汉防己甲素体外辅助多柔比星杀伤胃癌细胞及机制研究

目的探讨中药活性成分汉防己甲素是否能在体外辅助多柔比星杀伤胃癌细胞并研究其机制。方法噻唑蓝(MTT)法检测胃癌细胞系MGC-803相对细胞活力。Western blot实验检测MGC-803细胞中小窝蛋白-1(caveolin-1)表达水平、蛋白激酶B(AKT)和B淋巴细胞瘤-2蛋白(Bcl-2)相关细胞死亡激动子(Bad)磷酸化水平、半胱天冬酶-9(caspase-9)和半胱天冬酶-3(caspase-3)活化水平。免疫共沉淀法检测Bad与大分子B淋巴细胞瘤蛋白(Bcl-xl)及Bcl-2相互作用。流式细胞术检测MGC-803细胞的凋亡。结果汉防己甲素+多柔比星组MGC-803相对细胞活力(0.34±0.03)显著低于多柔比星(0.79±0.06)(P0.05),汉防己甲素+多柔比星组MGC-803的细胞凋亡率显著高于多柔比星组[(40.32±3.51)%比(12.23±1.13)%,P0.05]。汉防己甲素+多柔比星组MGC-803细胞的caveolin-1表达水平、AKT和Bad的磷酸化水平均低于多柔比星组,而汉防己甲素+多柔比星组MGC-803细胞的Bad与Bcl-xl及Bcl-2结合水平、caspase-9和caspase-3活化水平均高于多柔比星组。汉防己甲素+多柔比星+caveolin-1质粒组MGC-803相对细胞活力显著高于汉防己甲素+多柔比星组[(0.71±0.06)比(0.34±0.03),P0.05],而其细胞凋亡率显著低于汉防己甲素+多柔比星组[(15.94±1.22)%比(40.32±3.51)%,P0.05]。结论汉防己甲素可能通过caveolin-1/AKT/Bad途径增强多柔比星对胃癌细胞的凋亡诱导活性。     

Survey: Chinese children get inadequate sleep

Background The identification of vulnerable plaques before rupture is an important clinical goal. The purpose of the present study was to assess the difference in plaque composition among patients with acute coronary syndrome （ACS） and stable coronary artery disease （SCAD） by intravascular ultrasound virtual histologic analysis. Methods One hundred and thirty-nine patients were divided into ACS group and SCAD group according to clinical presentation. A total of 229 de novo lesions with 〉50% stenosis in native coronary arteries with diameters 〉2.5 mm were studied with intravascular ultrasonography. Geometric and compositional data were obtained using intravascular ultrasound virtual histology software. Results There were no significant differences in overall lesions for fibrous （（52.0±11.9）% vs （54.3±8.5）%, P〉0.05）, fibrolipidic （（12.3±10.1）% vs （13.8±9.5）%,P〈0.05）, calcium （（14.0±9.1）% vs （19.3±13.1）%, P〉0.05）, or necrotic core （（22.0±11.1）% vs （19.7±5.4）%, P〉0.05） percentages in ACS and SCAD patients, respectively. There were also no significant differences in culprit lesions for fibrous （（46.4±12.0）% vs （53.6±8.8）%, P〉0.05）, fibrolipidic （（9.1±9.0）% vs （12.9±9.7）%, P〉0.05）, calcium （（16.6±9.7）% vs （21.8±26.3）%, P〉0.05）, or necrotic core （（28.0±12.6）% vs （20.6±5.2）%, P〉0.05） percentages in ACS and SCAD patients, respectively. High density lipoprotein-cholesterol levels 〉1.04 mmol/L were associated with more fibrolipidic （（14.5±10.4）% vs （7.1±6.5）%, P〈0.05） and less necrotic core （（20.6±9.7）% vs （27.9±12.6）%,P〈0.05） percentages in the cohort with ACS. Conclusions In this study, coronary plaque composition assessed by intravascular ultrasound virtual histologic analysis was not significantly different between ACS and SCAD patients. The anatomic relationship of the specific plaque components to the lumen of the vessel was more important than th     

