共查询到20条相似文献,搜索用时 234 毫秒
1.
ZHUANG Wei XIE Liang-di XU Chang-sheng WANG Hua-jun SHEN Yi-hua CHEN Ming 《园艺学报》2013,29(11):2030-2033
AIM: To investigate the effects of transplantation of adipose stromal vascular fraction (SVF) on the cardiac function in adriamycin-induced heart failure rats. METHODS: SVF was isolated from adipose tissue of a Sprague-Dawley (SD) rat by collagenase digestion and marked with green fluorescent protein (GFP) in vitro. Twenty-eight SD rats were randomized into normal control group (n=8), adriamycin control group (n=10) and SVF treatment group (n=10). Adriamycin at dose of 15 mg/kg was intraperitoneally injected into the rats twice a week for 4 weeks to induce heart failure. SVF cells (05 mL, 1×107/L) were injected via penis vein, and PBS vehicle was injected into the control animals in the same way. Four weeks later, the cardiac function was determined by multichannel physiologic recorder via cardiac catheterization. SVF was demonstrated in the myocardium by frozen section fluorescence microscopy. The CD31 expression was determined by an immunohistochemical test. RESULTS: Compared with adriamycin control group, SVF transplantation increased left ventricular peak systolic pressure [LVSP, (13565±21.58) mmHg vs (10558±2262) mmHg, P<005], left ventricular pressure maximal rise rate [+dp/dtmax, (4 81565±56624) mmHg/s vs (3 53550±46528) mmHg/s, P<005], and left ventricular pressure maximal decline rate [-dp/dtmax, (3 67756±46775) mmHg/s vs (2 73865±51251) mmHg/s, P<005]. The results of the CD31 immunohistochemical test showed that the nuclear staining and granule distribution were more uniform, and the number of blood vessels per visual field increased in SVF treatment group as compared with adriamycin control group (P<005). CONCLUSION: SVF transplantation improves the cardiac function in the rat model of heart failure, possibly and partly through the promotion of myocardial neovascularization. 相似文献
2.
XU Ya-nan YANG Long YANG Tian-he DENG Chun-yu LUO Lin QIN Zhi-fang TANG Qian YANG Jun 《园艺学报》2014,30(8):1489-1492
AIM:To investigate the effects of mechanical stretch on transient outward potassium current (Ito), inward rectifier potassium current (IK1) and action potential duration(APD) of cultured neonatal rat atrial myocytes. METHODS:Neonatal rat atrial myocytes were isolated and cultured on silicone sheeting with or without stretch for 24 h. The silicone membrane area was increased by 12% in stretched group. The cells without stretch served as control. Ito, IK1 and APD were recorded by the technique of whole-cell patch clamp. RESULTS:Compared with control group, Ito density in stretched myocytes was significantly reduced [(16±04) pA/pF vs (121±29) pA/pF, P<001], whereas IK1 density was increased [(-108±08) pA/pF vs (-88±09) pA/pF, P<001]. The APDs at 50% and 90% levels of repolarization (APD50 and APD90) in the stretched cells were obviously decreased than those in non-stretched cells [(105±14) ms vs (155±24) ms, (300±28) ms vs (563±36) ms, P<001]. CONCLUSION:Stretch stimulation leads to the reduction of Ito density, the increase in IK1 density and the shortness of APD in cultured rat atrial neonatal myocytes, which may contribute to atrial electrical remodeling induced by pressure overload. 相似文献
3.
