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| 1 | 益气活血方基于miR-124调控Wnt通路促进神经再生显示文摘目的探讨益气活血方(脑络欣通)对MCAO-R气虚血瘀证大鼠神经再生的影响及可能的作用机制。方法随机数字表法将大鼠分成4组:正常组、模型组、脑络欣通组、通心络组,其中脑络欣通组和通心络组分别用脑络欣通溶液、通心络溶液灌胃。观察各组大鼠生命状态并进行神经功能缺损、气虚证和血瘀证评分,运用激光多普勒仪动态监测局部脑血流量(r CBF),TTC染色检测脑梗死体积,免疫组化结合免疫荧光染色检测脑组织Nestin和Brd U表达,荧光定量PCR检测mi RNA-124水平,Western blotting检测Wnt3a、GSK3β和β-catenin蛋白表达水平。结果脑络欣通和通心络都能改善模型大鼠神经功能,降低气虚证和血瘀证评分,减少脑梗死体积,r CBF提高(P<0.01);脑络欣通和通心络组Brd U表达增强,与正常组比较,其他3组阳性细胞数明显增多(P<0.01),与模型组比较,脑络欣通和通心络组显著增多,Nestin表达明显增强(P<0.01)。脑络欣通能抑制模型大鼠脑组织mi RNA-124和Wnt3a应激性的高表达,同时提高β-catenin的表达水平(P<0.01)。但脑络欣通和通心络对模型大鼠GSK3β蛋白表达均无明显影响(P>0.05)。结论脑络欣通可能通过影响脑组织mi RNA-124的表达而激活Wnt通路,从而发挥对气虚血瘀型脑缺血的神经保护以及神经再生的作用。 | 谭辉 王键 尹婷婷 何玲 邓勇 李凤 王玉凤 | 2017 | 南方医科大学学报2017，37，8： | 11 |
| 2 | Interplay of SOX transcription factors and microRNAs in the brain under physiological and pathological conditions显示文摘Precise tuning of gene expression,accomplished by regulato ry networks of transcription factors,epigenetic modifiers,and microRNAs,is crucial for the proper neural development and function of the brain cells.The SOX transcription factors are involved in regulating diverse cellular processes during embryonic and adult neurogenesis,such as maintaining the cell stemness,cell prolife ration,cell fate decisions,and terminal diffe rentiation into neurons and glial cells.MicroRNAs represent a class of small non-coding RNAs that play important roles in the regulation of gene expression.Together with other gene regulatory factors,microRNAs regulate different processes during neurogenesis and orchestrate the spatial and temporal expression important for neurodevelopment.The emerging data point to a complex regulatory network between SOX transcription factors and microRNAs that govern distinct cellular activities in the developing and adult brain.Deregulated SOX/mic roRNA interplay in signaling pathways that influence the homeostasis and plasticity in the brain has been revealed in various brain pathologies,including neurodegenerative disorders,traumatic brain injury,and cancer.Therapeutic strategies that target SOX/microRNA interplay have emerged in recent years as a promising tool to target neural tissue regeneration and enhance neuro restoration.N umerous studies have confirmed complex intera ctions between microRNAs and SOX-specific mRNAs regulating key features of glioblastoma.Keeping in mind the crucial roles of SOX genes and microRNAs in neural development,we focus this review on SOX/microRNAs interplay in the brain during development and adulthood in physiological and pathological conditions.Special focus was made on their interplay in brain pathologies to summarize current knowledge and highlight potential future development of molecular therapies. | Milena Stevanovic Danijela Stanisavljevic Ninkovic Marija Mojsin Danijela Drakulic Marija Schwirtlich | 2022 | Neural Regeneration Research2022，17，11： | 2 |
| 3 | microRNA在亨廷顿病中的研究进展显示文摘亨廷顿病(Huntington’s disease,HD)是神经退行性疾病(neurodegenerative disorders)中一种单基因遗传病,由亨廷顿基因(the huntingtin gene,HTT)第一个外显子中的CAG三核苷酸序列重复扩增引起,尚无法治愈。HTT编码的蛋白产物被称为亨廷顿蛋白(Huntingtin protein,Htt)。突变亨廷顿蛋白(mutated huntingtin protein,mHtt)容易形成聚集体,具有毒性,导致一系列细胞学异常和神经元功能障碍。microRNA(miRNA)在基因转录后水平调控中起重要作用,其表达的改变与HD病理过程有关,成为治疗HD的潜在生物标志物。近年来,对一些特定miRNA在HD中调控机制及靶基因预测方面的研究可为HD提供潜在的治疗方法。本文就miRNA在HD中的相关研究进展进行综述。 | 姜兵兵 | 2020 | 中国临床药理学与治疗学2020，25，6： | 2 |
| 4 | 微小RNA在衰老及衰老性疾病发生发展中的调控作用显示文摘近年来,随着表观遗传学的发展,微小RNA(miRNA)在基因表达调控方面的作用已经成为研究热点。miRNA是机体内一类高度保守的内源性非编码单链小分子RNA,它可以通过降解靶mRNA或抑制靶蛋白翻译以调控基因的表达。本文主要围绕miRNA在衰老及衰老相关性疾病(神经退行性疾病、骨质疏松、动脉粥样硬化和肿瘤等)发生发展中的调控作用以及中药的干预作用作一综述。 | 孙丽娥 金国琴 | 2018 | 生命的化学2018，38，2： | 2 |