Predictors of left atrial appendage stunning after electrical cardioversion of non-valvular atrial fibrillation

Atrialfibrillation (AF)isthemostcommon persistentarrhythmia,leadingtoembolismsfrequently 1Restorationofsinusrhythmimprovescardiacfunctionalcapacity,alleviatespalpitation ,andreducestheriskofembolisms Direct currentcardioversionhastheadvantageofimmediaterestorationofsinusrhythm ,butitisfrequentlyassociatedwithtransientatrialmechanicaldysfunction ,i e “atrialstunning” ,whichmayincreasetheriskofsubsequentthromboembolicevents 2 　Withtheadventoftransesophagealechocardiography (TEE) ,leftatrial…     

Decreased small arterial compliance with increased serum vascular endothelial growth factor-A and circulating endothelial progenitor cell in dilated cardiomyopathy

Background Evidence showed that both myocardium and blood vessels were damaged in dilated cardiomyopathy （DCM）. However, the changes in arterial compliance, serum cytokines and circulating endothelial progenitor cells （EPC）, and their correlations remain unknown.
Methods Sixty-five DCM patients and 49 healthy volunteers were studied. Both large artery compliance （C1） and small artery compliance （C2） were measured with the CVProfUor DO-2020. Quantitative enzyme-linked immunosorbent assays （ELISAs） were used to measure the levels of vascular endothelial growth factor-A （VEGF-A） and VEGF receptor 2 （VEGF-R2）. Circulating EPC was assessed by EPC colony-forming assays and flow cytometry （CD133^＋/CD34^＋cells）. Phagocytized Dil-acLDL and binded FITC-UEA-I were used to analyze endothelial lineage marker expression by immunofluorescence.
Results Although C2 was markedly lower in DCM patients than in control group （（3.8±1.8） ml/mmHg × 100 vs （5.0±2.2） ml/mmHg × 100, P〈0.0001）, there was no statistically significant difference in C1 between the two groups （P〉0.05）. Levels of VEGF-A, the numbers of colony-forming units （CFU） and the fractions of EPC were obviously higher in DCM patients than in control group （（127.6±139.5） pg/ml vs （58.8±42.9） pg/ml, P〈0.0001; （2.5±1.5）% vs （0.5±0.3）%, P〈0.05; 23.5±12.8 vs 10.8±7.4, P〈0.01, respectively） and however, there was no significant difference in VEGF-R2 between two groups （P〉0.05）. LgVEGF-A was positively correlated with the number of EPC-CFU （r=-0.435; P〈0.05） and inversely correlated with C2 （r=-0.543; P〈0.001） in DCM patients. Conclusions The reduction of C2, a sensitive marker reflecting endothelial dysfunction, was observed in DCM patients and closely related to the increase in serum VEGF-A.     

Connective tissue growth factor is associated with the early renal hypertrophy in uninephrectomized diabetic rats

Structural remodeling in diabetic kidney ischaracterized by the early appearance ofhypertrophy in glomerular and tubular components, subsequently developing the thickness of glomerular and tubular basement membranes, and the progressive accumulation of extracellular matrix components.1 Recent studies have demonstrated that early renal hypertrophy is detrimental to the kidney in the long term and is a precursor of development of renal fibrosis.2,3 However, the exact mechanism of renal hypertrop…     