AIM:To investigate the effects of site-specific (α-1 repeat: 124HNFTAGDLGPSTIVGSAAFNMF145) antibody of Na+-Ca2+ exchanger (NCX) on the isolated rat heart functions and vascular tone and to compare them with the effects of Na+-K+ pump inhibitor ouabain and L-type Ca2+ channel agonist (±)Bay K8644. METHODS:The heart and thoracic aorta were rapidly isolated from the adult rats weighing 250~300 g. The hemodynamic indexes including left ventricular developed pressure, maximal rate of rise/decline of left ventricular pressure (±dp/dtmax) and coronary resistance were observed by Langendorff isolated heart perfusion system. The rings of thoracic aorta were mounted into the organ baths and the vascular tone was determined. RESULTS:At concentrations of 10, 20 and 40 nmol/L, the site-specific antibody of NCX enhanced the cardiac functions in a dose-dependent manner during the perfusion period with no arrhythmia. At the same time, it did not increase the coronary resistance. The antibody had no effect on the vascular tone of isolated thoracic aorta ring at the same concentrations. Ouabain at concnentration of 0.5 mmol/L and (±)Bay K8644 at concentration of 01 mmol/L had similar effects with the site-specific antibody of NCX at concentration of 40 nmol/L on left ventricular developed pressure and +dp/dtmax of isolated rat hearts during perfusion, but (±)Bay K8644 (01 mmol/L) didn’t have significant effect on -dp/dtmax. Ouabain (0.5 mmol/L) even reduced -dp/dtmax as compared with the control. After administration of ouabain (0.5 mmol/L) for 5 min, most isolated hearts appeared premature pulse more than 5 beats/min. (±)Bay K8644 (0.1 mmol/L) did not induce arrhythmia during all the time of exposure. CONCLUSION: The site-specific (α-1 repeat: 124HNFTAGDLGPSTIVGSAAFNMF145) antibody of NCX enhances both systolic and diastolic functions of isolated rat hearts without arrhythmia. Meanwhile, this antibody doesn’t increase coronary resistance during perfusion and vascular tone in isolated thoracic aorta rings. 相似文献
4.
AIM: To explore the relationship between 3-nitrotyrosine (3-NT) level in hearts or blood and myocardial cell apoptosis in rat diabetic cardiomyopathy (DCM). METHODS: Sixty Sprague-Dawley (SD) rats (male, 8-week-old) were randomly divided into 4 groups: normal group, diabetic cardiomyopathy group (DCM group), diabetic rats treated with valsartan (40 mg·kg-1·d-1, D+V group) and DCM rats treated with valsartan (40 mg·kg-1·d-1, DCM+V group). Apoptotic index (AI) of rat cardiac myocytes was examined by TUNEL. The expression index (EI) of 3-NT in rat cardiac myocytes was examined by immunohistochemistry. The 3-NT concentration in rat serum was examined by ELISA. RESULTS: (1) Significant differences of the heart weight indexes among the 4 groups were observed (P<0.01). The heart weight indexes in DCM group and DCM+V group were higher than those in normal group and D+V group (P<0.01). (2) The EI of 3-NT in the cardiac myocytes was positively correlated with the AI of the cardiac myocytes in the same group (P<0.01), but the concentration of 3-NT in blood had no correlation with the AI of cardiac myocytes (P>0.05). (3) The difference of AI of cardiac myocytes among the 4 groups had statistical significance (P<0.01). The arrangement from high to low of AI was DCM group > D+V group and DCM+V group > N group (P<0.05). (4) The EI of 3-NT in DCM group was the highest as compared to other groups (P<0.05). (5) No statistical difference of 3-NT concentration in blood among the 4 groups was observed (P>0.05). CONCLUSION: (1) The expression of 3-NT in DCM myocardial tissues in SD rats is significantly increased and closely correlated with the apoptosis in myocardial cells. Valsartan inhibits 3-NT expression in DCM myocardial cells, thus inhibits the DCM myocardium apoptosis. (2) The 3-NT level in blood can not be true for reflection of 3-NT expression in DCM myocardial tissues and its effect on myocardial cell apoptosis. 相似文献
5.
AIM: To observe the influence of simvastatin on insulin secretion function of mouse pancreatic beta cell line MIN6 and to explore its possible mechanisms.
METHODS: MIN6 cells were randomly divided into normal control group and low-, middle-and high-concentration simvastatin treatment groups, which were cultured for 48 h with high-glucose DMEM containing 15% fetal bovine serum plus 0, 2, 5 and 10 μmol/L simvastatin, respectively. The insulin secretion of MIN6 cells was measured by radioimmunoassay. The content of ATP in MIN6 cells was measured by biochemiluminescence method. The mRNA and protein expression levels of inwardly rectifying potassium channel 6.2 (Kir6.2), voltage-dependent calcium channel 1.2 (CaV1.2) and glucose transporter 2 (GLUT2) were detected by real-time fluorescence quantitative PCR and Western blotting, respectively.
