犬切牙压低移动过程中牙周组织骨保护素/核因子κB受体活化因子配体的表达**

背景：骨保护素及核因子κB受体活化因子配体是调控破骨细胞生成和活化的关键因子,机械力可影响牙周膜细胞和成骨细胞骨保护素及核因子κB受体活化因子配体的表达。 目的：观察犬切牙压低移动过程中牙周组织中骨保护素/核因子κB受体活化因子配体的表达。 方法：采用微型种植体作为支抗,将犬切牙分别施加牵引力1,2,4,12周,并设置对照组进行比较。牵引后切取犬切牙连同牙龈及牙槽骨组织块,制作组织切片进行骨保护素及核因子κB受体活化因子配体免疫组织化学染色,用Image-Proplus软件半定量分析图像平均吸光度值。 结果与结论：与对照组相比,核因子κB受体活化因子配体和骨保护素分别在在施加牵引力1和2周表达最显著,其平均吸光度值在施加牵引力1和2周时可达到峰值(P < 0.05),随后逐渐下降,施加牵引力12周恢复至对照组水平。结果证实,正畸牙压低移动过程中核因子κB受体活化因子配体及骨保护素的表达变化规律与骨改建过程一致,骨保护素/核因子κB受体活化因子配体系统是牙周组织改建的重要调节因素。     

三七总皂苷干预股骨头缺血性坏死兔成骨细胞护骨素基因的表达*

背景：前期研究已明确三七总皂苷能抑制乙醇诱导的兔骨髓基质干细胞成脂分化。 目的：进一步观察三七总皂苷对兔成骨细胞的增殖和分化以及骨保护素、细胞核因子κB受体活化因子配体mRNA表达的影响。 方法：白酒灌胃4周制备新西兰兔股骨头缺血坏死模型,随机分为生理盐水组、复方骨肽组和三七总皂苷组。通过组织块培养法提取各组兔成骨细胞,检测细胞的分化,骨保护素、细胞核因子κB受体活化因子配体基因表达情况,检测各目的基因杂交信号的强弱。 结果与结论：三七总皂苷组兔碱性磷酸酶活性、钙结节计数及骨保护素、细胞核因子κB受体活化因子配体的表达强度、骨保护素mRNA/细胞核因子κB受体活化因子配体mRNA均高于生理盐水组(P < 0.01);与复方骨肽组效果接近。证实三七总皂苷能够促进兔成骨细胞的增殖和分化,并能提高成骨细胞的骨保护素mRNA的相对表达量而对其细胞核因子κB受体活化因子配体mRNA有抑制作用。     

去卵巢后大鼠骨组织中核因子κB受体活化因子配体和骨保护素表达的变化

背景：核因子κB受体活化因子配体在破骨细胞分化、活化和存活的生理过程中起十分重要的作用。骨保护素作为核因子κB受体活化因子配体的诱骗受体，对破骨细胞有相反作用。 目的：观察去卵巢后大鼠骨组织内核因子κB受体活化因子配体、骨保护素mRNA、蛋白表达和骨密度的时间变化规律。 设计、时间及地点：随机对照动物实验，于2006-05/10在四川大学华西医院移植免疫实验室完成。 材料：6月龄健康雌性SD大鼠50只，体质量300~320 g。随机平均分成去卵巢组和对照组。 方法：建立去卵巢大鼠模型，于术后2，4，6，8，10周取股骨髁。 主要观察指标：测量股骨髁的骨密度，检测骨组织核因子κB受体活化因子配体、骨保护素的mRNA、蛋白表达情况。 结果：去卵巢后大鼠股骨髁的骨密度与对照组相比于第6周开始出现显著降低(P < 0.05)；核因子κB受体活化因子配体mRNA水平在第4周达到高峰，蛋白水平在第6周达到高峰，此后均呈持续高表达，与对照组相比，各时间点表达水平差异具有显著性(P < 0.05)；骨保护素 mRNA水平在第4周达到高峰，蛋白水平在第2周达到高峰，此后均迅速下降，与对照组相比，各时间点表达水平差异具有显著性(P < 0.05)。 结论：大鼠去卵巢后股骨髁是骨密度变化的敏感部位；核因子κB受体活化因子配体持续高表达，骨保护素表达短期内升高，迅速降低是骨质疏松的直接原因。     

