简介:Objectives:Apoptosisisrecognizedasanimportantmechanismincontrast-inducednephropathy(CIN).Cordycepssinensis(CS),atime-honoredtonicfoodandherbalmedicineinChina,canimprovethemicrocirculation,increasethetolerancetoischemiainpatientswithmicrocirculatorydisorders.AsCShasbeenfoundtoberenoprotectiveandanti-apoptoticinmultiplekidneyinjuries,wehypothesizedthatCSwouldpreventCIN.TheobjectiveofthisresearchistostudythemechanismofCSontubularepithelialcellapoptosisindiabeticCINrats.
简介:Thepanaxnotoginsengsaponin(PNS)hadbeenclinicallyusedforthetreatmentofcardiovasculardiseasesandstrokeinChina.IthadbeendemonstratedthatPNScouldprotectcardiomyocytesfrominjuryinducedbyischemi-a,buttheunderlyingmolecularmechanismsofthisprotectiveeffectwerestillunclear.ThisstudywasaimedtoinvestigatetheprotectiveeffectandmolecularmechanismsofPNSonapoptosisinH9c2cellsinvitroandratmyocardialischemiainjurymodelinvivo.Annexin-V/PIassayshewthatPNScouldprotectH9c2cellsfromapoptosisinducedbyserum,glucoseandoxygendeprivation(SGOD)inadose-dependentmanner.However,theanti-apoptoticeffectofPNSwasreversedbyLY294002,aspecificPI3Kinhibitor.ThisantiapoptoticeffectofPNSwasconfirmedbyJC-1,aspecificprobeofmitochondrialmembranepotentialstaining.PNScouldsignificantlyincreasephos-AktinH9c2cellsbyWesternblotassaysanditseffectcouldbeinhibitedbyLY294002.Furthermore,PNScouldimproveischemic-inducedleftventricularfunctionasreflectedbyEF,LVDdandLVDs.PNScouldalsoinhibitedcellularapoptosisinmyocardialtissuesinischemicratsbyTUNELassay.PNSadministrationalsoincreasedtheexpressionofphos-Aktinratischemicmyocardialtissues.TheseresultssuggestedthatPNScouldprotectmyocardialcellsfromapoptosisinducedbyischemiainvitromodelandinvivomodelthroughactivating-PI3K/AktsignalpathwaywhichmaybemeaningfulforfurtherunderstandingthemolecularmechanismsofcardiacprotectionofPNS.Andtheresultsmightbeusefulintreatmentofmyocardialischemiainfuture.
简介:目的:观察热应激诱导心肌热休克蛋白(HSP)70表达上调,对兔快速心房起搏致房颤心肌钙激活钾通道(KCa)3.1表达的影响。方法:将24只新西兰大白兔随机分为假手术组(n=8,仅植入电极而不起博)、起搏组(n=8,以600次/min快速起搏右心房6h)和热应激起搏组(热应激组,n=8,先行热应激预处理,再行与起搏组一样的快速起搏)。结果:与假手术组和起搏组比较,热应激组心脏各部位HSP70mRNA和蛋白表达显著上调[HSP70蛋白,左房:(39.00±3.21)比(39.75±2.82)比(69.75±3.45),右房:(38.38±2.92)比(39.50±3.89)比(69.00±2.93),左心耳:(37.75±3.28)比(39.00±3.89)比(68.63±3.23),右心耳:(37.00±3.85)比(38.38±3.74)比(68.75±2.82)],P均〈0.01,而起搏组和假手术组间无显著性差异(P〉0.05);与起搏组KCa3.1mRNA和蛋白表达量显著下调比较,热应激组心脏各部位KCa3.1mRNA和蛋白表达量显著上调[KCa3.1蛋白,左房:(21.25±1.67)比(24.00±2.62),右房:(21.13±1.96)比(23.75±1.83),左心耳:(21.00±2.07)比(23.75±1.67),右心耳:(20.88±2.03)比(23.50±2.45)],P均〈0.05,且热应激组与假手术组间无显著差异(P〉0.05)。结论:热应激可诱导心房起搏心肌热休克蛋白(HSP)70表达上调,抑制KCa3.1mRNA和蛋白表达量显著下降。
简介:目的探讨严重多发骨折患者血清IL-6、TNF水平变化情况及其与疾病变化的关系,为临床治疗提供依据。方法选取2014年7月~2015年4月我科收治的严重多发骨折患者40例(ISS评分≥16分)开展回顾性分析,同时以40例健康志愿者作为对照,采用酶联兔疫吸附剂测定法(ELISA)准确测定严重多发骨折患者与健康.6-愿者血清IL-6、TNF值,观察严重多发骨折患者不同时间段血清IL-6、TNF水平变化情况及其与健康志愿者的比较。结果严重多发骨折患者骨折第2d、手术当天(骨折第6d)、术后第2d(骨折第8d)IL-6值显著高于健康志愿者,差异具有统计学意义(P〈0.05);骨折第2d、手术当天(骨折第6d)、术后第2d(骨折第8d)TNF值显著高于健康志愿者,差异具有统计学意义(P〈0.05);40例严重多发骨折患者IL-6、TNF值呈现为一个先升高后降低的趋势,骨折第2d患者IL-6、TNF值均开始升高,在手术当天(骨折第6d)达到顶峰,然后逐渐降低。结论骨折及手术创伤均可致患者体内IL-6、TNF升高,通过血清IL-6、TNF水平监测,可为严重多发骨折患者临床手术治疗、感染控制等提供重要依据。
简介:目的探讨老年杓型与非杓型高血压患者踝臂指数(anklebrachialindex,ABI)的异常情况及临床意义。方法选择老年原发性高血压患者79例进行24h动态血压监测,分为非杓型组52例和杓型组27例。测定ABI、高敏C反应蛋白(highsensitiveC—reactiveprotein,hs—CRP)、髓过氧化物酶(myeloperoxidase,MPo)水平和血管内皮功能。结果非杓型组ABI、肱动脉内皮依赖性舒张功能较杓型组明显降低,MPO、hs—CRP较杓型组明显升高,差异有统计学意义(P〈0.05)。非杓型组患者ABI与hs—CRP和MPO呈负相关(r=-0.723,r=-0.719,P〈0.01),与肱动脉内皮依赖性舒张功能呈正相关(r=0.917,P〈0.01)。结论ABI降低与斑块不稳定、炎性反应及血管内皮功能受损密切相关,对评价夜间老年高血压患者动脉结构、功能的损害程度、判断预后、指导合理治疗有重要的临床意义。