RESULTS: Compared with normal control group, middle-and high-concentration simvastatin treatment markedly decreased the synthesis and secretion of insulin in MIN6 cells (P<005). The content of ATP in MIN6 cells was markedly decreased in simvastatin treatment groups (P<005). The mRNA expression level of Kir6.2 in MIN6 cells was significantly up-regulated in simvastatin treatment groups (P<001), while the mRNA expression levels of CaV1.2 and GLUT2 were significantly down-regulated in middle-and high-concentration simvastatin treatment groups (P<001). The protein expression of Kir6.2 was significantly increased but that of CaV1.2 was significantly decreased in middle-and high-concentration simvastatin treatment groups (P<001), and the protein expression level of GLUT2 was markedly decreased in high-concentration simvastatin treatment group (P<001).
CONCLUSION: Simvastatin inhibits insulin synthesis and secretion in mouse pancreatic beta cell line MIN6 via suppressing ATP production, up-regulating the expression of Kir6.2 and down-regulating the expression of CaV1.2 and GLUT2. 相似文献
6.
AIM: To observe the change of L-type voltage-gated Ca2+ channel current during focal brain ischemia in the normal rats and the rats with diabetes mellitus (DM). METHODS: Combination of high-fat diet with streptozotocin (STZ) was used to establish DM animal model. The operation of middle cerebral artery occlusion (MCAO) with monofilament on the rats was performed. The animals were divided into sham operation group, MCAO 1 h group, MCAO 3 h group, MCAO 6 h group, MCAO 24 h group, DM sham operation group, DM+MCAO 1 h group, DM+MCAO 3 h group, DM+MCAO 6 h group and DM+MCAO 24 h group. The score of neural function was determined to judge the degree of palsy in the rats in MCAO 24 h group and DM+MCAO 24 h group. The changes of L-type voltage-gated Ca2+ channel current of cortex neurons during ischemia were measured using the whole-cell patch clamp technique. RESULTS: The rats in DM+MCAO 24 h group awaked slowly, and the degree of semiplegia was more serious than that in the rats in MCAO 24 h group. The score of neural function in DM+MCAO group was higher than that in MCAO group (P<0.05). The longer the ischemic time was, the higher L-type voltage-gated Ca2+ channel current was observed in MCAO group and DM+MCAO group (P<0.05). L-type voltage-gated Ca2+ channel current in DM+MCAO group was higher than that in MCAO group at each time point(P<0.05). CONCLUSION: The aggratation of ischemic injury during DM+MCAO is probably associated with Ca2+ overload induced by calcium channel opening and current increasing. 相似文献
7.
MA Ying-chun ZHENG Meng-xiao HUANG Lin-jing WANG Yuan-yuan YING Lei WANG Wan-tie 《园艺学报》2014,30(9):1645-1650
AIM:To investigate the effects of voltage-dependent K+ channel 1.5 (Kv1.5) on the proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia+hypercapnia condition and the relationship with mitogen-activated protein kinase(MAPK) signal pathway. METHODS:The PASMCs isolated from the male SD rat were cultured under hypoxia+hypercapnia condition, and randomly divided into normal group (N group), hypoxia+hypercapnia group (HH group), hypoxia+hypercapnia+DMSO incubation group (HD group), hypoxia+hypercapnia+U0126 (an extracellular signal-regulated kinase 1/2 inhibitor) incubation group (HU group), hypoxia+hypercapnia+SB203580 (a p38 mitogen-activated protein kinase inhibitor) incubation group (HS group), and hypoxia+hypercapnia+anisomycin (an agonist of MAPK) incubation group (HA group). Cell Counting Kit-8 was used to detect the cell viability. The protein expression of Kv1.5, PCNA and Bax was detected by Western blotting. RESULTS:Compared with N group, the cell viability and PCNA protein expression in HH group and HD group were significantly raised (P<001), but Kv1.5 and Bax proteins were significantly decreased (P<0.01). No difference between HH group and HD group was observed (P>005). Compared with HD group, the cell viability and PCNA protein expression in HU group, HS group and HA group were decreased (P<0.05 or P<0.01), but Kv1.5 protein and Bax protein were raised (P<0.01), with the most significant changes in HA group. CONCLUSION:The regulation of Kv1.5 to the proliferation and apoptosis of PASMCs under hypoxia+hypercapnia condition might have a relationship with the activation of MAPK signal pathway. 相似文献
8.
