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Microglia are critical nervous system-specific cells influencing brain development, maintenance of the neural environment, response to injury, and repair. They contribute to neuronal proliferation and differentiation, pruning of dying neurons, synaptic remodeling and clearance of debris and aberrant proteins. Colonization of the brain occurs during gestation with an expansion following birth with localization stimulated by programmed neuronal death, synaptic pruning, and axonal degeneration. Changes in microglia phenotype relate to cellular processes including specific neurotransmitter, pattern recognition, or immune-related receptor activation. Upon activation, microglia cells have the capacity to release a number of substances, e.g., cytokines, chemokines, nitric oxide, and reactive oxygen species, which could be detrimental or beneficial to the surrounding cells. With aging, microglia shift their morphology and may display diminished capacity for normal functions related to migration, clearance, and the ability to shift from a pro-inflammatory to an anti-inflammatory state to regulate injury and repair. This shift in microglia potentially contributes to increased susceptibility and neurodegeneration as a function of age. In the current review, information is provided on the colonization of the brain by microglia, the expression of various pattern recognition receptors to regulate migration and phagocytosis, and the shift in related functions that occur in normal aging.  相似文献
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Vascular endothelial dysfunction is regarded as a primary phenotypic expression of normal human aging. This senescence-induced disorder is the likely culprit underlying the increased cardiovascular and metabolic disease risks associated with aging. The rate of this age-dependent deterioration is largely influenced by the poor-quality lifestyle choice, such as smoking, sedentary daily life, chronic alcohol ingestion, high salt intake, unbalanced diet, and mental stress; and it is accelerated by cardiovascular and metabolic diseases. Although minimizing these detrimental factors is the best course of action, nonetheless chronological age steadily impairs endothelial function through reduced endothelial nitric oxide synthase (eNOS) expression/action, accelerated nitric oxide (NO) degradation, increased phosphodiesterase activity, inhibition of NOS activity by endogenous NOS inhibitors, increased production of reactive oxygen species, inflammatory reactions, decreased endothelial progenitor cell number and function, and impaired telomerase activity or telomere shortening. Endothelial dysfunction in regional vasculatures results in cerebral hypoperfusion triggering cognitive dysfunction and Alzheimer's disease, coronary artery insufficiency, penile erectile dysfunction, and circulatory failures in other organs and tissues. Possible prophylactic measures to minimize age-related endothelial dysfunction are also summarized in this review.  相似文献
