KIOM-79 inhibits high glucose or AGEs-induced VEGF expression in human retinal pigment epithelial cells

We evaluated whether KIOM-79, a mixture of extracts obtained from Puerariae lobata, Magnolia officinalis, Glycyrrhiza uralensis and Euphorbia pekinensis, could inhibit vascular endothelial growth factor (VEGF) expression in human retinal pigment epithelial (RPE) cells cultured under high glucose (HG, 25mM) or S100b (a specific ligand of the receptor for advance glycation end products (RAGE), 5microg/ml). In this study, the effect of KIOM-79 on HG or S100b-induced VEGF expression was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, RT-PCR, ELISA, and Western blot on human RPE cells. The MTT assay (p<0.01) revealed that KIOM-79 (up to 1mg/ml) had no effect on cell growth. HG or S100b induced an increase in expression of VEGF at both mRNA and protein levels (p<0.05; p<0.01 versus control). The increase in VEGF expression by HG or S100b was dose- and time-dependently prevented by KIOM-79 (p<0.05 versus 25mM glucose; p<0.01 versus S100b). Also, KIOM-79 inhibited protein kinase C (PKC)-alpha/beta(alpha) and p38 mitogen-activated protein kinase (MAPK) activation. Our results demonstrate that KIOM-79 can inhibit VEGF expression via inhibition of the MAPK and PKC pathway.     

银杏叶提取物GBE50对缺氧致内皮细胞功能的影响

目的初步探讨缺氧对人脐静脉内皮细胞功能的影响,以及银杏叶提取物GBE50在其中的作用。方法应用流式细胞技术、TUNEL、RT—PCR及Western blot等方法,探讨缺氧及GBE50对内皮细胞功能的影响。结果缺氧干预内皮细胞24h后,细胞活性氧（reactive oxygen species,ROS）水平及早期、晚期凋亡率均明显增加,伴随内皮素（endothelin-1,ET-1）mRNA水平及内皮型一氧化氮合成酶（endothelial oxide synthase,eNOS）蛋白水平的升高。缺氧前4h给予GBE50干预后发现,GBE5025μg／ml时可显著降低细胞早期及晚期凋亡率及ET-1 mRNA水平（P〈0．05）,部分降低因缺氧导致的ROS水平及eNOS蛋白表达的增高（P〉0．05）。结论缺氧可导致血管内皮功能障碍,而GBE50可部分或显著逆转缺氧所致的内皮功能障碍,GBE50对缺氧所致的内皮功能障碍有一定的保护作用。     

搜风祛痰法对血管紧张素Ⅱ诱导血管内皮细胞iNOS mRNA及ET-1 mRNA表达的影响

目的观察搜风祛痰法对血管紧张素Ⅱ致体外培养人脐静脉内皮细胞（HUVECs）iNOS及ET-1 mRNA表达的影响。方法制备兔活心汤含药血清。采用酶消化法培养HUVECs2-3代用于实验,采用RT-PCR法测定内皮细胞iNOSmRNA及ET-1 mRNA。结果活心汤可抑制AngⅡ导致的内皮细胞损伤,减少iNOSmRNA及ET-1 mRNA的表达。结论活心汤可抑制AngⅡ所致的HUVECs损伤,保护血管内皮细胞功能。     

搜风祛痰法中药对AngⅡ诱导人脐静脉内皮细胞NF-κB mRNA及ET-1 mRNA表达的影响

目的观察搜风祛痰法对血管紧张素Ⅱ致体外培养人脐静脉内皮细胞（HUVECs）核转录因子（NF-κB）mRNA及内皮素-1（ET-1）mRNA表达的影响。方法制备兔活心汤含药血清。采用酶消化法培养HUVECs2-3代用于实验,采用RT-PCR法测定内皮细胞NF-κB mRNA及ET-1 mRNA,随机分为5组：正常对照组,血管紧张素Ⅱ（AngⅡ）组,低浓度中药血清＋AngⅡ组,中浓度中药血清＋AngⅡ组,高浓度中药血清＋AngⅡ组。结果活心汤可抑制AngⅡ导致的内皮细胞损伤,减少NF-κB mRNA及ET-1 mRNA的表达。结论活心汤可抑制AngⅡ所致的HUVECs损伤,保护血管内皮细胞功能。     

