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| 1 | Neuronal autophagy aggravates microglial inflammatory injury by downregulating CX3CL1/fractalkine after ischemic stroke显示文摘Ischemic stroke often induces excessive neuronal autophagy, resulting in brain damage; meanwhile, inflammatory responses stimulated by ischemia exacerbate neural injury. However, interactions between neuronal autophagy and microglial inflammation following ischemic stroke are poorly understood. CX3CL1/fractalkine, a membrane-bound chemokine expressed on neurons, can suppress microglial inflammation by binding to its receptor CX3CR1 on microglia. In the present study, to investigate whether autophagy could alter CX3CL1 expression on neurons and consequently change microglial inflammatory activity, middle cerebral artery occlusion(MCAO) was established in Sprague-Dawley rats to model ischemic stroke, and tissues from the ischemic penumbra were obtained to evaluate autophagy level and microglial inflammatory activity. MCAO rats were administered 3-methyladenine(autophagy inhibitor) or Tat-Beclin 1(autophagy inducer). Western blot assays were conducted to quantify expression of Beclin-1, nuclear factor kappa Bp65(NF-κB), light chain 3B(LC3B), and CX3CL1 in ischemic penumbra. Moreover, immunofluorescence staining was performed to quantify numbers of LC3B-, CX3CL1-, and Iba-1-positive cells in ischemic penumbra. In addition, enzyme linked immunosorbent assays were utilized to analyze concentrations of tumor necrosis factor alpha(TNF-α), interleukin 6(IL-6), interleukin 1 beta(IL-1β), and prostaglandin E2(PGE2). A dry/wet weight method was used to detect brain water content, while 2,3,5,-triphenyltetrazolium chloride staining was utilized to measure infarct volume. The results demonstrated that autophagy signaling(Beclin-1 and LC3B expression) in penumbra was prominently activated by MCAO, while CX3CL1 expression on autophagic neurons was significantly reduced and microglial inflammation was markedly activated. However, after inhibition of autophagy signaling with 3-methyladenine, CX3CL1 expression on neurons was obviously increased, whereas Iba-1 and NF-κB expression was downregulated; TNF-α, IL-6, IL-1β, and PGE2 levels were decreased; and cerebral edema was obviously mitigated. In contrast, after treatment with the autophagy inducer Tat-Beclin 1, CX3CL1 expression on neurons was further reduced; Iba-1 and NF-κB expression was increased; TNF-α, IL-6, IL-1β, and PGE2 levels were enhanced; and cerebral edema was aggravated. Our study suggests that ischemia-induced neuronal autophagy facilitates microglial inflammatory injury after ischemic stroke, and the efficacy of this process may be associated with downregulated CX3CL1 expression on autophagic neurons. | Hong-Yun He Lu Ren Tao Guo Yi-Hao Deng | 2019 | Neural Regeneration Research2019，14，2： | 25 |
