抑制细胞间缝隙连接通讯功能对星形胶质细胞缺氧/复氧损伤的保护作用

目的研究抑制细胞缝隙连接通讯功能对星形胶质细胞缺氧/复氧损伤的影响.方法原代培养的新生SD大鼠大脑皮层星形胶质细胞分为正常对照组、空白对照组及细胞缝隙连接抑制剂18-α-甘草次酸和油酸酰胺组.荧光示踪法检测星形胶质细胞的缝隙连接通讯功能; MTT法检测抑制缝隙连接通讯功能对缺氧/复氧损伤星形胶质细胞存活率的影响; Annexin V/碘化丙啶双染流式细胞术及Hoechst 33258荧光染色法检测抑制缝隙连接通讯功能对缺氧/复氧损伤星形胶质细胞凋亡的影响.结果与正常对照组相比, 空白对照组星形胶质细胞缝隙连接通讯功能明显增强( P＜0.01), 细胞存活率明显降低( P＜0.01), 细胞凋亡明显增加( P＜0.01);与空白对照组相比, 18-α-甘草次酸及油酸酰胺可显著降低星形胶质细胞缝隙连接通讯功能(均 P＜0.01), 减轻缺氧/复氧损伤引起的星形胶质细胞存活率的降低(均 P＜0.01), 且可减少缺氧/复氧损伤引起的星形胶质细胞凋亡(均 P＜0.01). 结论抑制细胞间缝隙连接通讯功能对星形胶质细胞缺氧/复氧损伤具有保护作用.     

神经胶质细胞参与吗啡耐受机制及治疗的研究进展

 吗啡是临床上常用的强效镇痛药，然而长期应用会导致其镇痛效能降低，发生吗啡耐受。以往对吗啡耐受机制的研究主要集中在脊髓神经元敏化等中枢神经元机制，近年来越来越多的学者开始关注神经胶质细胞，特别是小胶质细胞和星形胶质细胞，在吗啡耐受形成中的作用。本文简要综述了神经胶质细胞参与吗啡耐受的作用机制及其治疗的研究进展，为解决临床上中重度疼痛治疗中的难点问题提供新的解决思路与依据。     

针刺双向良性调控星形胶质细胞治疗脊髓损伤的研究进展＊

随着近年来交通和工业的快速发展，脊髓损伤患者也不断增加，现已成为严重的社会负担，但却一直没有理想的治疗方案。继发性损伤是脊髓损伤后分子和细胞发生的一系列复杂的级联反应。它是SCI的重要组成部分，阐明继发性损伤的机制，针对不同的机制采取不同的干预措施是主要的治疗策略。而星形胶质细胞作为中枢神经系统中数量最多的细胞，在脊髓损伤后发挥了重要作用，受到研究人员的广泛关注，许多研究证明针刺可通过调节星形胶质细胞而发挥治疗作用，故本文综述了星形胶质细胞在脊髓损伤后的作用，以及针刺对其的干预影响，并提出日后研究的展望。     

抑制病理性疼痛相关胶质细胞活化药物的研究进展

背景 病理性疼痛的产生和持续机制十分复杂.近些年越来越多的研究者关注到脊髓胶质细胞在病理性疼痛中所发挥的作用,其中胶质细胞活化和增殖的抑制剂成为了研究的重点.目的 系统阐述胶质细胞在病理性疼痛中的作用和部分胶质细胞抑制剂的作用机制及研究进展.内容 胶质细胞不仅具有营养和支持作用,还参与了病理性疼痛,已有许多实验证实了应用胶质细胞抑制剂可以减弱胶质细胞的激活从而削弱疼痛反应.趋向 期望能为进一步的药物实验研究提供有价值的思路和借鉴.     

CNS: Not an immunoprivilaged site anymore but a virtual secondary lymphoid organ

The cardinal dogma of central nervous system (CNS) immunology believed brain is an immune privileged site, but scientific evidences gathered so far have overturned this notion proving that CNS is no longer an immune privileged site, but rather an actively regulated site of immune surveillance. Landmark discovery of lymphatic system surrounding the duramater of the brain, made possible by high resolution live imaging technology has given new dimension to neuro-immunology. Here, we discuss the immune privilege status of CNS in light of the previous and current findings, taking into account the differences between a healthy state and changes that occur during an inflammatory response. Cerebrospinal fluid (CSF) along with interstitial fluid (ISF) drain activated T cells, natural killer cells, macrophages and dendritic cells from brain to regional lymph nodes present in the head and neck region. To keep an eye on inflammation, this system hosts an army of regulatory T cells (CD25+ FoxP3+) that regulate T cell hyper activation, proliferation and cytokine production. This review is an attempt to fill the gaps in our understanding of neuroimmune interactions, role of innate and adaptive immune system in maintaining homeostasis, interplay of different immune cells, immune tolerance, knowledge of communication pathways between the CNS and the peripheral immune system and lastly how interruption of immune surveillance leads to neurodegenerative diseases. We envisage that discoveries should be made not only to decipher underlying cellular and molecular mechanisms of immune trafficking, but should aid in identifying targeted cell populations for therapeutic intervention in neurodegenerative and autoimmune disorders.     