鸦胆子油乳对人肺癌A549细胞血管内皮 生长因子表达的影响

目的：研究鸦胆子油乳对人肺癌A549细胞血管内皮生长因子(vascular endothelial growth factor，VEGF)表达的影响。方法：以健康人外周血单个核细胞(peripheral polymorphonuclear neutrophil，PMN)为正常对照，分别用不同剂量的鸦胆子油乳(0.5，1.25，2.5，5 g·L-1)与人肺癌A549细胞共育48 h，采用定量sandwich酶免疫技术和RT-PCR法分别测定PMN细胞和A549细胞培养上清液VEGF分泌和细胞内VEGF mRNA的表达，未加药组采用等量RPMI 1640培养液。结果：A549细胞上清液VEGF分泌量较外周血单个核细胞显著上升(120.73 vs 21.21，P<0.05)，2.5 g·L-1鸦胆子油乳作用48 h能使A549细胞VEGF分泌显著减少(20.30 vs 120.73，P<0.05)。A549细胞VEGF mRNA表达较骨髓单个核细胞也显著上升(0.957 3 vs 0.464 9，P<0.05)，鸦胆子油乳(0.5，1.25，2.5 g·L-1)作用48 h对A549细胞VEGF mRNA表达无显著影响，5 g·L-1鸦胆子油乳可显著降低A549细胞VEGF mRNA表达(0.468 2 vs 0.957 3，P<0.05)。结论：鸦胆子油乳能降低A549细胞VEGF的分泌和表达，该作用可能是其抗肿瘤的作用机制之一。     

Effects of quercetin on the release of endothelin, prostacyclin and tissue plasminogen activator from human endothelial cells in culture

Quercetin and related flavonoids are naturally occurring polyphenolic compounds with multiple pharmacological activities. Using cultured human umbilical vein endothelial cells, we investigated the effects of quercetin on endothelin (ET-1) and tissue plasminogen activator (t-PA) release induced by thrombin. We observed that when endothelial cells pretreated with 5 or 50 microM of quercetin were incubated for 4 and 24 h with thrombin, ET-1 concentration-dependently decreased (n = 6, P < 0.01, at 4 h IC50 = 1.54 microM, at 24 h IC50 = 2.78 microM). Under the same experimental conditions, quercetin significantly increased t-PA (n = 6, P < 0.01, at 4 h EC50 = 0.71 microM and at 24 hrs EC50 = 0.74 microM). In the same preparation, we evaluated prostacyclin (PGI2) release, induced by thrombin activated platelets, as determined by a 6-Keto-PGF1alpha radioimmunoassay. Following the treatment of cultured endothelial cells with activated platelets, the concentration of 6-Keto-PGF1alpha was significantly increased (P < 0.01). Quercetin (1, 5, and 20 microM) inhibited PGI2, in a concentration-dependent manner (n = 6, P < 0.05). Our data indicate that quercetin modulates the release of ET-1, t-PA, and PGI2 from vascular endothelial cells.     

中药脑心通对血管内皮细胞一氧化氮和内皮素-1的影响

目的 观察脑心通对氧化低密度脂蛋白(Ox-LDL)诱导的人脐静脉内皮细胞(HUVEC) 一氧化氮(NO)和内皮素-1(ET-1)分泌量的影响.方法 以培养HUVEC作为靶细胞,在内皮细胞培养基中加入Ox-LDL(50 mg/L)制备细胞损伤模型,并以不同浓度脑心通含药血清预先进行干预,分别采用硝酸还原酶法和放免法检测细胞上清液中的NO及ET-1的含量.结果 Ox-LDL作用HUVEC 24h后,HUVEC上清液中NO含量明显降低,而ET-1的含量明显升高,均明显高于正常对照组(P＜0.05);而预先加入脑心通含药血清或阿托伐他汀药液组NO含量明显升高,且在加入步长脑心通含药血清组,这种作用在一定剂量范围内随药物剂量的增加而增强(P＜0.05).结论 步长脑心通能够通过促进内皮细胞NO的合成与释放从而发挥对血管内皮细胞的保护作用,有利于减轻或抑制动脉粥样硬化的形成与发展.     