骨保护素与脑血管疾病

骨保护素（osteoprotegerin,OPG）是肿瘤坏死因子（TNF）受体家族的成员之一,与核因子-κB受体活化因子配体（receptor activator of nuclear factorκB ligand,RANKL）、核因子-κB受体活化因子（receptor activator ofnuclear factorκB,RANK）共同构成骨保护素系统。该系统     

脂联素对成骨细胞护骨素和核转录因子κB受体活化素配体表达的影响

背景：在骨组织中,护骨素的主要作用是抑制破骨细胞的形成和活性,核转录因子κB受体活化素配体的主要作用为刺激破骨细胞的分化和活性,抑制破骨细胞的凋亡。护骨素/核转录因子κB受体活化素配体在破骨功能调控中起重要作用。近来研究发现脂联素促进成骨细胞增殖和分化,脂联素与骨代谢相互偶联。但脂联素对破骨细胞的作用不明。 目的：观察脂联素对成骨细胞核转录因子κB受体活化素配体和护骨素表达的影响,进一步分析其对破骨细胞生成的作用。 设计、时间及地点：对比观察实验,于2007-06/2008-12在中南大学湘雅二医院代谢内分泌研究所实验室完成。 材料：外科手术取正常成人髂前上棘松质骨用于细胞培养,临床标本由湘雅医院提供。 方法：分别用0,3,10和30 mg/L脂联素干预人成骨细胞48 h,检测护骨素和核转录因子κB受体活化素配体 mRNA与蛋白表达。并用脂联素干预成骨细胞与外周血单核细胞共同培养系统,观察其对破骨细胞生成的影响。 主要观察指标：分别采用荧光定量聚合酶链反应和酶联免疫吸附法检测人成骨细胞护骨素和核转录因子κB受体活化素配体mRNA与蛋白表达,抗酒石酸磷酸酶染色确定为破骨细胞。 结果：脂联素呈剂量依赖性抑制人成骨细胞护骨素 mRNA与蛋白质的表达(P < 0.05)。脂联素呈剂量依赖性促进人成骨细胞核转录因子κB受体活化素配体mRNA与蛋白的表达(P < 0.05)。脂联素干预成骨细胞与外周血单核细胞共同培养系统可诱导破骨细胞生成。 结论：脂联素可通过诱导成骨细胞核转录因子κB受体活化素配体表达、抑制护骨素表达,诱导破骨细胞生成。     

大鼠磨牙加力移动龈沟液中核因子κB受体活化子配体/骨保护素的表达变化

背景：核因子κB受体活化子配体和骨保护素系统参与破牙骨质细胞的形成并调节牙根吸收过程,而不同力值大小及加力时间下龈沟液中核因子κB受体活化子配体和骨保护素的表达变化是否可以作为判断牙根吸收的量化指标鲜有报道。 目的：探讨核因子κB受体活化子配体和骨保护素表达变化与力值大小及加力时间的相关性。 方法：雄性SD大鼠随机分成0.49 N,0.98 N和1.47 N力值组,每组按照加力时间分为加力0,3,7,10,14,21及 28 d亚组。各组大鼠建立大鼠正畸牙模型,采用吸潮纸尖法提取实验牙的龈沟液,应用ELISA法测定不同力值和加力时间龈沟液核因子κB受体活化子配体和骨保护素的浓度及比值变化。 结果与结论：加力不同时间点不同力值加载组组间大鼠龈沟液中核因子κB受体活化子配体/骨保护素的浓度比值比较差异均具有显著性意义(P < 0.01),力值越大,该比值越大。0.49 N加力组在加力的前21 d,随着加力时间的延长,大鼠龈沟液中核因子κB受体活化子配体/骨保护素的值逐渐增高(P < 0.01);第28天的核因子κB受体活化子配体/骨保护素的比值趋于稳定。0.98 N和1.97 N加力组,随着加力时间的延长,大鼠龈沟液中核因子κB受体活化子配体/骨保护素的值均持续逐渐增高(P < 0.01)。结果表明,大鼠龈沟液中核因子κB受体活化子配体和骨保护素的比值与力值大小及作用时间具有相关性,可用于正畸牙根吸收的临床检测指标。 关键词：龈沟液;正畸牙;核因子κB受体活化子配体;骨保护素;牙根吸收     