| 2 | 外泌体与缺血性脑卒中及针灸干预机制显示文摘近年来的研究发现一些特异性治疗性外泌体可作为缺血性脑卒中(ischemic stroke,IS)治疗的新靶点,本文旨在研究外泌体作为细胞间通讯新介质对于IS的诊断及对于受损脑组织的保护作用,讨论外泌体中微小核糖核酸(microRNAs,miRNA)作为缺血性中风的新兴生物标志物和治疗靶标的潜在临床应用。进一步探讨针灸对外泌体的影响,外泌体对针灸刺激的应答作用,为阐述针灸治疗IS的机制提供新思路,为发挥针灸治疗优势提供科学依据。 | 李巧凤 彭拥军 李忠仁 洪浩 储继红 蔡云 | 2020 | 世界科学技术-中医药现代化2020，22，1： | 8 |
| 3 | miR-145对TNF-α诱导人关节软骨细胞增殖、凋亡及炎症反应的影响显示文摘目的明确miR-145在肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)诱导人关节软骨细胞增殖、凋亡及炎症反应中的作用。方法利用0、5、10、15及30 ng/ml TNF-α诱导人C-20/A4和CH8关节软骨细胞48 h,提取总RNA并反转录,采用实时荧光定量聚合酶链反应检测miR-145的表达水平。瞬时转染miR-145模拟物(mimics)至30 ng/ml TNF-α诱导的人C-20/A4和CH8细胞,分别采用噻唑蓝比色法[3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide,MTT]、蛋白质印迹及酶联免疫吸附剂测定(enzyme-linked immunosorbnent assay,ELISA)观察细胞增殖、凋亡及炎症因子浓度的变化。结果随着TNF-α诱导浓度的提高,C-20/A4和CH8细胞中白介素-1β(interleukin-1β,IL-1β)、IL-6及IL-13的浓度呈剂量依赖性升高(P<0.05),而miR-145的表达水平呈剂量依赖性降低(P<0.05)。与对照组相比,miR-145 mimics显著提高C-20/A4和CH8细胞中miR-145的表达水平(P<0.05)。与对照组相比较,miR-145 mimics显著降低C-20/A4和CH8细胞增殖能力,并增加胱天蛋白酶3(caspase 3,CASP3)、cleaved CASP3、Bcl-2相关X蛋白(Bcl-2 related X protein,BAX)的表达水平及IL-1β、IL-6及IL-13的浓度(P<0.05)。结论miR-145在TNF-α诱导的人关节软骨细胞中呈剂量依赖性下调。体外过表达miR-145抑制TNF-α诱导的人关节软骨细胞增殖,促进凋亡及炎症反应。 | 阿布都艾尼·热吾提 肖伟 周文正 车立新 徐江波 孙俊刚 | 2021 | 中国骨与关节杂志2021，10，7： | 3 |
| 4 | miR-21a-5p靶向MATN2抑制LPS诱导的巨噬细胞损伤的实验研究显示文摘目的miR-21a-5p对脂多糖(LPS)处理的RAW264.7巨噬细胞的调控作用及分子机制研究。方法实时荧光定量PCR(qRT-PCR)检测不同浓度LPS处理的巨噬细胞中miR-21a-5p水平;应用miR-21a-5p模拟物(mimics)和阴性对照(miRNA-NC)分别转染LPS处理的巨噬细胞,MTT法检测细胞活力,流式细胞术检测细胞凋亡比例;ELISA检测炎性细胞因子水平;TargetScan数据库分析miR-21a-5p的潜在靶基因,蛋白免疫印迹技术(Western blot法)检测MATN2蛋白表达水平;双荧光素酶实验验证miR-21a-5p和MATN2之间的关系。结果随着LPS处理浓度的增加,miR-21a-5p水平逐渐降低。miR-21a-5p mimics转染RAW264.7巨噬细胞后miR-21a-5p水平显著升高。上调LPS处理的巨噬细胞miR-21a-5p水平后,细胞活力显著升高,细胞凋亡比例降低;促炎性细胞因子TNF-α、IL-6和IL-1β水平降低。qRT-PCR和Western blot法结果表明,上调miR-21a-5p水平后,MATN2蛋白表达和mRNA水平明显降低,而下调miR-21a-5p水平后,MATN2蛋白表达和mRNA明显升高。双荧光素酶报告实验显示miR-21a-5p靶向MATN2的mRNA的3′非编码区(3′UTR)。结论miR-21a-5p可以靶向MATN2抑制LPS诱导的巨噬细胞损伤。 | 王立刚 王颖 王涵 | 2021 | 医学研究杂志2021，50，5： | 2 |
| 5 | microRNA调控小胶质细胞激活极化的研究进展显示文摘微小RNA(microRNA,miRNA)是一类长约22个核苷酸的内源性非编码RNA,参与调控细胞增殖、分化、代谢、凋亡的各个方面。小胶质细胞是中枢神经系统的固有免疫细胞,参与介导免疫炎症反应,在众多神经系统疾病的发生、发展及康复过程中扮演重要角色。激活的小胶质细胞能够极化为M1和M2两种类型。M1型主要促进炎症反应的发生,M2型则具有抗炎和促进神经修复的功能。近年来研究发现,miRNA可以调控小胶质细胞的激活极化过程,影响多种神经系统疾病的进程。该文对miRNA的生物学作用及对小胶质细胞激活极化的调控进行综述。 | 于涛(综述) 王华(审校) | 2020 | 国际儿科学杂志2020，47，8： | 0 |
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