黄芩素通过SIRT1/p53途径提高宫颈癌细胞对顺铂的敏感性

目的: 探讨中药活性成分黄芩素是否对顺铂有协同抗宫颈癌效应并研究其机制。方法: MTT实验检测宫颈癌细胞系Hela的细胞活力;流式细胞术检测Hela细胞的凋亡;western blot实验检测Hela细胞中SIRT1、p53、乙酰化p53、Puma的表达水平及caspase-3的活化水平。结果: 顺铂联合黄芩素对Hela的细胞活力抑制率(66.3±5.7)和凋亡诱导率(38.4±3.2)显著高于顺铂单治疗组的的细胞活力抑制率(18.1±1.4,P<0.05)和凋亡诱导率(10.4±0.9,P<0.05)。顺铂联合黄芩素治疗组的SIRT1表达水平显著低于顺铂单治疗组,同时顺铂联合黄芩素治疗组的p53乙酰化水平和表达水平、Puma表达水平及caspase-3活化水平均显著高于顺铂单治疗组。另外,顺铂+黄芩素+SIRT1质粒组Hela的细胞活力抑制率(25.7±2.1)和凋亡诱导率(14.5±1.1)显著低于顺铂联合黄芩素组Hela的细胞活力抑制率(66.3±5.7,P<0.05)和凋亡诱导率(38.4±3.2,P<0.05)。结论: 黄芩素通过SIRT1/p53途径增强顺铂对宫颈癌细胞的杀伤活性。     

槲皮素通过SIRT1/ROS/DR5途径发挥对TRAIL的协同抗前列腺癌活性

目的: 探讨中药活性成分槲皮素是否对TRAIL有协同抗前列腺癌效应并研究其机制。方法: MTT实验检测前列腺癌细胞系PC3的细胞活力;流式细胞术检测PC3细胞的凋亡和ROS的产生;western blot实验检测PC3细胞中SIRT1、DR5的表达水平及caspase-8、caspase-3的活化水平。结果: TRAIL联合槲皮素对PC3的细胞活力抑制率(64.7±5.2)和凋亡诱导率(34.7±2.6)显著高于TRAIL单治疗组的细胞活力抑制率(16.9±1.4,P<0.05)和凋亡诱导率(9.1±0.8,P<0.05)。TRAIL联合槲皮素治疗组的SIRT1表达水平显著低于TRAIL单治疗组,同时TRAIL联合槲皮素治疗组的DR5表达水平、ROS产生水平及caspase-8、caspase-3活化水平均显著高于TRAIL单治疗组。另外,TRAIL+槲皮素+SIRT1质粒组PC3的细胞活力抑制率(23.4±1.9)和凋亡诱导率(12.5±1.2)及TRAIL+槲皮素+NAC组PC3的细胞活力抑制率(21.5±1.8)和凋亡诱导率(11.3±1.1)均显著低于TRAIL联合槲皮素组PC3的细胞活力抑制率(64.7±5.2,P<0.05)和凋亡诱导率(34.7±2.6,P<0.05)。结论: 槲皮素通过SIRT1/ROS/DR5途径发挥对TRAIL的协同抗前列腺癌活性。     

Monocyte chemoattractant protein-1 expression in renal tissue is associated with monocyte recruitment and tubulo-interstitial lesions in patients with lupus nephritis

目的　观察狼疮性肾炎 (LN)患者肾组织中单核细胞趋化因子 (MCP 1)的分布及其与肾间质单核细胞浸润和间质病变的关系 ,探讨其在LN患者肾小管间质病变中的作用。方法　采用PAP四层法对 18例LN患者肾组织MCP 1,CD68 ,CD4 ,及CD8 进行免疫组化染色。同时取 8例微小病变型肾病患者作为对照。结果　 18例患者肾组织中均有不同程度的MCP 1染色阳性。其主要位于肾小管基侧膜 (16/ 18例 )及间质小血管壁 (9/ 18例 )上。对照组MCP 1阳性的小管明显低于狼疮性肾炎患者 (7 4± 6 2 %vs 2 6 7± 2 2 8% ,P <0 0 1)。LN患者肾间质中CD4 ,CD8 及CD68 细胞数明显高于对照。其MCP 1阳性小管数与间质CD68 细胞浸润及间质病变的程度明显相关。而与CD4 ,CD8 细胞浸润程度及患者尿蛋白的多少无相关性。结论　LN患者肾小管MCP 1表达增加可能是导致间质单核细胞浸润及肾小管间质损伤的一个重要原因     

Electrical remodeling of membrane ionic channels of hypertrophied ventricular myocytes from spontaneously hypertensive rats