颌间牵引力对成年大鼠髁状突核因子κB受体活化因子配基/骨保护素的调控

背景：颌间不对称牵引是正畸中调整下颌位置和咬合关系的常规手段,常用于成人偏颌畸形的代偿性矫治。牵引力对成年颞下颌关节的影响尚存在争议。 目的：创建下颌骨单侧前上牵引的大鼠动物模型,验证颌间牵引力大小不同对髁状突软骨下骨核因子κB受体活化因子配基/骨保护素表达的影响是否一致。 设计、时间及地点：随机分组设计,对照动物实验,于2005-03/2007-03 在四川大学口腔生物医学工程教育部重点实验室完成。 材料：3月龄雄性SD大鼠180只分为对照组(n=20)、重力组(n=80)和轻力组(n=80)。 方法：在160只SD大鼠左侧眼眶前下方4 mm左右做平行于眼睑的切口以暴露颧弓,在左下颌角附近下唇下方1 cm,距离腹部中线5 mm处做另一切口。用镍钛拉簧连接固定左侧下颌角和同侧颧弓前部,用测力计确定其伸长所产生的力值为实验所需拉力值(40 g或120 g),28 d后撤除镍钛拉簧。对照组大鼠同样进行手术但不放置弹簧。 主要观察指标：加力3,7,14,28 d及撤除外力后3,7,14,28 d,以免疫组织化学半定量检测双侧髁状突软骨下骨中核因子κB受体活化因子配基/骨保护素表达。 结果：骨保护素在大鼠髁突软骨全层均有表达,软骨下骨、肥大带浅层和部分成熟软骨细胞表达较强。核因子κB受体活化因子配基在大鼠髁突软骨的全层均有表达,成熟的软骨细胞表达较强。与对照组比较,轻力组加力侧核因子κB受体活化因子配基的表达在前3 d明显升高(P < 0.01),第7天表达量恢复正常水平,到14 d以后出现第2个高峰(P < 0.01),撤除外力后3~7 d核因子κB受体活化因子配基表达量又再次升高(P < 0.01),直到撤力14 d才开始回落。除了第7天外,重力组核因子κB受体活化因子配基表达比轻力组强烈(P < 0.01)。在28 d内,轻重力对骨保护素表达影响不明显。加力侧骨保护素表达在第3天没有明显变化,7 d表达量减少(P < 0.01),到14 d以后出现第1个高峰,撤除外力后3 d骨保护素表达量又再次下降(P < 0.01),直到撤力后7 d才出现第2个高峰。轻力和重力组大鼠加力侧髁状突核因子κB受体活化因子配基/骨保护素比值没有相关性(r＝0.005,P > 0.05)。 结论：轻、重牵引力作用对软骨下骨中骨保护素表达的量和变化规律是一致的;同时,核因子活化受体核因子κB受体活化因子配基对应力反应的表达曲线形态基本一致。     