Sinomenine suppresses TNF-alpha-induced VCAM-1 expression in human umbilical vein endothelial cells

Sinomenine (SN), an alkaloid prepared from the root of Sinomenium acutum Rehd. Et wils, is used to alleviate the symptoms of rheumatism in Chinese medicine. In the present study, the potential inhibition of TNF-alpha-induced VCAM-1 expression on human umbilical vein endothelial cells (HUVECs) was evaluated in vitro. HUVECs were isolated from freshly collected umbilical cords. Positive controls were stimulated with TNF-alpha, omitting SN. Negative controls were cultured omitting TNF-alpha and SN. Experimental groups were co-cultured with TNF-alpha and SN at different concentrations (0.25, 0.5, and 1.0 mol/L), or TNF-alpha and Dexamethasone (Dex) at a concentration of 1.0 x 10(-6) mol/L. Cells were harvested after culturing with the above drugs for 12 h. VCAM-1 mRNA expression was detected by real-time quantitative PCR, and VCAM-1 expression was detected by flow cytometry. The experimental data indicated that VCAM-1 mRNA and VCAM-1 were induced by TNF-alpha. The relative VCAM-1 mRNA expression decreased in the experimental groups (p<0.05). Concentrations of SN at 0.5 and 1.0 mol/L inhibited expression of VCAM-1 (p<0.05). SN at concentration of 0.25 mol/L and Dex at concentration of 1.0 x 10(-6) mol/L did not show an inhibitory effect on VCAM-1 expression in TNF-alpha-induced HUVECs. Our preliminary data indicates that SN has an inhibitory effect in vitro on TNF-alpha-induced VCAM-1 expression at both mRNA level and protein level in HUVECs, and suggests that SN may be a novel method of immunotherapy for rheumatic carditis or rheumatic heart disease.     

生芪降糖颗粒对胰岛素抵抗鼠的作用及机制研究

目的 观察生芪降糖颗粒干预胰岛素抵抗（IR）模型大鼠的作用,并探讨其作用机制。方法 选取Wistar大鼠以高脂饮食、链脲佐菌素腹腔注射制造IR模型,随机分组分别给予不同剂量的生芪降糖颗粒、罗格列酮治疗,同时设立正常对照组,观察血糖以及主动脉内皮素-1（ET-1）、蛋白激酶（PKC）蛋白表达的变化。结果 生芪降糖颗粒中、高剂量组和罗格列酮组大鼠的血糖均明显下降,并以生芪降糖颗粒高剂量组下降最明显。模型组主动脉ET-1、PKC表达量较正常组显著升高（P〈0．05）。罗格列酮组和生芪降糖颗粒高剂量组主动脉ET-1、PKC表达量较模型组均下降,与模型组比较差异具有显著性（P〈0．05）,且呈剂量依赖性。结论 生芪降糖颗粒通过降糖、抑制ET-1、PKC表达等作用,改善血管内皮功能,从而起到胰岛素增敏及减轻胰岛素抵抗的作用。     

Salvia Miltiorrhiza Induces VEGF Expression and Regulates Expression of VEGF Receptors in Osteoblastic Cells

