简介:目的观察脑出血后LINGO-1表达的变化,探讨维甲酸对脑出血后LINGO-1表达的影响。方法将72只SD大鼠随机分为假手术组、模型组和维甲酸治疗组,选取造模后1d、3d、7d和14d为观察点。制备脑出血模型,Longa评分法评价神经功能缺损程度,RT-PCR法检测LINGO-1mRNA的表达,Westernblot法检测LINGO-1蛋白的表达。结果模型组Longa评分7d最高,14d出现下降;LONG-1mRNA3d表达最高,7-14d出现下降;LONG-1蛋白7d到高峰,14d出现下降。维甲酸治疗组在14dLonga评分较模型组下降(P〈0.05);在7d和14dLINGO-1mRNA表达较模型组下降(P〈0.05);在14dLINGO-1蛋白表达较模型组下降(P〈0.05)。结论脑出血后LINGO-1表达明显上调,呈先上升后下降的变化规律。维甲酸可以降低LINGO-1mRNA和蛋白的表达及神经功能评分。
简介:BackgroundNowadays,thestudiesmainlyfocusonthefunctionofdecreasingtheinflammatoryfactorandimprovingthefunctionsofendothelium,buttheeffectsofstatinsonventricularremodelingarerarelystudied.MethodsThe2-kindey,1-cliphypertensiverats(2K1C,Goldblatt)werepreparedwithSprague-Dawley(SD)rat.SDratswererandomlydividedintothreegroups:controlrats,hypertensiveratsandhypertensiveratstreatedwithatorvastatin(2mg·kg-1·d-1).After6weeks,systolicbloodpressure(SBP)wasmeasuredusingthetail-cuffmethod.TheplasmaconcentrationofangiotensinⅡandreninactivityweredeterminedbyradioimmunoassay.Theheartweight,theratioofleftventricularweightandbodyweightwascalculated.ResultsTheplasmaconcentrationofangiotensinⅡ(106.4±7.8)ng/Landreninactivity(20.6±2.4)ng/Lweresignificantlyincreaedinhypertensiveratscomparedwithnormalrats[(72.3±5.4)ng/Land(12.5±3.7)ng/L](P<0.01).Theheartweight(1.46±0.09)g,theratio3.54±0.19(×10-3)ofleftventricularweightandbodyweightinhypertensiveratswereobviouslyhigherthanthatinnormalrats[(0.98±0.07)gand(2.28±0.06)×10-3](P<0.01).Aftertreatmentwithatorvastatin,theplasmaconcentrationofangiotensinⅡ(68.3±6.9)ng/Landreninactivity(8.7±2.3)ng/L,heartweight(1.05±0.04)g,theratio2.36±0.07(×10-3)aboveweredecreasedsignificantly,therewerenodifferencebetweenthegroupofhypertensiveratsandthenormal.ConclusionsAtorvastatincandecreasetheratioofleftventricularweightandbodyweightandhastheeffectsoncardiovascularremodelinginhypertensiverats.
简介:Thestudyaimedtoinvestigatetheeffectsofivabradineonthelevelsofhypoxia-induciblefactor-1alpha(HIF-1α)andVEGFinserumofrabbitwithacutemyocardialinfarction(AMI).MethodsAMImodelwasestablishedbyligatingtheleftanteriordescendingbranchofthecoronaryarteryinNewZealandwhiterabbits.Twentyfiverabbitswererandomlydividedinto4groups:sham-operated(S),myocardial-infarction(M)withbisoprololtreatment(M+B)andivabradine-treated(I+M).Themedicaltreatmentbeganimmediatelyafterinfarctionandcontinuedfor3weeks.Serumofeachrabbitwasobtainedatthefollowingtimepoints(24hbeforetheoperation,24h,3d,1week,2weeksand3weeksaftertheoperation).ELISAwasusedtomeasurethelevelsofHIF-1αandVEGFofeachsample.ECGandheartrates(beforeandaftertreatment)wereanalyzed.ResultsBaselineheartrateshowednosignificantdifferencesbetweenthe3infarctedgroups(M,M+B,M+I).ThreeweekslatertheheartratesweresignificantlyloweringroupM+BandgroupM+IthaningroupM.However,therewasnostatisticdifferencebetweenthetwodrug-treatedgroups(P=0.848).ThelevelsofHIF-1αandVEGFingroupsM,M+BandM+I)increasedsignificantlycomparedwithgroupS(P<0.01).TheproductionsofHIF-1αandVEGFwereloweringroupM+BandgroupM+IcomparedwithgroupM(P<0.01).TherewasnostatisticaldifferencebetweenthegroupM+BandgroupM+I(P>0.05),andthecorrelativeanalysisrevealedthattheproductionofHIF-1αwaspositivelycorrelatedwiththatofVEGF(r=0.732,P<0.01).ConclusionIvabradinecanreduceheartrateandmeanwhiledecreasetheserumlevelsofHIF-1αandVEGFafterAMI.