XIA Zhen LI Ju-xiang DING Hao SUN Guo-fang HONG Kui WU Yan-qing CHENG Xiao-shu 《园艺学报》2013,29(12):2121-2127
AIM:To investigate the role of endoplasmic reticulum stress (ERS) in the process of Bim-mediated cardiomyocyte apoptosis induced by hypoxia. METHODS:Cardiomyocytes were isolated from neonatal Sprague-Dawley rats aged 1~3 days, and primarily cultured in vitro. The antibody targeting α-striated muscle actin was used to identify the cardiomyocytes. The siRNAs targeting bim were transfected into cardiomyocytes with liposome, followed by detecting the expression of Bim by Western blotting. Cardiomyocytes were divided into five groups: blank control group, hypoxia group, hypoxia+liposome group, hypoxia+negative control siRNA group and hypoxia+Bim-siRNA group. The cell viability was determined by MTT assay, and the cell apoptotic rate and the intracellular calcium concentration were measured by flow cytometry. The protein expression of caspase-12 and inositol 1,4,5-triphosphate (IP3) was detected by Western blotting. RESULTS:Immunohistochemical identification confirmed that rat cardiomyocytes were successfully cultured. Green fluorescence was observed in the cells transfected with negative control siRNA under fluorescence microscope. The expression of Bim was obviously inhibited after transfected with Bim-siRNAs and the silencing efficiency of Bim-siRNA-2 was the highest (86.73%). Compared with blank control group, the viability of cardiomyocytes in hypoxia group was significantly reduced (P<005). Compared with hypoxia+negative control siRNA group, the viability of cardiomyocytes in hypoxia+Bim-siRNA group was significantly increased (P<005). The apoptotic rate and the intracellular calcium concentration of cardiomyocytes were obviously increased in hypoxia group (P<0.01), and were both decreased after bim silencing (P<005 or P<0.01). The expression of caspase-12 and IP3 was up-regulated in hypoxia group (P<005), and was down-regulated after bim silencing (P<005 or P<0.01). CONCLUSION: Cardiomyocyte apoptosis induced by hypoxia can be inhibited by silencing the expression of bim gene. Caspase-12 and IP3, as markers of ERS, may participate in the process of Bim-mediated cardiomyocyte apoptosis induced by hypoxia. 相似文献
9.
ZHANG Ling SUN Meng SHI Bo TANG Li-li WU Cun-zao CAI Yong XIA Peng ZHENG Shao-ling YANG Yi-rong CHEN Bi-cheng 《园艺学报》2014,30(8):1363-1367
AIM:To investigate the effect of immunosuppressant FK506 on serum glucose in rats and to explore its mechanism. METHODS:Sprague-Dawley rats (n=12) were randomly divided into drug group and normal group. The rats in drug group were intraperitoneally injected with FK506 at dose of 1 mg·kg-1·d-1 and the rats in normal group received saline (1 mL·kg-1·d-1, ip) for 14 d. The fasting weight and fasting glucose were regularly measured every 2 d. Visceral fat was isolated from the rats at the end of experiment. The mRNA expression of adiponectin, leptin, visfatin, resistin, retinol-binding protein 4 (RBP4) and peroxisome proliferator-activated receptors γ (PPAR-γ) was determined by real-time fluorescence quantitative PCR. The protein expression of PPAR-γ and adiponectin was measured by Western blotting. RESULTS:Compared with normal group, the concentration of fasting blood glucose in model group was significantly increased from the 10th day (P<0.05). At day 14, the fasting blood glucose of the model group increased from (5.10±062) mmol/L to (7.73 ± 0.73) mmol/L. No significant change of blood glucose in normal group between the 10th day and the 14th day [from (4.66 ± 0.32) mmol/L to (5.80±0.10) mmol/L] was observed. Compared with normal group, the mRNA expression of PPAR-γ, adiponectin and leptin in the adipose tissue of model group was significantly decreased (P<001), whereas the expression of visfatin, resistin and RBP4 was significantly increased (P<005). Compared with normal group, the expression of PPAR-γ and adiponectin in model group was decreased (P<001). CONCLUSION:FK506 may decrease the expression of PPAR-γ to change the expression of adipocytokines and induce hyperglycemia in rats. 相似文献
10.