| 5 | microRNA与认知功能疾病显示文摘microRNA是一类长约22个核苷酸的非编码RNA,广泛参与神经发育、组织分化和神经突触形成等多种生命进程。认知与神经发育、组织分化和神经突触形成关系密切。因此microRNA在认知功能改变这一病理生理过程中起到非常重要的作用。本文将从microRNA在神经发育、突触形成、在神经退行性疾病和术后认知功能障碍发病机理中的作用等方面作一综述。 | 廖明锋 张志发 陈堃 李璐 吴娅琴 龙思 王学仁 | 2017 | 生命的化学2017，37，4： | 1 |
| 6 | Altered microRNA expression in animal models of Huntington’s disease and potential therapeutic strategies显示文摘A review of recent animal models of Huntington’s disease showed many microRNAs had altered expression levels in the striatum and cerebral cortex,and which were mostly downregulated.Among the altered microRNAs were miR-9/9*,miR-29b,miR-124a,miR-132,miR-128,miR-139,miR-122,miR-138,miR-23b,miR-135b,miR-181(all downregulated)and miR-448(upregulated),and similar changes had been previously found in Huntington’s disease patients.In the animal cell studies,the altered microRNAs included miR-9,miR-9*,miR-135b,miR-222(all downregulated)and miR-214(upregulated).In the animal models,overexpression of miR-155 and miR-196a caused a decrease in mutant huntingtin mRNA and protein level,lowered the mutant huntingtin aggregates in striatum and cortex,and improved performance in behavioral tests.Improved performance in behavioral tests also occurred with overexpression of miR-132 and miR-124.In the animal cell models,overexpression of miR-22 increased the viability of rat primary cortical and striatal neurons infected with mutant huntingtin and decreased huntingtin-enriched foci of≥2μm.Also,overexpression of miR-22 enhanced the survival of rat primary striatal neurons treated with 3-nitropropionic acid.Exogenous expression of miR-214,miR-146a,miR-150,and miR-125b decreased endogenous expression of huntingtin mRNA and protein in HdhQ111/HdhQ111 cells.Further studies with animal models of Huntington’s disease are warranted to validate these findings and identify specific microRNAs whose overexpression inhibits the production of mutant huntingtin protein and other harmful processes and may provide a more effective means of treating Huntington’s disease in patients and slowing its progression. | Bridget Martinez Philip V.Peplow | 2021 | Neural Regeneration Research2021，16，11： | 1 |
| 7 | 外泌体MicroRNA在亨廷顿舞蹈病发生发展中的作用显示文摘亨廷顿舞蹈病(Huntington’s disease,HD)是一种遗传性神经退行性疾病,其特征为运动障碍、进行性认知功能下降及精神障碍,可严重影响患者的生活质量。外泌体微小RNA(MicroRNA)是一种由蛋白质生物合成的内源性非编码RNA分子。最新研究表明,外泌体MicroRNA广泛参与HD发生发展,不仅参与其发病机制,还在基因预测及机制调控等方面表现出潜在的研究价值。因此,探讨外泌体MicroRNA在HD发生发展中的作用可为HD的研究提供新方向。 | 王璐璐 董露露 王天俊 | 2022 | 卒中与神经疾病2022，29，4： | 0 |
| 8 | Mitochondria in Huntington’s disease:implications in pathogenesis and mitochondrial-targeted therapeutic strategies显示文摘Huntington’s disease is a genetic disease caused by expanded CAG repeats on exon 1 of the huntingtin gene located on chromosome 4.Compelling evidence implicates impaired mitochondrial energetics,altered mitochondrial biogenesis and quality control,disturbed mitochondrial trafficking,oxidative stress and mitochondrial calcium dyshomeostasis in the pathogenesis of the disorder.Unfortunately,conventional mitochondrial-targeted molecules,such as cysteamine,creatine,coenzyme Q10,or triheptanoin,yielded negative or inconclusive results.However,future therapeutic strategies,aiming to restore mitochondrial biogenesis,improving the fission/fusion balance,and improving mitochondrial trafficking,could prove useful tools in improving the phenotype of Huntington’s disease and,used in combination with genome-editing methods,could lead to a cure for the disease. | Anamaria Jurcau Carolina Maria Jurcau | 2023 | Neural Regeneration Research2023，18，7： | 0 |
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