刺五加多糖对氧化损伤大鼠的海马神经元OGG1 mRNA表达的影响

目的 研究刺五加多糖(ASPS)对氧化损伤的海马神经元OGG1 mRNA表达的影响,为揭示ASPS具有抵抗氧化损伤提供有力的实验依据.方法 运用海马神经细胞原代培养技术,采用H2O2诱导建立细胞氧化损伤模型.观察细胞形态学变化;MTT法测定细胞活性;化学比色法检测细胞匀浆液中过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力;RT-PCR法检测OGG1 mRNA的表达.结果 形态学观察显示,与模型组比较,ASPS组细胞损伤程度明显减轻;ASPS组细胞活性(0.46)比模型组细胞活性(0.36)高(P＜0.01) ; SOD、GSH-Px活力ASPS组显著高于模型组; ASPS能够明显提高OGG1 mRNA的表达.结论 ASPS能够增强OGG1 mRNA的表达,并对海马神经元氧化损伤有保护作用.     

丹黄方对部分肝叶切除大鼠肝组织中Tec的影响

目的探讨丹黄方对部分肝叶切除大鼠肝组织中Tec mRNA表达的影响。方法采用部分肝叶切除肝再生模型。24只大鼠随机分为假手术组、手术组、丹黄方组和pHGF组。除假手术组外其余三组接受部分肝叶切除手术。从手术前3天至手术后48小时,丹黄方组给与丹黄方灌胃（10g/kg）及腹腔注射生理盐水（4．0ml/kg）,每天一次;促肝细胞生长素（pHGF）组给与生理盐水灌胃（4．0ml／kg）和腹腔注射pHGF（1ml/100g）,每天一次;手术组及假手术组仅给与生理盐水（4．0ml／kg）灌胃和腹腔注射。采用RT—PCR方法检测Tec mRNA的表达。结果丹黄方组肝组织中Tec mRNA的表达显著高于假手术组和手术组,P〈0．01;与pHGF组比较无显著差异,P〉0．05。结论丹黄方具有促进部分肝叶切除大鼠肝组织中Tec mRNA的表达的作用。     

dsRNA抑制SAG3表达对弓形虫入侵蛋白ROP2、MIC2的影响

目的观察表面抗原3（SAG3）对弓形虫入侵相关蛋白的影响,为深入研究弓形虫的致病机制奠定基础。方法用电穿孔的方法将针对SAG3基因3-′UTR区的dsRNA转入弓形虫速殖子体内,转染后的虫体感染Hela细胞,转染后2 h提取总RNA,RT-PCR检测SAG3的抑制效率,同时检测弓形虫入侵蛋白ROP2、MIC2的表达情况。结果dsRNA电穿孔转染弓形虫速殖子后抑制SAG3 mRNA表达,ROP2、MIC2的表达量显著低于对照组。结论抑制SAG3的表达影响ROP2、MIC2的表达。     

血清survivin抗体及基因表达检测对肺癌的诊断价值

目的探讨血清survivin抗体及基因表达对肺癌的诊断价值。方法收集47例肺癌患者和30例健康对照组的外周血标本,分别采用ELISA法、RT-PCR法检测血清中survivin抗体和survivin mRNA的表达水平。结果肺癌患者血清中survivin抗体和survivin mRNA表达水平均高于对照组（P均〈0.05）,肺癌患者血清血清survivin抗体表达与血清survivin mRNA的表达呈正相关（r=0.367,P〈0.01）。结论血清survivin基因及抗体检测对临床肺癌诊断有重要价值。     

膀胱内翻性乳头状瘤中EphA2蛋白、mRNA的表达及意义

目的观察膀胱内翻性乳头状瘤（IPB）组织中受体酪氨酸激酶（EphA2）蛋白、mRNA的表达,并探讨其意义。方法采用免疫组化sP法检测26例IPB（IPB组）、15例低级别膀胱移行细胞癌（BTCC组）和10例正常膀胱组织中的EphA2蛋白。采用逆转录实时定量PCR技术检测各组EphA2 mRNA的表达。结果IPB组、BTCC组EphA2蛋白的表达量（IA值）分别为13826±3996和13112±3587,与对照组的8364±3915相比,P均〈0．05;IPB组与BTCC组相比P〉0．05。以对照组为1,IPB组与BTCC组EphA2 mRNA表达分别上调（2．12±0．95）和（2,01±0．86）倍;IPB与BTCC组比较,P〉0．05。结论IPB组织中EphA2过表达,其可能促进了膀胱内翻性乳头状瘤的癌性转化。     

The ADAMs family: coordinators of nervous system development, plasticity and repair

A disintegrin and metalloprotease (ADAM) transmembrane proteins have metalloprotease, integrin-binding, intracellular signaling and cell adhesion activities. In contrast to other metalloproteases, ADAMs are particularly important for cleavage-dependent activation of proteins such as Notch, amyloid precursor protein (APP) and transforming growth factor alpha (TGFalpha), and can bind integrins. Not surprisingly, ADAMs have been shown or suggested to play important roles in the development of the nervous system, where they regulate proliferation, migration, differentiation and survival of various cells, as well as axonal growth and myelination. On the eleventh anniversary of the naming of this family of proteins, the relatively unknown ADAMs are emerging as potential therapeutic targets for neural repair. For example, over-expression of ADAM10, one of the alpha-secretases for APP, can prevent amyloid formation and hippocampal defects in an Alzheimer mouse model. Another example of this potential neural repair role is the finding that ADAM21 is uniquely associated with neurogenesis and growing axons of the adult brain. This comprehensive review will discuss the growing literature about the roles of ADAMs in the developing and adult nervous system, and their potential roles in neurological disorders. Most excitingly, the expanding understanding of their normal roles suggests that they can be manipulated to promote neural repair in the degenerating and injured adult nervous system.