Traumatic brain injury can be categorized into primary and secondary injuries.Secondary injuries are the main cause of disability following traumatic brain injury,which involves a complex multicellular cascade.Microgl...Traumatic brain injury can be categorized into primary and secondary injuries.Secondary injuries are the main cause of disability following traumatic brain injury,which involves a complex multicellular cascade.Microglia play an important role in secondary injury and can be activated in response to traumatic brain injury.In this article,we review the origin and classification of microglia as well as the dynamic changes of microglia in traumatic brain injury.We also clarify the microglial polarization pathways and the therapeutic drugs targeting activated microglia.We found that regulating the signaling pathways involved in pro-inflammatory and anti-inflammatory microglia,such as the Toll-like receptor 4/nuclear factor-kappa B,mitogen-activated protein kinase,Janus kinase/signal transducer and activator of transcription,phosphoinositide 3-kinase/protein kinase B,Notch,and high mobility group box 1 pathways,can alleviate the inflammatory response triggered by microglia in traumatic brain injury,thereby exerting neuroprotective effects.We also reviewed the strategies developed on the basis of these pathways,such as drug and cell replacement therapies.Drugs that modulate inflammatory factors,such as rosuvastatin,have been shown to promote the polarization of antiinflammatory microglia and reduce the inflammatory response caused by traumatic brain injury.Mesenchymal stem cells possess anti-inflammatory properties,and clinical studies have confirmed their significant efficacy and safety in patients with traumatic brain injury.Additionally,advancements in mesenchymal stem cell-delivery methods—such as combinations of novel biomaterials,genetic engineering,and mesenchymal stem cell exosome therapy—have greatly enhanced the efficiency and therapeutic effects of mesenchymal stem cells in animal models.However,numerous challenges in the application of drug and mesenchymal stem cell treatment strategies remain to be addressed.In the future,new technologies,such as single-cell RNA sequencing and transcriptome analysis,can facilitate further experimental studies.Moreover,research involving non-human primates can help translate these treatment strategies to clinical practice.展开更多
目的 分析创伤性颅脑损伤血清miR-31-5p、miR-129-5p水平及其与神经功能的关系。方法 回顾性选取2022年8月—2025年8月东南大学附属徐州市中心医院收治的创伤性颅脑损伤患者169例,根据格拉斯哥昏迷量表(Glasgow coma scale,GCS)评分将...目的 分析创伤性颅脑损伤血清miR-31-5p、miR-129-5p水平及其与神经功能的关系。方法 回顾性选取2022年8月—2025年8月东南大学附属徐州市中心医院收治的创伤性颅脑损伤患者169例,根据格拉斯哥昏迷量表(Glasgow coma scale,GCS)评分将患者分为轻型组(n=64)、中型组(n=54)、重型组(n=51)。另选同期东南大学附属徐州市中心医院体检的健康者100例为对照组。比较所有受试者血清miR-31-5p、miR-129-5p水平、美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分。采用Pearson相关分析血清miR-31-5p、miR-129-5p水平与NIHSS评分的相关性,采用受试者工作特征(receiver operating characteristic,ROC)曲线分析血清miR-31-5p、miR-129-5p水平对创伤性颅脑损伤患者发生神经功能缺损的诊断价值。结果 重型组、中型组、轻型组血清miR-31-5p水平、NIHSS评分均高于对照组,血清miR-129-5p水平均低于对照组,重型组、中型组血清miR-31-5p水平、NIHSS评分均高于轻型组,血清miR-129-5p水平均低于轻型组,重型组血清miR-31-5p水平、NIHSS评分均高于中型组,血清miR-129-5p水平低于中型组(P<0.05)。血清miR-31-5p水平与NIHSS评分呈正相关(r=0.666,P<0.05),血清miR-129-5p水平与NIHSS评分呈负相关(r=-0.715,P<0.05)。ROC结果显示,血清miR-31-5p、miR-129-5p水平联合诊断创伤性颅脑损伤患者神经功能缺损的敏感度为99.3%,特异度为92.9%,AUC为0.951,预测价值较高。结论 血清miR-31-5p水平升高、miR-129-5p水平降低与创伤性颅脑损伤患者神经功能缺损程度密切相关,二者联合检测对评估神经功能缺损具有较高预测价值。展开更多
目的系统梳理创伤性脑损伤(TBI)后神经元凋亡机制的研究进展,识别该领域研究热点与难点,为未来研究方向提供参考。方法基于Web of Science核心合集数据库,检索2001—2025年间主题为TBI神经元凋亡的相关文献,运用VOSviewer、CiteSpace及...目的系统梳理创伤性脑损伤(TBI)后神经元凋亡机制的研究进展,识别该领域研究热点与难点,为未来研究方向提供参考。方法基于Web of Science核心合集数据库,检索2001—2025年间主题为TBI神经元凋亡的相关文献,运用VOSviewer、CiteSpace及R软件,从文献数量、国家分布、期刊来源及关键词等维度进行文献计量分析。结果共纳入TBI神经元凋亡领域文献3666篇,年发文量呈持续增长趋势。中国(1488篇)和美国(1015篇)为发文量前两位的国家,合计占比达68%。主要研究机构包括宾夕法尼亚州立大学、匹兹堡大学及苏州大学等。相关研究主要发表于Journal of Neurotrauma、Brain Research等期刊。早期研究聚焦于氧化应激、钙超载及Bcl-2家族蛋白介导的线粒体凋亡途径,2010年后逐渐拓展至多机制交叉调控。关键词共现分析显示,凋亡、炎症与氧化应激为核心机制,并与阿尔茨海默病、脑缺血等神经退行性疾病存在关联。结论STBI后神经元凋亡机制研究正从基础通路探索逐步拓展至神经修复、跨疾病关联及靶向治疗等方向。然而,该领域基础研究成果在向临床转化过程中仍面临诸多挑战,转化策略有待进一步系统探索。展开更多