This study investigated in vitro whether Salvia Miltiorrhiza Bunge (SM) induces vascular endothelial growth factor (VEGF) expression and regulates expression of VEGF receptors 1 (VEGFR‐1) and 2 (VEGFR‐2) on osteoblasts. MC3T3‐E1 cells were cultured with SM and VEGF at points 24, 48 and 72 h. A blank control was included. The mRNA expression of VEGF, VEGFR‐1 and VEGFR‐2 was examined using real‐time polymerase chain reaction. VEGF protein expression was examined using enzyme linked immunosorbent assay. SM increased VEGF mRNA expression by 21% at 24 h (p < 0.05), 5% (p < 0.05) at 48 h and 74% (p < 0.001) at 72 h, while external VEGF intervention decreased the internal VEGF expression by 51% at 24 h (p < 0.001) and increased it by 126% at 72 h (p < 0.001). SM increased VEGF protein at 72 h (p < 0.05). VEGFR‐1 mRNA expression, in response to SM, decreased by 8% (p < 0.05) at 72 h and decreased following VEGF at 24 and 72 h by 20% (p < 0.001) and 15%, respectively, (p < 0.001). VEGFR‐2 mRNA expression increased following SM at 24 and 48 h by 25% (p < 0.05) and 73% (p < 0.05), respectively, and decreased at 72 h by 13% (p < 0.05). It was concluded that SM modulated expression of VEGF and its receptors in MC3T3‐E1 cells. Copyright © 2013 John Wiley & Sons, Ltd.     

小檗碱对HeLa细胞诱导的血管内皮细胞增殖作用的影响

目的:探讨小檗碱对HeLa细胞诱导血管内皮细胞增殖作用的影响及其作用机制.方法:用MTT法检测小檗碱对HUVECs增殖及HeLa细胞条件培养液诱导HUVECs增殖的影响;用ELISA检测HeLa细胞上清液中VEGF的含量.结果:在0～48h范围内小檗碱对HUVECs的增殖有明显抑制作用,并有浓度时间依赖关系;经浓度为5μg/ml～40μg/ml小檗碱作用后的HeLa细胞条件培养液对HUVECs增殖的抑制率为24.4%～44.2%,而HeLa细胞条件培养液对HUVECs增殖有明显促进作用;小檗碱抑制HeLa细胞VEGF的表达.结论:小檗碱可能通过抑制HeLa细胞VEGF的表达从而抑制肿瘤血管生成.     

Effect of brain functional recovery decoction on expression of vascular endothelial growth factor and Ang-1 protein in a rat cerebral ischemia reperfusion model

OBJECTIVE: To investigate the effect of brain functional recovery decoction(BFRD) on expression of vascular endothelial growth factor(VEGF) and angiopoietin-1(Ang-1) protein in rats with cerebral ischemia reperfusion injury, and to explore the mechanism of action of BFRD.METHODS: Using the suture-occlusion method, a Wistar rat model of focal cerebral ischemia reperfusion was established. The rats were randomly divided into treatment group, model group, and sham operation group. The treatment group was administered BFRD. In situ hybridization was used to detect VEGF m RNA expression. Immunohistochemistry was used to observe expression of Ang-1 protein.RESULTS: VEGF mRNA expression was greater in the model group compared with the sham operation group(P 0.05); Ang-1 protein expression was more obvious in the treatment group than the model group(P 0.05).CONCLUSION: BFRD promoted VEGF m RNA and Ang-1 protein expression in the brains of rats with cerebral ischemia, suggesting increased angiogenesis.     

