简介：目的探讨松花粉对脑衰老的作用及其相关机制。方法以100mg/kgD-半乳糖皮下注射建立小鼠衰老模型,灌胃给予模型小鼠高、中、低三个剂量（500mg/kg、1000mg/kg、1500mg/kg）的松花粉,并以非酶糖基化抑制剂盐酸氨基胍（AG）为阳性对照,连续给药8周后,采用跳台法测定小鼠的学习记忆能力。处死小鼠获取血清及脑组织,检测晚期糖基化终末产物（AGE）水平,超氧化物歧化酶（SOD）活力、MDA水平以及炎症因子IL-6和TNF-α水平等衰老相关指标。结果跳台法检测模型组较正常组潜伏期显著缩短,5min内错误次数显著增加（P〈0.05）,而松花粉处理后能显著逆转这一变化（P〈0.05）,高剂量组效果最佳;同时,松花粉处理组能显著抑制模型组血清及脑组织中AGE水平及IL-6、TNF-α水平的升高（P〈0.05）,提高血清及脑组织SOD活力（P〈0.05）并下调MDA水平（P〈0.01）。结论松花粉能显著改善衰老模型小鼠的学习记忆功能,并上调抗氧化活性和降低衰老相关的炎症介质水平,抑制体内非酶糖基化可能是其发挥延缓衰老作用的机制之一。

简介：BackgroundOurpreviousstudyshowedthe150mg/mLfetalcardiacsupernatant(FCS)couldinducedifferentiationofBMSCsintocardiomyocye-likecellswithoutcardiomyocytetouch,butdifferentiationefficiencyisnothighenough.Inhibitionofglycogensynthasekinase-3enhancedtheproliferationandsurvivesofstemcells.Wetestedif6-bromoindirubin-3-oxime(BIO,glycogensynthasekinase-3inhibitor)enhancestheeffectsofFCSondifferentiationofBMSCsandexplorethegrowthfactorsinFCS.MethodsBMSCswereisolatedfromthefemurandtibiaoffour-week-oldmaleSprague-Dawleyratsandco-culturedwithFCS(150mg/mL)thatwasmadefromfetalheartsfromnineteen-daypregnantWistarrats.BIOwithdifferentconcentration(0,1,10,and100nM)wasintroducedinculturedishes.Transforminggrowthfactorbeta1(TGF-β1),bonemorphogeneticprotein2(BMP-2)andAktincardiacsupernatantandculturemediumwereassayedwithELISAmethods.ResultsAfterco-culturingwithFCS,beatingmyotubeswereobservedin25.9%BMSCsdishesafter1to2weeks’culture.ThelevelsofTGF-β1andBMP-2inFCSconcentrationswerenomorethanthatinyoungandadultcardiacsupernatant.AllBIOgroupssignificantlyenhancedtheeffectsofFCSondifferentiationofBMSCsintothecardiomyocyte-likecells(1nM,83%;10nM,73%;100nM,100%).AktlevelswerehigherinBMSCsculturalmediumwithFCS.ConclusionsFCScouldinducethedifferentiationofBMSCsintothecardiomyocyte-likecells.TGF-β1andBMP-2mightnotplayaroleinthedifferentiationofBMSCsinducedbyFCS.BIOenhancedtheeffectsofFCSonthedifferentiationofBMSCsintocardiomyocyte-likecells,whichmightinvolvetheAktpathway.