基金supported by the Natural Science Foundation of Yunnan Province,No.202401AS070086(to ZW)the National Key Research and Development Program of China,No.2018YFA0801403(to ZW)+1 种基金Yunnan Science and Technology Talent and Platform Plan,No.202105AC160041(to ZW)the Natural Science Foundation of China,No.31960120(to ZW)。
文摘Traumatic brain injury can be categorized into primary and secondary injuries.Secondary injuries are the main cause of disability following traumatic brain injury,which involves a complex multicellular cascade.Microglia play an important role in secondary injury and can be activated in response to traumatic brain injury.In this article,we review the origin and classification of microglia as well as the dynamic changes of microglia in traumatic brain injury.We also clarify the microglial polarization pathways and the therapeutic drugs targeting activated microglia.We found that regulating the signaling pathways involved in pro-inflammatory and anti-inflammatory microglia,such as the Toll-like receptor 4/nuclear factor-kappa B,mitogen-activated protein kinase,Janus kinase/signal transducer and activator of transcription,phosphoinositide 3-kinase/protein kinase B,Notch,and high mobility group box 1 pathways,can alleviate the inflammatory response triggered by microglia in traumatic brain injury,thereby exerting neuroprotective effects.We also reviewed the strategies developed on the basis of these pathways,such as drug and cell replacement therapies.Drugs that modulate inflammatory factors,such as rosuvastatin,have been shown to promote the polarization of antiinflammatory microglia and reduce the inflammatory response caused by traumatic brain injury.Mesenchymal stem cells possess anti-inflammatory properties,and clinical studies have confirmed their significant efficacy and safety in patients with traumatic brain injury.Additionally,advancements in mesenchymal stem cell-delivery methods—such as combinations of novel biomaterials,genetic engineering,and mesenchymal stem cell exosome therapy—have greatly enhanced the efficiency and therapeutic effects of mesenchymal stem cells in animal models.However,numerous challenges in the application of drug and mesenchymal stem cell treatment strategies remain to be addressed.In the future,new technologies,such as single-cell RNA sequencing and transcriptome analysis,can facilitate further experimental studies.Moreover,research involving non-human primates can help translate these treatment strategies to clinical practice.
文摘目的 分析创伤性颅脑损伤血清miR-31-5p、miR-129-5p水平及其与神经功能的关系。方法 回顾性选取2022年8月—2025年8月东南大学附属徐州市中心医院收治的创伤性颅脑损伤患者169例,根据格拉斯哥昏迷量表(Glasgow coma scale,GCS)评分将患者分为轻型组(n=64)、中型组(n=54)、重型组(n=51)。另选同期东南大学附属徐州市中心医院体检的健康者100例为对照组。比较所有受试者血清miR-31-5p、miR-129-5p水平、美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分。采用Pearson相关分析血清miR-31-5p、miR-129-5p水平与NIHSS评分的相关性,采用受试者工作特征(receiver operating characteristic,ROC)曲线分析血清miR-31-5p、miR-129-5p水平对创伤性颅脑损伤患者发生神经功能缺损的诊断价值。结果 重型组、中型组、轻型组血清miR-31-5p水平、NIHSS评分均高于对照组,血清miR-129-5p水平均低于对照组,重型组、中型组血清miR-31-5p水平、NIHSS评分均高于轻型组,血清miR-129-5p水平均低于轻型组,重型组血清miR-31-5p水平、NIHSS评分均高于中型组,血清miR-129-5p水平低于中型组(P<0.05)。血清miR-31-5p水平与NIHSS评分呈正相关(r=0.666,P<0.05),血清miR-129-5p水平与NIHSS评分呈负相关(r=-0.715,P<0.05)。ROC结果显示,血清miR-31-5p、miR-129-5p水平联合诊断创伤性颅脑损伤患者神经功能缺损的敏感度为99.3%,特异度为92.9%,AUC为0.951,预测价值较高。结论 血清miR-31-5p水平升高、miR-129-5p水平降低与创伤性颅脑损伤患者神经功能缺损程度密切相关,二者联合检测对评估神经功能缺损具有较高预测价值。
文摘目的系统梳理创伤性脑损伤(TBI)后神经元凋亡机制的研究进展,识别该领域研究热点与难点,为未来研究方向提供参考。方法基于Web of Science核心合集数据库,检索2001—2025年间主题为TBI神经元凋亡的相关文献,运用VOSviewer、CiteSpace及R软件,从文献数量、国家分布、期刊来源及关键词等维度进行文献计量分析。结果共纳入TBI神经元凋亡领域文献3666篇,年发文量呈持续增长趋势。中国(1488篇)和美国(1015篇)为发文量前两位的国家,合计占比达68%。主要研究机构包括宾夕法尼亚州立大学、匹兹堡大学及苏州大学等。相关研究主要发表于Journal of Neurotrauma、Brain Research等期刊。早期研究聚焦于氧化应激、钙超载及Bcl-2家族蛋白介导的线粒体凋亡途径,2010年后逐渐拓展至多机制交叉调控。关键词共现分析显示,凋亡、炎症与氧化应激为核心机制,并与阿尔茨海默病、脑缺血等神经退行性疾病存在关联。结论STBI后神经元凋亡机制研究正从基础通路探索逐步拓展至神经修复、跨疾病关联及靶向治疗等方向。然而,该领域基础研究成果在向临床转化过程中仍面临诸多挑战,转化策略有待进一步系统探索。