人工关节磨损钛微粒诱导破骨的分子生物学机制

背景：人工关节磨损微粒可刺激人单核巨噬细胞产生大量炎性破骨细胞因子,导致假体周围骨溶解,但其具体作用途径尚不清楚。 目的：分析钛微粒诱导溶骨的分子生物学机制。 方法：巨噬细胞与清洁钛微粒、细菌内毒素结合钛微粒和细菌内毒素联合培养。4,8,16,32 h采用反转录聚合酶链反应技术和电泳迁移率变动分析法检测巨噬细胞核激活因子受体mRNA、骨保护素mRNA表达及核转录因子κB DNA的结合活性。 结果与结论：清洁钛微粒刺激巨噬细胞核激活因子受体 mRNA与骨保护素mRNA比例失衡,促进溶骨。细菌内毒素组并未检测到核激活因子受体 mRNA表达,4 h时骨保护素mRNA表达轻度一过性增加,提示细菌内毒素并未通过核激活因子受体/骨保护素信号系统调控溶骨,而更多的通过核转录因子κB/炎性细胞因子信号通路,诱发溶骨。细菌内毒素结合钛微粒后,两种溶骨信号机制可能同时发生,并协同作用。     

重组核因子κB活化因子受体蛋白对破骨细胞活性的抑制作用

背景：核因子κB活化因子受体直接参与破骨细胞的活性及功能调节,在骨吸收类疾病发病中具有重要意义。通过基因工程得到的可溶性核因子κB活化因子受体蛋白可能为防治骨质疏松等骨吸收类疾病提供了新的有效手段。 目的：观察重组重组核因子κB活化因子受体蛋白对体外培养破骨细胞活化、吸收活性的影响。 方法：取新生24 h内SD大鼠胎鼠的四肢长骨,机械分离获得破骨细胞,采用不同浓度重组重组核因子κB活化因子受体蛋白干预后,行抗酒石酸酸性磷酸酶染色及骨吸收陷窝甲苯胺蓝染色,观察其对破骨细胞的生长情况。 结果与结论：重组核因子κB活化因子受体蛋白对破骨细胞作用3 d后,破骨细胞数量明显减少,以10-4 mol/L重组核因子κB活化因子受体蛋白最为显著。核因子κB活化因子受体蛋白作用9 d时,骨片吸收陷窝数明显减少。由此认为,在体外重组核因子κB活化因子受体蛋白可以有效抑制破骨细胞活化及骨吸收活性。     

唑来膦酸对大鼠成骨细胞增殖、分化和护骨素/核因子κB受体激动剂配体mRNA表达的影响☆

背景：在应用于预防和治疗假体周围骨溶解时，唑来膦酸可在发挥抑制破骨细胞作用的同时而不影响成骨功能。 目的：观察唑来膦酸对大鼠成骨细胞功能的影响，验证其应用于人工关节置换后假体周围骨溶解的可行性。 设计、时间及地点：观察对照实验，于2007-03/2008-03在华北煤炭医学院中心实验室完成。 材料：新生24 h内SD大鼠，唑来膦酸标准品。 方法：体外培养新生大鼠颅盖骨来源的成骨细胞，应用不同浓度唑来膦酸进行干预，实验组细胞培养基中唑来膦酸终浓度为10-4~10-11 mol/L，对照组不加药, 只加等量细胞悬液和培养基。唑来膦酸干预后分别于第1，2，3，5，7天采用四甲基偶氮唑盐比色法测定吸光度，检测唑来膦酸对成骨细胞增殖的影响；第3天和第5天分别采用荧光定量聚合酶链反应测护骨素和核因子κB受体激动剂配体mRNA表达，以硝基苯基质动力学法测定各组细胞碱性磷酸酶活性。 主要观察指标：成骨细胞增殖情况和碱性磷酸酶活性，护骨素、核因子κB受体激动剂配体mRNA表达水平。 结果：唑来膦酸浓度≥10-5 mol/L时抑制成骨细胞增殖，10-6~10-11 mol/L则不影响细胞增殖。唑来膦酸浓度为10-7 ~10-11 mol/L时碱性磷酸酶活性无变化，而成骨细胞的护骨素mRNA表达增加，核因子κB受体激动剂配体mRNA的表达下降。 结论：唑来膦酸在低浓度时不影响成骨细胞增殖及分化，通过降低成骨细胞核因子κB受体激动剂配体/护骨素的比率而抑制破骨细胞分化，可应用于人工关节置换后假体周围骨溶解。     

Treatment with Anti-interferon-γ Monoclonal Antibodies Modifies Experimental Autoimmune Encephalomyelitis in Interferon-γ Receptor Knockout Mice