大黄素对脂多糖诱导的内皮细胞损伤Rho/ROCK信号通路的影响

目的:探讨大黄素对脂多糖(LPS)诱导损伤的人脐静脉血管内皮细胞(HUVECs)骨架及通透性影响的作用机制。方法:HUECs分为五组:正常对照组、内皮炎症损伤模型组(0.2μg/m L LPS)、大黄素干预组(10μmol/L大黄素+0.2μg/m L LPS)、抑制剂对照组(0.2μg/m L LPS+50μmol/L Y27632)、西药对照组(10-5mol/L缬沙坦+0.2μg/m L LPS)。首先,以内皮细胞生物学功能PCR基因芯片技术筛选可能的基因改变。结合基因芯片结果和文献中各基因功能,拟定观察Rho/ROCK通路相关的和可能涉及调节细胞骨架的基因,如纤连蛋白(FN)、整合素A5(ITGA5)、Ras同源基因家族成员(Rho A)、肌球蛋白轻链磷酸酶(MLCP)、磷脂酰肌醇-4,5-二磷酸肌醇3-激酶(PI3K)、黏着斑激酶(FAK)、血管内皮生长因子(VEGF)、血管内皮生长因子受体2(VEGFR2)的m RNA表达水平,进行实时荧光定量PCR验证,同时以Western blotting对ITGA5、Rho A、4,5-二磷酸磷脂酰肌醇(PIP2)和磷酸化的肌球蛋白轻链(PMLC)进行蛋白水平的研究。结果:1LPS组Rho/ROCK通路相关基因(FN、ITGA5、Rho A、MLCP、PI3K、FAK、VEGF、VEGFR2)表达显著升高,ITGA5、Rho A、PIP2、PMLC的蛋白表达亦升高,与正常对照组比较,差异均有统计学意义(P0.05)。2与LPS组比较,Y27632组、缬沙坦组的FN、ITGA5、Rho A、PI3K、FAK、VEGF、VEGFR2基因表达下降,MLCP表达上升,差异均有统计学意义(P0.05);ITGA5、PIP2的蛋白表达下降;缬沙坦组PMLC表达降低,差异有统计学意义(P0.05)。3与LPS组比较,大黄素组FN、PI3K、FAK表达降低,MLCP表达上升,差异均有统计学意义(P0.05);PIP2蛋白表达下降,差异有统计学意义(P0.05)。结论:LPS可激活Rho/ROCK信号通路,成功构建HUVECs内皮损伤模型;Y27632和缬沙坦可阻断Rho/ROCK通路,对细胞骨架有较强的保护作用;大黄素可轻度抑制Rho/ROCK通路,同时可能通过调节PI3K、MLCP表达而影响其他通路(如AKT和/或FAK-PI3K信号通路)从而发挥对内皮细胞损伤的干预作用。     

痰瘀同治方含药血清对ox-LDL损伤人脐静脉内皮细胞 NF-κB和ICAM-1表达的影响

目的:观察痰瘀同治方含药血清对氧化型低密度脂蛋白(ox-LDL)损伤的人脐静脉内皮细胞(HUVECs)核因子-κB(NF-κB)的活化和细胞间黏附分子-1(ICAM-1)表达的影响,探讨痰瘀同治方抗动脉粥样硬化的分子机制.方法:SD大鼠随机分为正常组,痰瘀同治方低、中、高剂量组( 24,48,72 g·kg-1·d-1)和辛伐他汀组(18 mg·kg-1·d-1),制备含药血清.体外培养HUVECs,实验分为6组:①正常组;②模型组;③痰瘀同治方低剂量组;④痰瘀同治方中剂量组;⑤痰瘀同治方高剂量组;⑥辛伐他汀组.其中①、②组用20％正常鼠血清,③～⑥组用20％各组含药血清,除正常组外其余各组加入100 mg·L-1 ox-LDL刺激3h或24 h后进行各项指标测定.Real-time PCR法检测HUVECs NF-κB p65和ICAM-1mRNA表达,Western blotting检测ICAM-1蛋白表达,细胞免疫荧光法检测NF-κB p65核移位变化.结果:HUVECs经ox-LDL刺激后NF-κB p65和ICAM-1的表达与正常组比较均明显升高(P＜0.01).痰瘀同治方和辛伐他汀含药血清能显著降低NF-κB p65 mRNA表达及抑制其核移位(P＜0.05),降低ICAM-1 mRNA和蛋白表达(P＜0.05),其中以辛伐他汀和痰瘀同治方大剂量含药血清作用尤为显著(P＜0.01).结论:痰瘀同治方能够通过抑制血管内皮细胞NF-κB通路,降低ICAM-1表达,进而减少炎症反应,这可能是其抗动脉粥样硬化分子机制之一.     

