蛇床子素减轻脂多糖诱导的大鼠学习记忆减退

目的观察蛇床子素对脂多糖诱导的大鼠学习记忆减退的作用,并初探其可能的作用机制。方法 40只雄性SD大鼠随机分为假手术组、模型组、阳性药组及蛇床子素组。阳性药组、蛇床子素组分别每日1次灌胃布洛芬、蛇床子素40 mg.kg-1,连续12 d,假手术组、模型组灌胃等体积的生理盐水,3 d后侧脑室注射脂多糖诱导大鼠的神经炎症模型,制模后d 5开始Morris水迷宫检测大鼠的空间记忆能力,连续5 d。Morris水迷宫检测结束后,处死大鼠,HE染色观察大鼠海马神经元损伤情况,real time RT-PCR法测定海马肿瘤坏死因子α(Tnf-α)、白细胞介素-1β(Il-1β)、诱导型一氧化氮合酶(Nos2)及环氧合酶-2(Cox-2)的mRNA表达。结果侧脑室注射脂多糖后,大鼠在定向航行实验中的逃避潜伏期显著增加(P<0.05),空间探索实验中的校正逃避潜伏期缩短(P<0.05),海马神经元明显受损,且海马Tnf-α、Il-1β、Nos2及Cox-2的mRNA表达增加(P<0.05);然而,蛇床子素及布洛芬明显缩短了大鼠的定向航行实验中的逃避潜伏期(P<0.05),延长了空间探索实验中的校正逃避潜伏期(P<0.05),减轻了海马神经元损伤,且降低海马Tnf-α、Il-1β、Nos2及Cox-2的mRNA表达。结论蛇床子素可减轻脂多糖诱导的大鼠学习记忆减退及海马神经元损伤,其机制与抑制炎症相关基因的mRNA表达有关。     

蛇床子素抑制小胶质细胞激活改善血管性痴呆大鼠学习记忆能力

目的 观察蛇床子素(Ost)对双侧颈总动脉结扎(BCCAO)致血管性痴呆(VD)大鼠认知功能的影响,并探讨其作用机制.方法 将雄性SD大鼠随机分为假手术组、Ost正常对照(40 mg·kg-1)组、模型组和Ost 20、40 mg·kg-1组(均n=16).永久性结扎大鼠双侧颈总动脉致模后第2日给药,每日1次,持续28...     

The effect of icariin on promoting neurogenesis and angiogenesis and its mechanism

OBJECTIVE To observe the effects of icariin(ICA) on neurogenesis and angiogenesis after ischemia,and investigate the possible mechanism.METHODS The rats were subjected to middle cerebral artery occlusion(MCAo)-reperfusion injury with thread embolus,24 h later ICA was intragastrically administrated to rats at doses of 20,40 and 80 mg·kg-1 once a day,respectively,continuously for 28 d.The behavioral test was performed using the neurological severity score(NSS) 18 scores at 24,72 h,7,14,21 and 28 d after ischemia,resepectively.Rats were sacrificed 28 d after MCAo,infarct volume was evaluated by TTC staining.The mRNA expression of brain-derived neurotrophic factor(BDNF) and its receptor TrkB and VEGF and its receptor VEGFR2 were detected by RT-PCR,and the protein expression of BDNF,TrkB,VEGF and VEGFR 2 were determined by Western blotting.RESULTS ICA obviously attenuated neurological functional deficit score,as well as infarction volume.ICA raised the number of BrdU/NeuN and BrdU/GFAP positive cells in the ischemia periphery zone of rats 28 d after ischemia.At the same time,ICA noticeablely enhanced the mRNA expression of VEGF,VEGFR2,BDNF and TrkB,and the protein expression of VEGF and BDNF and TrkB were increased 28 d after ischemia.CONCLUSION The results showed that ICA may promote neurogenesis and angiogenesis after ischemia in rats,and the possible mechanism might be,at least partly,due to an increase of BDNF and its receptor TrkB,VEGF and its receptor VEGFR2 in the brain.     

淫羊藿苷的神经药理作用及分子机制研究进展

近年来关于淫羊藿苷对中枢神经系统药理作用的研究日益增多。为进一步推进淫羊藿苷用于防治中枢神经系统疾病的研究,本文结合国内外对淫羊藿苷的研究报道,系统地综述了淫羊藿苷的抗痴呆、抗衰老、抗缺血性脑损伤、抗抑郁及神经保护等中枢神经系统的药理作用及作用机制。