Ｍｅｔｈｏｄｓ　Ｍｅｍｂｒａｎｅｉｏｎｉｃｃｈａｎｎｅｌｓｗｅｒｅｓｔｕｄｉｅｄｉｎｅｎｚｙｍａｔｉｃａｌｌｙｄｉｓｐｅｒｓｅｄｓｐｏｎｔａｎｅｏｕｓｌｙｈｙｐｅｒｔｅｎｓｉｖｅｒａｔｓ (ＳＨＲｓ)ｌｅｆｔｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓｕｓｉｎｇｔｈｅｗｈｏｌｅ ｃｅｌｌｃｏｎｆｉｇｕｒａｔｉｏｎｏｆｐａｔｃｈ ｃｌａｍｐｔｅｃｈｎｉｑｕｅ ,ｗｉｔｈｎｏｒｍａｌＷｉｓｔａｒｒａｔｓｖｅｎｔｒｉｃｕｌａｒｍｙｏｃｙｔｅｓａｓｃｏｎｔｒｏｌｓ Ｗｅｏｂｓｅｒｖｅｄｄｅｐｏｌａｒｉｚｉｎｇｃｕｒｒ…     

The role of calcineurin in the lung fibroblasts proliferation and collagen synthesis induced by basic fibroblast growth factor

Objective To investigate the role of calcineurin (CaN) in the lung fibroblast proliferation and collagen synthesis induced by basic fibroblast growth factor (bFGF).Methods We used Western blot and immunohistochemical methods for investigating the content and distribution of calcineurin in the lung tissue. Calcineurin activity in different tissues was measured using 32P-labelled substrate. In the primary culture of lung fibroblasts, 3H-thymidine (3H-TdR) and 3H-proline incorporation methods were used to study the effect of cyclosporin A (CsA), an inhibitor of calcineurin, on the lung fibroblast DMA and collagen synthesis stimulated by bFGF.Results We found that calcineurin was expressed in lung tissue and has phosphatase activity (7.1±2.0 pmol Pi/mg pr/min). CsA (10~(-8)-10~(-6) mol/L) inhibited lung fibroblast 3H-TdR incorporation induced by bFGF in a dose-dependent manner, with the inhibitory rates by 20% , 46% and 66% (P< 0.01). CsA (10~(-7) -10~(-6) mol/L) inhibited 3H-proline incorporation in lung     

Tissue Doppler imaging study of right ventricular myocardial systolic activation in subjects with pulmonary arterial hypertension

Background Tissue Doppler imaging （TDI） has provided an objective means to quantify global and regional left ventricular （LV） and right ventricular （RV） function with improved accuracy and greater reproducibility than conventional echocardiography. This study was conducted to assess RV myocardial systolic activation by TDI in subjects with pulmonary arterial hypertension （PAH）. Methods A total of 30 patients with PAH and 30 healthy volunteers, all comparable in age and sex, underwent standard Doppler echo and TDI. Using pulsed Doppler echocardiography combined with TDI, the following regional parameters were evaluated in three different myocardial segments （RV basal lateral wall, basal septal, and LV basal lateral） on apical 4-chamber view： systolic （Sm）, early- and late-diastolic （Em and Am） peak velocities. RV myocardial systolic activation delay was defined as the difference in time to peak TDI systolic velocities between the RV basal lateral wall and basal septal. In addition, RV end-diastolic and end-systolic areas were measured to calculate RV fractional area change from the same apical 4-chamber view. Results Compared with the control group, patients with PAH showed increased RA and RV end-diastolic diameter （RA： （4.5±1.2）cm vs （3.0±0.8）cm, P〈0.05 and RV： （4.8±1.9）cm vs （3.4±0.5）cm, P〈0.05） and reduced RV fractional area change; （35±14）% vs （56±9）%, P〈0.05. These PAH patients showed lower myocardial peak velocities and a significant activation delay compared with controls （P〈0.05）. Moreover, a strong correlation between RV myocardial systolic activation delay and RV fractional area change was shown in patients with pulmonary arterial hypertension （r = -0.82）. Conclusions In PAH, RV myocardial systolic activation was markedly delayed, which was directly related to the RV fractional area change. RV myocardial systolic activation delay assessed by TDI could offer a unique approach to predict RV dysfunction.     