LIANG Qing LI Zi-cheng KUANG Su-hua HUANG Wei-qing HUANG Min-jian LIN Jun-min LIANG Zi-jing 《园艺学报》2013,29(8):1352-1357
AIM:To explore the in vivo effects of metoprolol on the expression of phosphorylated connexin 43 (p-Cx43) in myocardial tissues and the apoptosis of myocardial cells in rats with heart failure (HF).METHODS:One hundred Sprague-Dawley rats were randomly divided into 5 groups (each n=20): sham group, HF group, low-dose (1.25 mg·kg-1·d-1) metoprolol treatment (MetoA) group, middle-dose (5 mg·kg-1·d-1) metoprolol treatment (MetoB) group and high-dose (20 mg·kg-1·d-1) metoprolol treatment (MetoC) group.The rats in HF group and metoprolol treatment groups were subject to abdominal aortic ligation, and different doses of metoprolol were given 4 weeks later till 8 weeks after operation.Echocardiography was conducted to monitor the hemodynamic parameters at the 4th and 8th weeks, and the rat hearts were taken at the 8th week after operation.The morphological changes and the proliferation of collagen fibers in myocardial tissues were observed by HE and Masson staining, respectively.The expression level of p-Cx43 was detected by Western blotting and the apoptosis of myocardial cells was assessed by TUNEL method.The relationship between p-Cx43 expression level and apoptotic index was analyzed by Pearson’s correlation.RESULTS:(1) Echocardiography showed that metoprolol could effectively improved cardiac hemodynamics in HF rats, and pathological findings suggested that metoprolol could effectively reverse HF-induced cardiac remodeling in a dose-dependent manner within the therapeutic dose range.(2) Western blotting showed that p-Cx43 expression in HF group was significantly higher than that in sham group (P<001), and that in all metoprolol treatment groups was significantly decreased compared with HF group (P<005 or P<001), among which pairwise comparisons also showed significant differences (P<001).(3) The myocardial apoptotic index in HF group [(51.17±6.94)%] was significantly increased compared with sham group [(4.62±160)%, P<001].Compared with HF group, myocardial apoptotic indexes in MetoA group [(40.60±4.15)%], MetoB group [(30.66±4.00)%] and MetoC group [(22.24±5.69)%] were significantly decreased (P<001), among which pairwise comparisons also showed significant differences (P<001).(4) The expression level of p-Cx43 was positively correlated with the apoptotic index (r=0.905, P<001).CONCLUSION: The mechanism of metoprolol against HF-induced myocardial apoptosis may be related to inhibition of p-Cx43 expression. 相似文献
11.
AIM: To study the effect of panax notoginseng sponins (PNS) on L-type Ca2+ current in isolated right ventricle myocytes from chronic hypoxic rats. METHODS: Using whole cell patch clamp recording technique,we measured ICa-L in isolated right ventricle myocytes which were divided into three group:control group, chronic hy-poxic group and chronic hypoxic group with PNS(100 mg·kg-1·d-1). RESULTS: The result showed ICa-L of cells from chronic hypoxic group were significantly larger than the other two groups(P<0.05). CONCLUSION: PNS decreases L-type Ca2+ current of the right ventricle myocytes from chronic hypoxic rats. 相似文献
12.
AIM: To observe the effect of garlicin on sodium channel(INa) in isolated ventricular myocytes of rats. METHODS: The ventricular myocytes of rats were obtained by enzymatic dissociation and treated with different concentrations of garlicin. The change of INa was recorded by the technique of whole-cell patch clamp recording.RESULTS: Garlicin decreased the INa of isolated ventricular myocytes in a dose- and voltage-dependent manner. The current density was elevated to peak under the condition that the membrane voltage was -40 mV before treated with garlicin. The current density was decreased by 48% from peak after treated with 500 μmol/L garlicin . No significant change of the active curve with the use of garlicin was observed. The median inactive voltages of the inactive curves before and after garlicin treatment were (-88.61±9.60) mV and (-103.03±8.90) mV (P<0.01), respectively, and the slopes were -7.85±0.88 and -7.55±2.75 (P>0.05), respectively, indicating that garlicin made a shift to the negative direction. CONCLUSION: Garlicin treatment induced the current density-voltage curve of INa to shift up and significantly decreased the current density. The inactive curve of sodium channel moved to the left, while the current density was not decreased after treated with garlicin. Garlicin blocks sodium channel in its inactive state in a dose- and voltage-dependent manner. 相似文献
13.