The role of interferon-γ (IFN-γ) in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) is still controversial. We have studied the function of IFN-γ and its receptor in the EAE model using two different IFN-γ receptor knockout (IFN-γ R^−/−) mouse types: C57Bl/6×129Sv, with a disruption of the IFN-γ receptor cytoplasmic domain, and 129Sv, homozygous for a disrupted IFN-γ receptor gene. Mice were immunized with peptide 40-55 from rat myelin oligodendrocyte glycoprotein. A subgroup of mice was treated with anti-IFN-γ monoclonal antibodies (mAb) on day 8 postimmunization. Clinical scoring and both histological and immunohistochemical studies were undertaken for all groups. We hereby show that treatment with anti-IFN-γ mAb worsened the disease course of 129Sv wild-type mice. However, it decreased the mean daily score in IFN-γ R^−/− 129Sv and the incidence of the disease down to 50% in C57Bl/6×129Sv IFN-γ R^−/− mice. Moreover, after anti-IFN-γ mAb treatment, oxidative stress levels, metallothionein I and II antioxidant protein expression, and apoptoticneuronal death were increased in wild-type mice while decreased in IFN-γ R^−/− mice. These results suggest a putative alternative mechanism of action of this cytokine that works independent of its receptor.     

Ischemia preconditioning protects astrocytes from ischemic injury through 14‐3‐3γ

Stroke is a leading cause of death and disability, and new strategies are required to reduce neuronal injury and improve prognosis. Ischemia preconditioning (IPC) is an intrinsic phenomenon that protects cells from subsequent ischemic injury and might provide promising mechanisms for clinical treatment. In this study, primary astrocytes exhibited significantly less cell death than control when exposed to different durations of IPC (15, 30, 60, or 120 min). A 15‐min duration was the most effective IPC to protect astrocytes from 8‐hr‐ischemia injury. The protective mechanisms of IPC involve the upregulation of protective proteins, including 14‐3‐3γ, and attenuation of malondialdehyde (MDA) content and ATP depletion. 14‐3‐3γ is an antiapoptotic intracellular protein that was significantly upregulated for up to 84 hr after IPC. In addition, IPC promoted activation of the c‐Jun N‐terminal kinase (JNK), extracellular signal‐related kinase (ERK)?1/2, p38, and protein kinase B (Akt) signaling pathways. When JNK was specifically inhibited with SP600125, the upregulation of 14‐3‐3γ induced by IPC was almost completely abolished; however, there was no effect on ATP or MDA levels. This suggests that, even though both energy preservation and 14‐3‐3γ up‐regulation were turned on by IPC, they were controlled by different pathways. The ERK1/2, p38, and Akt signaling pathways were not involved in the 14‐3‐3γ upregulation and energy preservation. These results indicate that IPC could protect astrocytes from ischemia injury by inducing 14‐3‐3γ and by alleviating energy depletion through different pathways, suggesting multiple protection of IPC and providing new insights into potential stroke therapies. © 2015 Wiley Periodicals, Inc.     

Properties of γ-glutamyltransferase in developing rat brain

The activity and properties of brain γ-glutamyltransferase (EC 2.3,2.2) were studied in 7-, 14-and 90-day-old rats. The enzyme activity was highest in the pons-medulla and lowest in the cerebellum in each age group. The activity of glycylglycine, 10 protein amino acids, GABA and taurine as acceptor of the γ-glutamyl group was studied with 7-day-old and adult rats. The best acceptors were glycylglycine, lysine and methionine and the poorest taurine, valine and isoleucine. The relative acceptor activity of lysine changed most during development. K_m for the γ-glutamyl donor, γ-glutamyl-p-nitroanilide, with glycylglycine was about 3 mM in all experimental groups. It did not change during development but V increased about fivefold in all brain areas studied. A mixture of serine and borate strongly inhibited γ-glutamyltransferase in each age group. Potassium and magnesium ions had no measurable effect on the enzyme activity but sodium ions were stimulatory.     