Effects of Smac gene over-expression on the radiotherapeutic sensitivities of cervical cancer cell line HeLa

Background　Thesecondmitochondria derivedactivatorofcaspases(Smac) isanovelproapoptoticgene,whichplaysanimportantroleintheapoptosis inducingeffectsofirradiationontumorcells ThepurposeofthisstudywastoinvestigatetheeffectsofextrinsicSmacgenetransferanditsover expressioninradiotherapeuticsensitivitiesofcervicalcancercells Methods　AftertheSmacgenewastransferredintothecervicalcancercelllineHeLa, subclonedcellswereobtainedbypersistentG418selection CellularSmacgeneexpressionwasdetectedbyRT PCR…     

Alleviation of hypoxic pulmonary vascular structural remodeling by L-arginine

目的探讨L-精氨酸(L-Arg)对低氧性肺血管结构重建的干预作用及其可能机制.方法将18只Wistar大鼠配伍后随机分为对照组、低氧组和低氧+L-Arg组(共6个配伍组).以右心导管法测定肺动脉压力,并对大鼠肺组织标本进行显微结构观测和超微结构观察,同时以分光光度法测定血浆一氧化氮(NO)含量,并对肺组织以内皮素-1(ET-1) cRNA探针进行原位杂交,研究肺动脉内皮细胞ET-1 mRNA的表达.结果低氧组大鼠肺动脉平均压明显高于对照组(20.33±2.18?mm?Hg vs 15.38±1.05?mm?Hg, P<0.05).低氧后大鼠肺血管显微及超微结构发生明显改变,肺血管结构重建形成.同时低氧组大鼠血浆NO间接含量明显低于对照组 (P<0.05 ).低氧后肺动脉内皮细胞ET-1 mRNA表达明显增强.然而,低氧+L-Arg组大鼠PAMP较低氧组明显降低(16.73±1.35?mm?Hg vs 20.33±2.18?mm?Hg, P<0.05).L-Arg缓解了低氧性肺血管结构重建的形成.同时低氧+L-Arg组大鼠血浆NO间接含量明显高于低氧组(P<0.05).L-Arg使低氧大鼠肺动脉内皮细胞ET-1 mRNA表达明显受抑制.结论 L-Arg对低氧性肺血管结构重建以及低氧性肺动脉高压的形成有重要的调节作用,其机制可能与通过促进低氧大鼠体内NO生成,从而抑制肺动脉内皮细胞ET-1 mRNA表达有一定的关系.     

Efficacy of adaptive servoventilation in patients with congestive heart failure and Cheyne-Stokes respiration

Approximately 40% of patients with congestive heart failure (CHF) experience Cheyne-Stokesrespiration (CSR). Comparison between CHF patients with and without CSR has demonstrated that even though the left ventricle ejection fraction (LVEF) was similar at the beginning, those with CSR usually had a worse prognosis than those without CSR. The poor prognosis is associated with sleeping disordered breathing (SDB), intermittent hypoxemia and lower survival in CHF patients with CSR.1-4 …     

Sequential non-invasive mechanical ventilation following short-term invasive m echanical ventilation in COPD induced hypercapnic respiratory failure

ＩｎＣｈｉｎａ ,80 % - 90 %ｏｆｐａｔｉｅｎｔｓｗｉｔｈｃｈｒｏｎｉｃｏｂｓｔｒｕｃｔｉｖｅｐｕｌｍｏｎａｒｙｄｉｓｅａｓｅ (ＣＯＰＤ )ｅｘａｃｅｒｂａｔｅｄｂｅｃａｕｓｅｏｆｂｒｏｎｃｈｉａｌ ｐｕｌｍｏｎａｒｙｉｎｆｅｃｔｉｏｎ Ｓｏｍｅｏｆｔｈｏｓｅｅｘｐｅｒｉｅｎｃｉｎｇｓｅｖｅｒｅｒｅｓｐｉｒａｔｏｒｙｆａｉｌｕｒｅｏｆｔｅｎｒｅｑｕｉｒｅｍｅｃｈａｎｉｃａｌｖｅｎｔｉｌａｔｉｏｎ(ＭＶ) ,ｗｈｉｃｈｃａｎｈｅｌｐｔｏｃｏｎｔｒｏｌｐｕｌｍｏｎａｒｙｉｎｆｅｃｔｉｏｎａｎｄｔａｋｅｔｈｅｒ…     