WANG Hai-yan ZOU Zheng-yu DUAN Liang CHEN Xian LI Huan YUAN Shi-mei HE Tong-chuan ZHOU Lan 《园艺学报》2013,29(11):1928-1933
AIM: To investigate the effect of PI3K/Akt signaling pathway on S100A6-induced proliferation and migration of human osteosarcoma cell line 143B. METHODS: Recombinant human S100A6 protein (rhS100A6) was prepared. The 143B cells were treated with rhS100A6 in the presence or absence of PI3K inhibitor (LY294002 or wortmannin) exposure. The final concentrations of rhS100A6, LY294002 and wortmannin were 30 mg/L, 10 μmol/L and 0.5 μmol/L, respectively. The expression levels of total Akt (t-Akt) and phosphorylated Akt (p-Akt) in the 143B cells were analyzed by Western blotting. The cell proliferation and migration were determined by MTT and Transwell assays. RESULTS: rhS100A6 protein was successfully prepared, and significantly increased the proliferation and migration of 143B cells (P<005). rhS100A6 up-regulated the phosphorylation of Akt in 143B cells (P<005). Compared with rhS100A6 group, the level of p-Akt in 143B cells and the proliferation and migration of the cells were decreased in combined treatment group of rhS100A6 with LY294002 or wortmannin (P<005), where the proliferation rate at different time points dropped from 10.3% to 69.7% (P<005), and the migration rate dropped from 34.9% to 47.7% (P<005). CONCLUSION: To some extent, S100A6 promotes proliferation and migration of human ostersarcoma cell line 143B through PI3K/Akt signaling pathway. 相似文献
14.
QI Ben-ling LIU Hong-zhi CAO Lin-sheng CHENG Pei GUAN Si-ming LIU Cheng-yun ZHANG Hu-ping HE Ping WU Jian-ping 《园艺学报》2007,23(4):689-692
AIM: To investigate whether and how AT1 receptor blocker, valsartan, attenuates left ventricular remodeling and failure in a rat model of adriamycin(ADR)-induced dilated cardiomyopathy. METHODS: Weight-matched adult male Wistar rats were randomly divided into 3 groups as follows: 1) the ADR group, in which 2.5 mg/kg of ADR was weekly injected via a tail vein for 10 weeks (n=25); 2) concomitant AT1 receptor blocker valsartan and ADR, in which valsartan was administered by daily gavage at a dose of 30 mg·kg-1·d-1 (n=10); 3) control group (n=10). Hemodynamics and echocardiographic measurements were obtained at 12 weeks after treatment. Finally, left ventricle (LV) samples were collected at 12 weeks. The hydroxyproline content was determined by the methods of chloramines T. The expression of MMP-2, MMP-9 and tissue inhibitors of metalloproteinase-1 (TIMP-1) were measured by Western blotting. MMP-2 and -9 gelatinolytic activities were measured by gelatin zymography. RESULTS: Mortality was significantly lower in valsartan -treated rats than that in ADR rats (20% versus 40%, P<0.01). The dilatation of LV cavity was significantly attenuated in ADR-induced dilated cardiomyopathy rats given valsartan. Valsartan partially normalized LV contractile function, which was significantly reduced in ADR rats. The hydroxyproline content was increased in ADR-DCM group and significantly reduced by valsartan treatment (P<0.01). The protein levels of LV MMP-2 and MMP-9 were increased in ADR rats and attenuated by valsartan treatment (both P<0.01). However, no change in TIMP-1 was observed (P>0.05). The activities of LV myocardial MMP-2 and -9 gelatinolytic were increased significantly in ADR rats (both P<0.01) and attenuated by valsartan treatment (both P<0.01). CONCLUSION: Pretreatment with AT1 receptor blocker valsartan attenuates left ventricular remodeling and failure in a rat model of adriamycin-induced dilated cardiomyopathy. 相似文献
15.