Interferon-α and interferon-γ production capacity of idiopathic isolated optic neuritis patients

Interferon-α and interferon-γ production by idiopathic isolated optic neuritis (ON) patients was studied. The production capacity was compared with that in two control groups: patients with iritis and healthy control subjects. A sensitive and reliable interferon bioassay was applied for interferon level measurements.Statistically significant differences were not found between patients and control groups in either interferon-α production or interferon-γ production.     

14-3-3蛋白在人脑胶质瘤中的表达及生物学意义

目的检测14-3-3蛋白在人脑胶质瘤中的表达情况,探讨其在胶质瘤发生发展中的生物学意义。方法采用免疫组化亲和素-生物素过氧化物酶复合物(ABC)法检测5个胶质瘤细胞系(U251MG,U87MG,BT325,SHG44和C6)、121例人脑胶质瘤石蜡标本和10例正常脑组织中14-3-3蛋白的表达情况。分析14-3-3蛋白的表达在胶质瘤发生发展中的作用。结果在正常脑组织标本中,13-3-3蛋白主要表达于神经元的胞体和突起,仅在少数的胶质细胞中可见14-3-3蛋白的弱表达。然而,5个胶质瘤细胞系和绝大部分星形细胞瘤中可见14-3-3蛋白的阳性表达,其表达阳性率为:Ⅰ级78.6%(11/14),II级75%(18/24),III级76.2%(16/21),IV级80%(20/25)。不同恶性级别的星形细胞瘤中,14-3-3蛋白的阳性表达率无显著差别,但14-3-3蛋白的表达强度和范围有随肿瘤的恶性度增高而增加的趋势。其它类型的胶质瘤中也可见14-3-3蛋白的大量表达,其表达阳性率为:少突胶质细胞瘤66.7%(4/6),间变型少突胶质细胞瘤100%(4/4),室管膜瘤50%(2/4),间变型室管膜瘤66.7%(2/3),脉络从乳头状瘤100%(5/5),松果体细胞瘤100%(3/3),髓母细胞瘤66.7%(8/12)。结论14-3-3蛋白在人脑胶质瘤中有大量的表达。14-3-3蛋白表达上调可能是胶质瘤细胞对抗调亡的一种共同机制,以14-3-3蛋白为靶点有望成为一种有前景的新的胶质瘤生物学治疗方法。     

Regulation of expression of relaxin-3 and its receptor RXFP3 in the brain of diet-induced obese rats

An animal model closely related to human obesity is diet-induced obesity in Sprague–Dawley rats. These rats placed on a high-energy (HE) diet show wide distribution in body weight gain with a subset of animals developing diet-induced obesity (DIO) and the remaining animals showing a diet-resistant (DR) phenotype. Once obesity is established, DIO rats strongly defend their increased body weight against caloric restriction. There is evidence that neuropeptide relaxin-3 is involved in food intake regulation, but the levels of expression of relaxin-3 and its receptor have not been yet demonstrated in the DIO model. The present study investigated the brain expression of relaxin-3 and its cognate receptor RXFP3 in DIO and DR rats maintained on an HE diet since weaning. Expression of relaxin-3 and RXFP3 mRNAs was assessed by in situ hybridization in ad libitum, food-deprived (12 h) and refed (1 h) feeding states. The levels of expression of relaxin-3 in the medial portion of the nucleus incertus (NI) were higher in the DIO rats compared to the DR rats in the ad libitum-fed state. Food deprivation increased the levels of expression of relaxin-3 in the medial NI in DR but not DIO rats. The stronger expression of relaxin-3 in the ad libitum-fed state in the DIO rats was accompanied by low expression of the RXFP3 receptor in the paraventricular hypothalamic nucleus (PVN), supraoptic nucleus, central amygdala (CeA), NI, and nucleus of the solitary tract (NTS). Refeeding increased expression of RXFP3 in the paraventricular thalamic nucleus, parvocellular PVN, CeA, NI, and NTS in the DIO rats. These results provide evidence that DIO rats show a constitutive increase in relaxin-3 expression in the medial NI and that refeeding after food deprivation may enhance the orexigenic effects of relaxin-3 in DIO rats by rapid upregulation of the expression of RXFP3 in the specific brain regions involved in food intake regulation.     