Effect of arsenic trioxide on inhibition of restenosis after rabbit vascular injury and its mechanism

目的　探讨应用三氧化二砷 (As2 O3)预防血管损伤后再狭窄的效果及其作用机理。方法　观察As2 O3对培养兔血管平滑肌细胞 (VSMCs)凋亡的影响。 32只新西兰白兔随机分为 2、4周实验组和对照组 ,分别 10 %As2 O32 5mg·Kg 1·d 1或等量生理盐水腹腔注射 3天 ,应用球囊损伤左颈总动脉。处死动物取血管作形态学和免疫组化检测 ,并检查肝脏、肾脏组织学变化。结果　细胞形态学和DNA电泳梯形带证实 ,As2 O3诱导培养VSMCs凋亡 ,与药物浓度和作用时间呈依赖性。与对照组相比 ,2 wk实验组血管内膜增殖面积显著减少 (P <0 0 5 ) ,4 wk组内膜面积无明显差异 ;但 2 ,4 wk组的管腔面积均有明显增大 (P均 <0 0 5 )。与对照组相比 ,实验组 2 ,4 wk免疫组化显示bcl 2表达下调 (P均 <0 0 5 ) ,Bax表达上调 (P分别 <0 0 1,0 0 5 ) ,均与相对应的血管内膜增生受抑制 ,血管腔面积扩大相吻合结论　As2 O3诱导VSMCs凋亡和有效预防实验性血管损伤后再狭窄 ,均与下调bcl 2和上调bax表达有关     

Myocardial bridging detection by non-invasive multislice spiral computed tomography: comparison with intravascular ultrasound

Background Invasive intravascular ultrasound （IVUS） is current diagnostic standard for myocardial bridging （MB）. Non-invasive multislice computerized tomography coronary angiography （MSCT） technique has provided a good anatomical view of the tunnel artery now. Methods A total of 51 consecutive patients with atypical or typical angina scheduled for IVUS were enrolled in this study and MSCT was performed 7 days before IVUS. Coronary imaging was quantified using IVUS and MSCT. Four main vessels （left main artery （LMA）, left anterior descending （LAD）, left circumflex （LCX）, right coronary artery （RCA）） were examined. Results Forty-one out of 51 （80%） patients received metaprolol （25 mg） before the MSCT scan and 25 of them were current beta-blocker users. The mean heart rate was （64_＋3） beats per minute. A total of 51 patients underwent IVUS examination （30 with MB and 21 without MB） were chosen for this study. Twenty-eight out of 30 MB cases were correctly diagnosed by MSCT and 2 patients with MB were not detected. Comparison with IVUS, the sensitivity of detection by MSCT was 93%, specificity was 100%. The lumen diameter of the tunnel artery derived from MSCT and IVUS significantly decreased from （2.9±0.3） mm to （2.4±0.4） mm （P〈0.001） and from （3.3±0.3） mm to （2.6±0.5） mm （P〈0.001）, respectively. Minimal and maximal diameters of MB derived from MSCT were significantly smaller than those from IVUS （（2.4±0.4） mm vs （2.6±0.5） mm, P〈0.05 and （2.9±0.3） mm vs （3.3±0.3） mm, P〈0.05）, respectively. Conclusions MSCT offers a reliable non-invasive method for MB in LAD and atherosclerosis diagnosis with diagnostic accuracy comparable with invasive IVUS.     