乳宁Ⅱ号对TA2小鼠乳腺癌MA-891移植瘤中血管内皮生长因子表达的影响

目的研究乳宁Ⅱ号对TA2小鼠乳腺癌移植瘤中血管内皮生长因子(VEGF)表达及肺转移的影响。方法将体外培养的MA-891小鼠乳腺癌细胞接种于TA2小鼠右腋部皮下,造成小鼠移植瘤肺转移模型,同时予乳宁Ⅱ号治疗。结果乳宁Ⅱ号可抑制移植瘤生长,减少肺转移的发生(P<0．05),降低肿瘤组织中VEGF蛋白及VEGF mRNA表达(P<0．05)。结论乳宁Ⅱ号可通过降低肿瘤组织中VEGF蛋白及VEGF mRNA表达,发挥抑瘤和抗转移作用。     

青蒿琥酯对脂多糖致血管内皮细胞活化及损伤的保护作用

目的观察中药青蒿提取物青蒿琥酯(artesunate,AR)对脂多糖(lipololysaccharide ,LPS)诱导的人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)活化及损伤状态下的保护作用及相关机制．方法建立人脐静脉内皮细胞培养,细胞生长至融合状态后分别加入LPS及不同浓度的AR(0．04mg／L、0．2mg／L、1mg／L、5mg／L及20mg／L)共同孵育24h,ELISA方法检测培养上清中血管假性血友病因子(von Willebrand factor,vWF)含量,Western blot法检测细胞间黏附分子(ICAM—1)蛋白表达,原位杂交方法检测肿瘤坏死因子(TNFα)mRNA表达结果暴露于1ug／ml LPS后,HUVECs的vWF及ICAM1表达较对照组明显增加,加入AR后,随AR浓度增加明显下调LPS升高的vWF及ICAM—1表达,至AR为1mg／L时,其vWF与ICAM—1表达与LPS组比较差异均有显著性(P＜0．05)。AR抑制LPS升高的vWF及ICAM-1表达呈一定的浓度依赖方式．原位杂交显示在AR0．2mg／L及1mg／L时明显下调TNFα mR—NA表达,与LPS组比较差异有显著性(P＜0．05,P＜0．01)、结论青蒿琥酯对脂多糖诱导的HUVECs的活化及损伤有保护作用,可能与AR抑制TNFα mRNA表达有关。     

川芎嗪对急性冠脉综合征患者介入术后血小板活化及血管内皮功能的影响

目的探讨川芎嗪对冠脉介入治疗术后血小板活化状态及内皮功能的影响。方法80例急性冠脉综合征（ACS）患者随机分为川芎嗪治疗组（简称川芎嗪组,40例）和常规治疗组（简称常规组,40例）,两组病例在冠脉介入术前和术后次日采用流式细胞仪检测血小板活化指标CD62p、CD63及糖蛋白（GP）Ⅱb／Ⅲa受体复合物的表达水平;用双抗体夹心固相酶联免疫吸附试验（ELISA）测定血浆假血友病因子（vWF）的表达水平;用放射免疫测定法测定血浆内皮素1（ET-1）的表达水平;用酶法测定血浆一氧化氮（NO）的含量;用彩色多谱勒超声诊断仪测量内皮依赖性血管舒张（FMD）功能。静脉滴注川芎嗪治疗14天后复查上述指标并进行比较。结果与健康对照组比较,ACS患者术前CD62p、CD63、GPⅡb／Ⅲa受体复合物、vWF及ET-1均显著升高（P〈0．01）,FMD和NO显著降低（P〈0．01）。冠脉介入术后血小板活化有升高趋势,而vWF因子升高（P〈0．05）,FMD降低（P〈0．05）,但ET-1和NO水平差异无统计学意义（P〉0．05）。与常规组比较,川芎嗪组CD62p、CD63、vWF、ET-1及GPⅡb／Ⅲa的水平明显降低（P〈0．05,P〈0．01）,FMD水平增加（P〈0．05）。结论川芎嗪可用于冠状动脉介入术前、后预防和治疗冠脉内血栓及保护血管内皮功能。     