14-3-3蛋白在星形细胞瘤中的表达及意义

目的探讨14-3-3蛋白在星形细胞瘤中的表达与肿瘤病理分级和预后间的关系。方法采用免疫组化ABC法检测10例正常脑组织和67例确诊并有随访的人脑星形细胞瘤石蜡标本中14-3-3蛋白的表达情况。分析14-3-3蛋白的表达与肿瘤恶性程度及预后间的关系。结果在正常脑组织标本中，14-3-3蛋白主要表达于神经元胞体和突起，而在少数的胶质细胞中仅见其弱表达。绝大部分星形胶质细胞瘤中可见14-3-3蛋白阳性表达，其阳性表达率为：Ⅱ级76．5％（13／17），Ⅲ级76．2％（16／21），Ⅳ级79．3％（23／29）。不同恶性级别的星形细胞肿瘤中，14-3-3蛋白的阳性表达率无显著差别（P〉0．05），但14-3-3蛋白表达的强度和范围有随肿瘤的恶性度增高而增加的趋势（P〈0．05）。52例14-3-3蛋白阳性表达患者的生存期明显短于15例14-3-3蛋白表达阴性的患者（P〈0．01）。结论14-3-3蛋白在人脑星形细胞瘤中的表达上凋与肿瘤的恶性程度及预后相关。14-3-3蛋白有望成为星形细胞瘤基因治疗的新靶点。     

丁苯酞对大鼠局灶性脑缺血再灌注损伤后caspase-3表达的影响

目的:观察丁苯酞(NBP)对脑缺血再灌注损伤后的神经保护作用及caspase-3表达的影响。方法:SD大鼠46只随机分成假手术组(n=6)、缺血再灌注组(n=10)、NBP大剂量组(80mg·kg-1,n=10)、NBP中剂量组(40mg·kg-1,n=10)和NBP小剂量组(20mg·kg-1,n=10),采用ZeaLonga法制作局灶性脑缺血再灌注大鼠模型,观察NBP对大鼠脑缺血再灌注后的神经功能症状、组织形态学改变、以及对caspase-3表达的影响。结果:与假手术组相比,缺血再灌注组大鼠出现严重的神经功能缺失症状,光镜下脑组织出现明显的梗死缺血灶,皮质和海马区caspase-3表达增强;与缺血再灌注组比较,NBP治疗组能显著改善大鼠神经功能缺失症状,减少脑组织的梗死缺血损伤,降低caspase-3的表达,其中以NBP大剂量组的神经保护作用最为显著(P<0.001)。结论:NBP对大鼠局灶性脑缺血再灌注损伤具有保护作用,其作用机制可能与抑制caspase-3表达相关。     

Reliability of the task-related component (P3b) of P3 event-related potentials

Abstract Within session and between session reliabilities of the task-related component (P3b) of the P3 measures (amplitude, area and latency) and their habituation across eight sessions separated by 7–10 days, except for an interval of 1 month between the 6th and 7th sessions, were studied based on the difference waves, which were obtained by subtracting the ignored infrequent event-related potentials (ERP) from the target ERP elicited by a standard auditory oddball paradigm with eyes-open or eyes-closed conditions in 10 normal subjects. The within session reliabilities represented as Pearson correlation coefficients ( r ) were 0.57-0.66 for the three measures except for those for the latency and amplitude under the eyes-closed condition. The between session reliabilities expressed as intraclass correlation coefficients ( R ) ranged from 0.54 to 0.60 except for that for latency under eyes-closed conditions. Long-term habituation occurred within the first six sessions for the P3b amplitude and area, and dishabituation took place in the 7th session after an interval of 1 month, whereas no such phenomenon was observed for the P3b latency. Implications of the present results are discussed in terms of the clinical application of the P3 measures.