Opposite effects of WEB2086 on angiogenesis in atheromas and ischemic hindlimb of apoE gene deficient mice

Background  Our previous research has suggested that platelet activating factor receptor was related to atherosclerosis. The present study investigated the effect of a platelet activating factor receptor antagonist- WEB2086 on angiogenesis in aortal plaque and ischemic hindlimb of apolipoprotein E-deficient mice.
Methods  Eight-week-old apolipoprotein E-deficient mice were fed with a 0.15% cholesterol diet to develop advanced lesions. At age 32 weeks unilateral hindlimb ischemia was surgically induced and the mice were divided into two groups: with or without WEB2086 mixed with their drinking water (4.3 mg in 100 ml). At age 40 weeks blood was collected from the orbit for measurement of serum lipids and an enzyme linked immunosorbent assay was used to determine platelet activating factor and oxidized low density lipoprotein in the gastrocnemius and aorta. Whole-Mount CD31 stain and plaque-associated sprouting have been used to estimate angiogenesis in plaque from the aorta and laser Doppler perfusion imaging and immunohistochemical expression of von Willebrand factor have been used to estimate angiogenesis in ischemic hindlimb.
Results  The lipid composition of serum was not different between the groups. However, the amount of platelet activating factor and oxidized low density lipoprotein detected in the aorta was significantly higher than that in the gastrocnemius of ischemic hindlimb. The ratio of lesion to aorta levels was significantly reduced by administration of WEB2086, (31.52±6.18)% vs (55.58±8.34)%, P<0.01. The mean density of intimal capillaries in atherosclerotic plaque, (31.13±9.20)% vs (57.74±11.28)%, P<0.01, and the mean number of sprouts per aorta were significantly reduced, 183.92±34.17 vs 392.54±76.79, P<0.01, in the WEB2086 group. Blood flow (0.85±0.12 vs 0.45±0.06, P<0.01) and capillary density of ischemic hindlimb (1.18±0.17 vs 0.53±0.09, P<0.01) were markedly increased in apolipoprotein E-deficient mice treated with WEB2086 versus controls.
Conclusion  The study provides evidence that WEB2086 can inhibit angiogenesis in atherosclerotic plaque but promote it in ischemic hindlimb.

     

Imbalance of endogenous homocysteine and hydrogen sulfide metabolic pathway in essential hypertensive children

Background  Hypertension is a common disease of the cardiovascular system. So far, the pathogenesis of primary hypertension remains unclear. The elaboration of its pathogenesis is an important topic in the field which calls for urgent resolution. The aim of this study was to probe into the metabolic imbalance of homocysteine (Hcy) and hydrogen sulfide (H₂S) in children with essential hypertension, and its significance in the pathogenesis of essential hypertension.
Methods  Twenty-five children with essential hypertension and 30 healthy children with normal blood pressure were enrolled in the study. The medical history was investigated and a physical examination was conducted on the subjects. Plasma Hcy content was examined by fluorescence polarization immunoassay (FPIA). The plasma H₂S level was detected by a modified method with a sulfide electrode. Data were presented as mean±standard deviation. The t test was applied to the mean values of both groups. Pearson linear correlation analysis was applied to the plasma Hcy and H₂S as well as to the systolic pressure against the plasma H₂S/Hcy ratio.
Results  Plasma Hcy, an intermittent metabolite of the endogenous methionine pathway, was markedly increased but plasma H₂S, a final product of this pathway was significantly decreased in hypertensive cases when compared with normal subjects ((Hcy: (12.68±9.69) µmol/L vs (6.62±4.79) µmol/L (t=2.996, P<0.01); H₂S: (51.93±6.01) µmol/L vs (65.70±5.50) µmol/L) (t=-8.670, P<0.01)). The ratio of plasma H₂S/Hcy in children with hypertension was 5.83±2.91, while that of the control group was 11.60±3.30, and the difference is significant with a t=-6.610 and P<0.01. A negative correlation existed between plasma Hcy and H₂S concentrations, r=-0.379, P<0.05. And a negative correlation was found between systolic blood pressure and the plasma H₂S/Hcy ratio, r=-0.687, P<0.05.
Conclusion  There was a metabolic imbalance of homocysteine and hydrogen sulfide in essential hypertensive children.