二陈汤加味对慢性阻塞性肺疾病大鼠VEGF，VEGFR2，IL-4，ET-1的影响

目的:观察二陈汤加味对慢性阻塞性肺疾病(COPD)大鼠血管内皮生长因子(VEGF)及其受体2(VEGFR2),白细胞介素(IL)-4,内皮素-1(ET-1)及核转录因子-κB(NF-κB)的影响。方法:将50只SD大鼠随机分为5组,每组10只,组别为正常组、模型组、二陈汤加味低、中、高剂量组(10,20,40 g·kg~(-1)·d~(-1))。以烟熏合并脂多糖(LPS)气管滴注的方法制备COPD大鼠模型。成功造模后,治疗组灌胃给药,正常组及模型组灌胃等体积蒸馏水。光镜观察大鼠肺血管的病理变化,并测定肺血管壁厚度。酶联免疫吸附测定(ELISA)检测大鼠血清、支气管肺泡灌洗液(BALF)和肺组织匀浆液中IL-4的含量,实时荧光定量PCR(Real-time PCR)检测ET-1 mRNA表达;免疫组化检测肺组织VEGF,ET-1及VEGFR2的表达。结果:与正常组比较,模型组大鼠血清,BALF及肺组织匀浆液中IL-4含量均显著降低(P0.01);与模型组比较,二陈汤加味低、中、高剂量组IL-4含量均有程度不等的上升(P0.01)。与正常组比较,模型组肺组织ET-1 mRNA表达量显著升高(P0.01);与模型组比较,二陈汤加味低、中、高剂量组肺组织ET-1 mRNA表达量均显著降低(P0.01)。与正常组比较,模型组大鼠肺组织中的VEGF,VEGFR2表达增多,ET-1蛋白表达显著上升(P0.01),与模型组比较,二陈汤加味低、中、高剂量组VEGF,VEGFR2表达降低,ET-1蛋白表达显著降低(P0.01)。结论:二陈汤加味可能通过提升IL-4的含量,抑制VEGF,VEGFR2及ET-1的蛋白表达,从而减轻COPD大鼠肺组织炎症及肺血管重构的进程,减缓COPD及其并发症的进展。     

通心络胶囊联合津力达颗粒对2型糖尿病患者血糖及血管内皮功能的影响

目的：探讨通心络胶囊联合津力达颗粒对2型糖尿病(type 2 diabetes, T2DM)患者血糖及血管内皮功能的影响。方法将100例T2DM患者按随机数字表法分为2组各50例,2组患者均皮下注射门冬胰岛素30注射液、口服辛伐他汀降脂及肠溶阿司匹林抗血小板聚集,观察组在对照组基础上加服通心络胶囊及津力达颗粒。均治疗12周。采用双抗体两步夹心 ELISA 测定血管内皮生长因子(vascular endothelial growth factor, VEGF),采用放射免疫分析法测定内皮素-1(endothelin-1, ET-1),采用硝酸还原酶法测定NO,采用美国AU5800系列全自动生化分析仪测定血糖及HbAlc,并对结果进行比较。结果治疗后,观察组 FPG[(7.03±2.11)mmol/L 比(8.09±2.03)mmol/L,t＝1.911]、2hPG[(9.27±2.03)mmol/L比(12.06±3.54)mmol/L,t＝1.946]、HbAlc[(6.98±1.58)%比(8.06±2.13)%,t＝2.013]水平均低于对照组(P＜0.05)。与对照组治疗后比较,观察组VEGF[(684.61±84.37)ng/L比(514.28±79.52)ng/L,t＝2.136]、NO[(43.28±6.40)ng/L 比(34.64±6.70)ng/L,t＝2.097]水平升高(P＜0.05),ET-1[(53.13±7.24)μmol/L比(60.09±7.18)μmol/L,t＝2.271]下降(P＜0.05)。结论通心络胶囊联合联合津力达颗粒可降低T2DM患者血糖水平,改善血管内皮功能。