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目的:初步探讨人源化抗Aβ抗体对APP/PS1转基因鼠被动免疫治疗效果。方法选取36只APP/PS1转基因鼠,随机分为3组,每组各12只,分别予腹腔注射人源化抗Aβ抗体、鼠源性单克隆抗体、磷酸盐缓冲液(PBS),观察3组小鼠脑内淀粉样斑块积聚情况,测试其学习记忆能力,同时检测血清及脑内TNF-α含量。结果人源化抗Aβ抗体组、鼠源性单克隆抗体组小鼠空间辨别学习记忆能力均优于PBS对照组(P<0.05),人源化抗Aβ抗体组与鼠源性单克隆抗体组间比较差异无统计学意义(P>0.05);治疗后人源化抗Aβ抗体组与鼠源性单克隆抗体组小鼠大脑皮质、海马区棕色斑块沉积明显形态变小、数量变少、范围分散。人源化抗Aβ抗体组与鼠源性单克隆抗体组脑内TNF-α含量均较PBS对照组明显减少(P<0.05)。结论人源化抗Aβ抗体治疗转基因小鼠后明显改善其学习记忆能力,同时使其脑内TNF-α含量减少。  相似文献
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目的:研究线粒体分裂蛋白抑制剂(mdivi-1)能否减轻β淀粉样蛋白(Aβ)诱导的体外原代培养小鼠小胶质细胞的氧化应激损伤。方法:随机将体外原代培养BALB/C小鼠小胶质细胞分为con组、Aβ组、mdi组和 Aβ+mdi 组,con 组不予处理,Aβ组中加入 Aβ,mdi 组中加入 mdivi-1,Aβ+mdi 组分别加入2、5、10、20μmol/L mdivi-1后1 h加入Aβ。分别检测小胶质细胞存活率及凋亡、线粒体膜电位、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、8-羟基脱氧鸟苷(8-OHdG)含量。结果:与con组相比,Aβ组小胶质细胞存活率下降,凋亡增加,线粒体膜电位下降,MDA和8-OHdG含量升高,SOD活性下降,差异有统计学意义(<0.05);与Aβ组相比,Aβ+mdi组小胶质细胞存活率上升,凋亡减少,线粒体膜电位增加,细胞内MDA和8-OHdG水平下降,SOD活性上升,差异有统计学意义(<0.05)。结论:mdivi-1对Aβ诱导的体外原代培养小胶质细胞氧化应激损伤具有保护作用。  相似文献
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目的:研究线粒体分裂蛋白抑制剂对茁淀粉样蛋白(A茁)诱导小胶质细胞凋亡的作用及其机制。方法:随机将BV-2小胶质细胞分为con组、A茁组、mdi组和A茁+mdi组,con组不做特殊处理,mdi组培养基中加入10滋mol/L mdivi-1,A茁组培养基中加入20滋mol/L A茁,A茁+mdi组培养基分别加入2、5、10、20滋mol/L mdivi-1和20滋mol/L A茁。采用MTT法检测细胞存活率,TUNEL染色检测细胞凋亡,Western blot法检测Drp1、CytC和Caspase-3蛋白水平变化,RT-PCR法检测CA11b mRNA表达变化。结果:与con组相比,A茁组的细胞存活率明显下降,凋亡显著增加,CA11b mRNA上升,线粒体Drp1、细胞浆CytC和激活的 Cas-pase-3增加,差异有统计学意义(<0.05);与A茁组相比,A茁+mdi组的细胞存活率明显上升,凋亡显著减少,CA11b mRNA下降,线粒体Drp1、细胞浆CytC和激活的Caspase-3减少,差异有统计学意义(<0.05)。结论:线粒体分裂蛋白抑制剂对A茁诱导小胶质细胞凋亡有保护作用,其机制可能为抑制线粒体/CytC/Caspase-3凋亡途径。  相似文献
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目的:研究慢性低灌注后基质金属蛋白酶MMP-2、MMP-9和淀粉样物质A茁40表达的变化。方法:Wistar大鼠48只随机分为假手术组和缺血组各24只,缺血组大鼠结扎双侧颈总动脉,假手术组不造成缺血。免疫组化染色观察MMP-2、MMP-9和A茁40表达的变化。结果:缺血组大鼠低灌注后7 d,免疫组化染色显示MMP-2和A茁40在皮质的静脉内皮上有阳性表达;低灌注后14 d,MMP-2和A茁40在较小动脉内皮上阳性表达;低灌注后30 d在相对较大的动脉内皮上阳性表达;MMP-9在血管内皮未见表达。结论:慢性低灌注后A茁40在血管内皮沉积,MMP-2表达增加。  相似文献
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目的:初步探讨β淀粉样蛋白1~42(Aβ1~42)及D-半乳糖(D-gal)联合构建的复合型阿尔茨海默病(AD)模型,以及模型中硫氧还蛋白与凋亡相关蛋白的研究。方法采用44只2月龄雄性SD大鼠,共分4组,腹腔注射及侧脑室注射生理盐水的假手术组,腹腔注射D-gal及侧脑室注射Aβ1~42分别建立的D-gal组和Aβ1~42组,腹腔注射D-gal联合侧脑室注射Aβ1~42建立的复合AD模型组。免疫组织化学检测脑组织中Trx,细胞色素c(Cyto-c)及Caspase-9表达。结果与对照组相比,Aβ1~42组、D-gal组和复合模型组皮质、海马中Trx的表达下降,Cyto-c和Caspase-9的表达上升。与Aβ1~42组、D-gal组相比,复合模型组皮质、海马中Trx的表达下降;Cyto-c和Caspase-9的表达上升。结论在复合AD模型中神经细胞凋亡,Trx表达下降,而Cyto-c和Caspase-9表达上升。Trx参与神经细胞的凋亡过程。  相似文献
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背景:端粒酶可维持端粒长度,避免细胞复制性衰老和凋亡,其催化亚基端粒酶反转录酶还具有抗凋亡和调节细胞生存的作用。目的:观察人端粒酶反转录酶对β淀粉样蛋白1-40引起的人胚胎皮质神经元损伤的影响。方法:分离和培养12-16周龄人胚胎皮质神经元,将人端粒酶反转录酶基因重组腺病毒转染至神经元。免疫细胞化学法检测人端粒酶反转录酶基的表达,端粒重复序列扩增酶联免疫吸附法检测端粒酶活性。转染后第3天,给予10μmol/L β淀粉样蛋白1-40作用24 h 后,应用 MTT 检测细胞活力。荧光探针2’7’-二乙酰二氯荧光素标记检测细胞内活性氧水平,比色法测定细胞匀浆中谷胱甘肽含量。结果与结论:转染后第3天,人端粒酶反转录酶的表达最高,并重建了其端粒酶活性;10μmol/L β淀粉样蛋白1-40显著降低神经元的细胞活力和谷胱甘肽的含量(P <0.05和 P <0.01),升高活性氧水平(P <0.05)。转染了人端粒酶反转录酶基因的神经元能显著对抗β淀粉样蛋白1-40的毒性作用,增加细胞的活力和谷胱甘肽含量(P <0.05和 P <0.01),降低活性氧水平(P <0.05)。结果表明,人端粒酶反转录酶对β淀粉样蛋白1-40引起的人胚胎皮质神经元的损伤有明显保护作用。  相似文献
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