虾青素的抗肿瘤作用及其机制

通过论述虾青素的抗肿瘤作用及机制研究,旨在为临床肿瘤治疗相关研究及未来应用提供参考。     

溶血磷脂酸受体2调控胃癌细胞SGC-7901侵袭迁移以及增殖凋亡

为探讨LPA2是否可调节胃癌细胞SGC-7901的侵袭迁移及增殖凋亡,将LPA2 siRNA和pc DNA3.1-LPA2表达载体转染SGC-7901,转染后利用Western blotting检测LPA2、E-cadherin及Vimentin蛋白表达情况,Transwell实验检测细胞侵袭迁移能力,MTS实验检测细胞增殖,流式细胞仪检测凋亡情况。结果表明LPA2 siRNA对胃癌细胞SGC-7901敲除成功后,细胞内的E-cadherin表达增高,Vimentin表达降低;同时其侵袭、迁移和增殖能力降低,凋亡能力升高。细胞SGC-7901过表达LPA2后,细胞内的E-cadherin表达降低,Vimentin表达增加,其侵袭、迁移和增殖能力升高,凋亡能力降低。可见LPA2可调控胃癌细胞SGC-7901侵袭迁移以及增殖凋亡,为胃癌的治疗提供新的靶点。     

MPTP慢性帕金森病小鼠海马内氧化应激与细胞凋亡蛋白的表达

目的 观察 MPTP慢性帕金森病小鼠海马氧化应激指标及细胞凋亡相关蛋白的表达.方法 应用MPTP制备慢性帕金森病模型,观察行为学改变,Morris水迷宫实验,检测模型组和对照组小鼠海马内超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）及丙二醛（MDA）舍量变化,以及免疫组织化学方法、RT-PCR方法、Western blot方法检测海马Bax和Bel-2蛋白表达.结果 慢性帕金森病模型小鼠行为学特点为震颤、活动减少;水迷宫实验结果提示认知功能降低;与对照组海马比较：模型组海马SOD、GSH含量均下降,而MDA含量升高（P〈0.05）;模型组海马Bax蛋白表达增高,而Bel-2蛋白表达下降（P〈0.05）.结论 氧化应激在慢性帕全森病认知功能障碍发病机制中起重要作用,而Bax和Bcl-2蛋白参与了氧化应激诱导海马神经元凋亡的调控过程.     

白桦脂酸体外抗肿瘤的活性和机制

研究白桦脂醇（Betulin）和白桦脂酸（Betulinic Acid, BA）对3种癌细胞株的增殖抑制作用以及白桦脂酸诱导MCF 7细胞毒的分子机制. 应用结晶紫染色方法对白桦脂醇和白桦脂酸对肿瘤细胞的生长抑制作用进行筛选； 应用RT-PCR技术检测MCF 7细胞p21 mRNA, p53 mRNA, Bcl 2 mRNA和Bax mRNA的表达. 结果表明, 白桦脂醇和白桦脂酸有显著抑制肿瘤细胞生长的作用, 且有浓度依赖性; 白桦脂酸能够诱导MCF 7细胞凋亡, 并诱导其p21 mRNA和p53 mRNA表达增高, 但对其Bcl 2 mRNA和Bax mRNA 的表达无影响.     

Scavenger receptor family proteins: roles for atherosclerosis, host defence and disorders of the central nervous system

In this review, we summarize the structure and function of the scavenger receptor family of proteins including class A (type I and II macrophage scavenger receptors, MARCO), class B (CD36, scavenger receptor class BI), mucinlike (CD68/macrosialin, dSR-CI) and endothelial (LOX-1) receptors. Two motifs have been identified as ligand-binding domains a charged collagen structure of type I and II receptors, and an immunodominant domain of CD36. These structures can recognize a wide range of negatively charged macromolecules, including oxidized low-density lipoproteins, damaged or apoptotic cells, and pathogenic microorganisms. After binding, these ligands can be either internalized by endocytosis or phagocytosis, or remain at the cell surface and mediate adhesion or lipid transfer through caveolae. Under physiological conditions, scavenger receptors serve to scavenge or clean up cellular debris and other related materials, and they play a role in host defence. In pathological states, they mediate the recruitment, activation and transformation of macrophages and other cells which may be related to the development of atherosclerosis and to disorders caused by the accumulation of denatured materials, such as Alzheimer's disease. Received 17 September 1997; received after revision 16 March 1998; accepted 17 March 1998     

神经发育过程中的分子机制

叙述了脊椎动物神经分化、神经细胞迁移、神经细胞的凋亡过程中的某些分子机制及bHLH转录调控因子、RA、NMDA受体、Copases、bcl- 2家族在神经发育中的作用 .     

一氧化氮诱导棘阿米巴凋亡的初探

本实验旨在通过形态学和生物化学方法探讨NO对棘阿米巴凋亡的影响。将棘阿米巴在不同浓度的SNP（NO供体）处理条件下孵育一定时间，选用末端脱氧核苷酸转移酶（TdT）介导的d-UTP缺口末端标记法（TUNEL)、透射电镜观察可发现SNP（外源性NO供体）可诱导棘阿米巴滋养体随SNP剂量和时间的增长，逐渐产生凋亡的趋势；透射电镜下可见实验组（终浓度3mmol/L的SNP与棘阿米巴孵育9h和12h）棘阿米巴滋养体有凋亡的超微结构特征。结果表明NO可对棘阿米巴凋亡产生影响并发挥其抗棘阿米巴感染的作用。     

Compensatory caspase activation in MPP+-induced cell death in dopaminergic neurons

Many have hypothesized that cell death in Parkinsons disease is via apoptosis and, specifically, by the mitochondrial-mediated apoptotic pathway. We tested this hypothesis using a mouse dopaminergic cell line of mesencephalic origin, MN9D, challenged with the Parkinsonism-causing neurotoxin MPP⁺ (1-methyl-4-phenylpyridinium ion). Apoptosis was the main mode of cell death when the cells were subjected to MPP⁺ treatment under serum-free conditions for 24 h. Caspase-3 and caspase-9, however, were not activated, thus indicating the existence of alternate or compensatory cell death pathway(s) in dopaminergic neuronal cells. Using caspase inhibitors, we demonstrated that these pathways involve caspase-2, –8, –6 and –7. A time-course study indicated that activation of caspase-2 and –8 occurred upstream of caspase-6 and caspase-7. Upon MPP⁺ challenge, the apoptosis-inducing factor was translocated from the mitochondria into the MN9D cytosol and nucleus. These results suggest the existence of alternative apoptotic pathways in dopaminergic neurons.Received 20 September 2004; received after revision 5 November 2004; accepted 22 November 2004