubated with oxidized LDL (ox-LDL)to generate foam cells. Ghrelin of different concentrations were treated at different time points during foam cell formation. The ABCA1/ABCG1 protein and mRNA levels were detected by Western blotting and RT-PCR. The effect of variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer. RESULTS: Ghrelin reduced the content of lipid droplet in foam cells, and increased the efflux of intracellular cholesterol significantly. Ghrelin increased ABCA1 protein mass and mRNA level in dose-dependent manner. The changes of ABCG1 protein and mRNA level were the same as ABCA1. CONCLUSION: Ghrelin interfere atherosclerosis by up-regulating the expression of ABCA1 and ABCG1. 相似文献
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AIM: To investigate the effects of ghrelin on the expression of acyl coenzyme A:cholesterol acyltransferases-1 (ACAT-1) during the formation of foam cells. METHODS: The human monocytic leukemia cell line THP-1 was used in the study. The differentiation of THP-1 cells into macrophages was induced by phorbol 12-myristate 13-acetate (PMA). Macrophages were incubated with oxidized LDL (ox-LDL) to generate foam cells. Ghrelin of different concentrations were used during the formation of foam cells. The ACAT-1 protein and mRNA levels were detected by Western blotting and RT-PCR. The variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer. RESULTS: Ghrelin reduced the content of cholesterol ester in foam cells obviously. ACAT-1 protein and mRNA levels were also decreased. Ghrelin reduced ACAT-1 protein mass and mRNA level in a dose-dependent manner. CONCLUSION: Ghrelin might retard the formation of atherosclerosis via down-regulating the expression of ACAT-1. 相似文献
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YU Si-yang WANG Yan ZENG Gao-feng LIU Yang XU Jian-qiang ZENG Meng-ya TANG Ye-hua ZENG Zhi-ying SHI Xiao-qiao CHEN Ying ZHAO Guo-jun 《园艺学报》2016,32(5):863-868
AIM: To explore the role of nucleotide-binding oligomerization domain-like receptor protein 1 (NLRP1) inflammasome in atorvastatin-induced reduction of interleukin-1β (IL-1β) and interleukin-18 (IL-18) releases from the THP-1 macrophages. METHODS: Lipopolysaccharide (LPS, 10 μg/L) was used to trigger the secretion of IL-1β and IL-18 in the THP-1 macrophages. The cells were incubated with different concentrations of atorvastatin (1, 10 and 20 μmol/L) for 24 h, or treated with 10 μmol/L atorvastatin for different time (12 h, 24 h and 48 h). NLRP1 siRNA was transfected into the THP-1 cells. The mRNA expression of NLRP1 inflammasome was detected by RT-PCR. The protein expression of NLRP1 inflammasome was determined by Western blot. The secretion of proinflammatory cytokines IL-1β and IL-18 was quantified by ELISA. RESULTS: Atorvastatin inhibited the mRNA and protein expression of NLRP1 inflammasome in the THP-1 macrophages in a dose- and time-dependent manner. Transfection of NLRP1 siRNA significantly decreased the protein expression of NLRP1 and promoted the suppressive effect of atorvastatin on IL-1β and IL-18 secretion in the THP-1 macrophages. CONCLUSION: Atorvastatin inhibits the production of IL-1β and IL-18 in the macrophages through decreasing NLRP1 inflammasome expression, possibly contributing to the anti-inflammatory effect of atorvastatin on atherosclerosis. 相似文献