Effect of acupuncture on CD4+ CD25+ Foxp3+ regulatory T-cells in rats of embryo implantation failure
GAO Wei-na GUO Yue WANG Li-jun TANG Xiao LIU Ya-fei CHEN Zhen-yan ZHANG Ming-min HUANG Guang-ying 《园艺学报》2013,29(8):1464-1470
AIM:To observe the effect of acupuncture on CD4+ CD25+ Foxp3(forkhead box P3)+ regulatory T-cells(Treg cells) in rats with embryo implantation failure. METHODS:One hundred and forty-four pregnant rats were randomly divided into control group(N), mifepristone treatment group(M), mifepristone+acupuncture treatment group(A) and mifepristone+progestin treatment group(W). The rats in groups M, A and W were treated with mifepristone-sesame oil solution on day 1, while the rats in group N were injected with the same amount of sesame oil. The Housanli(ST36) and Sanyinjiao(SP6) points were selected for acupuncture. From day 1 to the time of death, the rats in group A were fasten up and then the acupuncture was performed. Accordingly, the rats in group N and group M were only fixed, and the rats in group W were given progestin. Implanted embryos in each group were counted. The proportions of CD4+ CD25+ Foxp3+ Treg cells in peripheral blood and CD4+ Foxp3+ Treg cells in the endometrium were detected by flow cytometry. The mRNA and protein levels of Foxp3 were determined by real-time PCR and Western blotting, respectively. RESULTS:Compared with group N, the number of implanted embryos, the percentages of CD4+ CD25+ Foxp3+ Treg cells in peripheral blood and CD4+ Foxp3+ Treg cells in the endometrium, and the expression of Foxp3 protein and mRNA in the endometrium were significantly decreased in group M(P<005). Compared with group M, the above indexes in group A and group W were significantly increased. CONCLUSION: The effect of acupuncture in rats with embryo implantation failure may be closely correlated with the modulation of CD4+ CD25+ Foxp3+ Treg cells. 相似文献
16.
DENG Chun-yu TANG Cheng-jing KUANG Su-juan QIAN Wei-min LI Zi-cheng WU Shu-lin SHAN Zhi-xin YANG Min YU Xi-yong LIN Shu-guang 《园艺学报》2008,24(1):84-88
AIM: The effects of breviscapin on transient outward potassium current (Ito) and inward rectifier potassium current (IK1) channel in isolated ventricular myocytes of rats were determined. The mechanism of breviscapin at the ionic channel level was explored. METHODS: Single ventricular myocyte of rats was isolated by enzymatic dissociation. The whole-cell patch-clamp recording technique was used to record the change of Ito and IK1 channel current influenced by breviscapin. RESULTS: Breviscapin decreased the Ito channel current in a dose-dependent and voltage-dependent manner in ventricular myocytes of rats. (1) The current-voltage curve was significantly decreased. Breviscapin at concentrations of 0.02, 0.05, 0.08, 0.10 g·L-1 respectively decreased Ito current density (10.07±0.50)%, (27.47±2.36)%, (42.72%±2.50)% and (56.09±5.60)%. Ito was inhibited in a voltage-dependent manner, showing a significant attenuating effect at test potentials from 0 to + 50 mV. (2) The Ito activation curve, the activation curve and the recovery curve were not altered. (3) Breviscapin did not affect IK1. CONCLUSION: Breviscapin concentration-dependently decreases Ito channel current in ventricular myocytes of rat. 相似文献
17.
MA Cai-yun ZHANG Li-ke DU Feng-he LU Ling-qiao WANG Hong-xia ZENG Xiang-jun FU Ping MAN Qing-qing 《园艺学报》2005,21(1):68-71
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.
AIM: To investigate the effects of breviscapine on INa channel in isolated rat ventricular myocytes. METHODS: Single cell of rat ventricular myocyte was isolated by enzymatic dissociation. The whole-cell patch-clamp recording technique was used to observe the change of INa channel current influenced by breviscapine. RESULTS: Breviscapine decreased the INa channel current in a dose-dependent and voltage-dependent manner in rat ventricular myocytes. The current-voltage curve was significantly decreased. Breviscapin at concentrations of 1, 3, 30, 100 mg/L respectively decreased INa current density, which were (7.98±0.60)%, (37.73±2.31)%, (65.58%±2.90)% and (88.09±5.60)%, respectively. INa was inhibited in a voltage-dependent manner, showing a significant attenuating effect at test potentials from -30 mV to 0. The INa inactivation curve was shifted to left and the activation curve was shifted to right. Breviscapine step down the recovery curve significantly. CONCLUSION: Breviscapine concentration-dependently decreased INa channel current in rat ventricular myocytes. 相似文献
19.