CO中毒迟发性脑病大鼠脑内星形胶质细胞和少突胶质细胞的表达及高压氧治疗对其表达的影响

目的探讨CO中毒迟发性脑病（DNS）大鼠脑内星形胶质细胞和少突胶质细胞的表达情况及高压氧（HBO）治疗对上述两种胶质细胞表达的影响，分析迟发性脑病的发病机制。方法建立DNS大鼠模型，用HE染色观察大鼠脑组织病理学变化，用免疫组织化学方法，采用小鼠抗大鼠神经胶质原纤维酸性蛋白（GFAP）单克隆抗体、小鼠抗大鼠RIP单克隆抗体检测大鼠脑内星形胶质细胞和少突胶质细胞的表达。结果HE染色标本上，正常对照组大鼠脑内细胞形态正常，DNS大鼠脑皮质出现大片疏松区，海马锥体细胞层稀疏，可见点片状坏死；HBO组坏死程度相对较轻。免疫组化结果显示，与对照组比较，DNS组GFAP表达明显增多（P〈0．05），且阳性细胞形态发生改变；RIP表达随损伤时间的推移逐渐减少（P〈0．05）；HBO组GFAP较7d组表达减少（P〈0．05），RIP较7d组表达增多（P〈0．05）。结论星形胶质细胞和少突胶质细胞在DNS的发病过程中起重要作用，高压氧治疗可针对胶质细胞改善患者脑组织损伤程度。     

Effects of Danggui-Shaoyao-San on the Influence of Spatial Learning and Memory Induced by Experimental Tooth Movement

Background:The pain caused by orthodontic treatment has been considered as tough problems in orthodontic practice.There is substantial literature on pain which has exactly effected on learning and memo...     

Estrogen-IGF-1 interactions in neuroprotection: Ischemic stroke as a case study

The steroid hormone 17b-estradiol and the peptide hormone insulin-like growth factor (IGF)-1 independently exert neuroprotective actions in neurologic diseases such as stroke. Only a few studies have directly addressed the interaction between the two hormone systems, however, there is a large literature that indicates potentially greater interactions between the 17b-estradiol and IGF-1 systems. The present review focuses on key issues related to this interaction including IGF-1 and sex differences and common activation of second messenger systems. Using ischemic stroke as a case study, this review also focuses on independent and cooperative actions of estrogen and IGF-1 on neuroprotection, blood brain barrier integrity, angiogenesis, inflammation and post-stroke epilepsy. Finally, the review also focuses on the astrocyte, a key mediator of post stroke repair, as a local source of 17b-estradiol and IGF-1. This review thus highlights areas where significant new research is needed to clarify the interactions between these two neuroprotectants.     

Noradrenergic Transmission at Alpha1-Adrenergic Receptors in the Ventral Periaqueductal Gray Modulates Arousal

Background

Dysregulation of arousal is symptomatic of numerous psychiatric disorders. Previous research has shown that the activity of dopamine (DA) neurons in the ventral periaqueductal gray (vPAG) tracks with arousal state, and lesions of vPAG^DA cells increase sleep. However, the circuitry controlling these wake-promoting DA neurons is unknown.

Downregulation of inflammatory markers by conjugated linoleic acid isomers in human cultured astrocytes

Objectives: Conjugated linoleic acid (CLA) isomers have been shown to possess anti-inflammatory activity in the central nervous system. In this study, we aimed to evaluate whether modulation of the fatty acid profile by the CLA isomers c9,t11 or t10,c12CLA was associated with changes in the expression of pro-inflammatory molecules in human astrocytes.

Methods: Cultured astrocytes were treated for 6 days with 100?µM fatty acids (c9,t11CLA or t10,c12CLA or oleic acid). Following the treatment, the fatty acid profile of the cell and pro-inflammatory molecule expression were assessed.

Results: Only the t10,c12CLA isomer induced a significant decrease in arachidonic acid and increased the ratio of docosahexaenoic acid/eicosapentaenoic acid, which constitutes indirect evidence of peroxisome proliferator-activated receptor alpha activation. Inhibition of tumour necrosis factor-α, interleukin-1β, and RANTES expression was observed in astrocytes treated with c9,t11CLA and t10,c12CLA.

Discussion: Current data demonstrate that CLA isomers, particularly t10,c12, may affect neuroinflammation by reducing the pro-inflammatory molecules in cultured astrocytes, suggesting a potential nutritional role of CLA isomers in modulating the astrocyte inflammatory response.