AIM: To evaluate the effects of atorvastatin on nitric oxide(NO), endothelin-1(ET-1)and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion(AMI/R). METHODS: Twenty-four rabbits were randomized into 3 groups: 8 in AMI/R group, 8 in atorvastatin-treated group(5 mg·kg-1·d-1)and 8 in sham-operated group. Animals in the former two groups were subjected to 60 min of coronary occlusion followed by 120 min of reperfusion. Data on haemodynamics were collected. NO in blood sample, and in normal, and in infarcted reflow and no-reflow myocardium were evaluated respectively by nitrate reductase method. The levels of ET-1 in blood sample, and in normal, infarcted reflow and no-reflow myocardium were determined by radioimmunoassay. RESULTS: (1)Compared to the baselines, the heart rate(HR), systolic blood pressure(SBP), diastolic blood pressure(DBP), left ventricular systolic pressure(LVSP), maximal rate of increase and decline in left ventricular pressure(±dp/dtmax)and cardiac output(CO)in AMI/R and atorvastatin-treated groups were significantly declined, whereas left ventricular end-diastolic pressure(LVEDP)was increased after 60 min of coronary occlusion and 120 min of reperfusion(P<0.05 or P<0.01). However, in atorvastatin-treated group, LVSP, LVEDP, ±dp/dtmax and CO at the time point of 120 min of reperfusion recovered more significantly than those at the time point of 60 min of coronary occlusion(P<0.01), which was more significant than those in AMI/R group(P<0.05 or P<0.01). Compared to AMI/R group, the SBP and DBP were significantly heigher in atorvastatin-treated group(P<0.01).(2)In atorvastatin-treated group, the levels of ET-1 in blood sample were significantly lower than those in AMI/R group(P<0.01), and the levels of NO were significantly higher(P<0.01). Moreover, the levels of NO or ET-1 in infarcted reflow myocardium were significantly lower than that in AMI/R group(P<0.05 or P<0.01).(3)Atorvastatin could ameliorate myocardial function. CONCLUSION: Atorvastatin is effective in increasing NO and reducing ET-1 in blood plasma and local myocardium, and in protection of endothelial cells. Atorvastatin also has a beneficial effect on improving left ventricular function during acute myocardial infarction and reperfusion in rabbits. 相似文献
20.
WANG Jing JIANG Yu-xin CUI Feng-juan MIN Zhi-xue ZHOU Ping-ping WANG Hai-hua 《园艺学报》2013,29(9):1573-1578
AIM:To investigate the effect of ginkgo-dipyridamole injection (GD) on ischemia/reperfusion (I/R) injury in rat hearts in vitro and its possible mechanism. METHODS:Forty male Sprague-Dawley rats were randomly divided into 5 groups (n=8): normal control (NC) group, I/R group, ischemic preconditioning (IPC)+I/R group, GD+I/R group and GD+LaCl3+I/R group. Cardiac function indexes, including heart rate (HR), left ventricular systolic pressure (LVSP) and the maximal rise/fall rate of left ventricular pressure (±dp/dtmax), were detected at 5 time points, including stabilizing point, 30 min after ischemia, and 5, 30 and 60 min after reperfusion. The activity of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary effluent at the five time points was assayed. The concentration of Ca2+ and the content of α-ketoglutarate dehydrogenase (α-OGDH) in myocardial mitochondria were determined at the end of the whole experiment. RESULTS:Compared with I/R group, the cardiac function indexes in IPC+I/R and GD+I/R groups were improved at the reperfusion period (P<0.05), the activity of LDH and CK in coronary effluent and the concentration of Ca2+ in mitochondria were significant reduced (P<0.01), and the content of α-OGDH was increased (P<0.05). However, the protective effect of GD was inhibited by LaCl3 (P<0.05). CONCLUSION:GD protects rat hearts against I/R injury by inhibiting calcium overload and improving mitochondrial enzyme activity to stabilize mitochondrial energy metabolism. 相似文献