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小胶质细胞活化介导的神经元损伤与抑郁症的研究进展

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中国药理学通报 2024年第1期40卷 12-15页

作者：何璎邹蔓姝韩远山王宇红湖南中医药大学科技创新中心湖南长沙410208 湖南中医药大学第一附属医院湖南长沙410000 抑郁类疾病中医药防治湖南省重点实验室湖南长沙410208

抑郁症是一种常见的神经障碍,其发病率高,复发性高,致残性高,但发病机制未明。近年来,胶质细胞对神经元的保护与攻击作用已成为神经疾病研究的前沿方向。小胶质细胞(microglia, MG)异常活化导致神经元损伤在抑郁症发病中具有重要作用,... 详细信息

抑郁症是一种常见的神经障碍,其发病率高,复发性高,致残性高,但发病机制未明。近年来,胶质细胞对神经元的保护与攻击作用已成为神经疾病研究的前沿方向。小胶质细胞(microglia, MG)异常活化导致神经元损伤在抑郁症发病中具有重要作用,该文通过GeenMedical、CNKI等进行文献检索,对MG活化相关通路及关键靶标在抑郁症中的研究进行归纳总结,为进一步的临床研究提供理论性的依据。

关键词：小胶质细胞神经元损伤抑郁症炎症作用机制免疫反应

Compound Chai Jin Jie Yu Tablets,Acts as An Antidepressant by Promoting Synaptic Function in the Hippocampal Neurons

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Digital Chinese Medicine 2020年第2期3卷 80-95页

作者： LI Zi-Rong han yuan-shan WU Meng-Yao LIU Jian JIN Shi ZhanG Xi WANG Yu-Hong State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan Hunan University of Chinese MedicineChangshaHunan 410208China The First Hospital of Hunan University of Chinese Medicine ChangshaHunan 410007China Qianjin Pharmaceutical Co. Ltd.ZhuzhouHunan 412000China Hunan Provincial Brain Hospital ChangshaHunan 410007China

Objective To investigate the effectiveness of compound Chai Jin Jie Yu Tablets(CJJYT)in ameliorating cognitive impairment associated with depression and its potential mechanism of *** In vitro experiments,the hippocampus was isolated from the whole brain of the fetal rat and cultured into hippocampal neuron cells.50μM corticosterone(CORT)was added to each group 18 h before the experiment for modeling depression,with the exception of the control *** modeling,the blank serum group was added with 10%blank serum,the CJJYT group and the venlafaxine group were added with the corresponding 10%drug-containing serum,and the control group and the model group were added with equal volumes of culture *** intracellular Ca^2+mean fluorescence intensity,miniature excitatory postsynaptic current(mEPSC)current amplitude,and frequency of different hippocampal neurons were evaluated as indicators of synaptic function in the hippocampal *** addition,the expression of synaptic plasticity related proteins,synaptophysin-α(SYN-α),N-methyl-D-aspartate receptor 2A(NR2A),N-methyl-Daspartate receptor 2B(NR2B),post synaptic density 95 protein(PSD-95),calcium/calmodulin dependent protein kinaseⅡ(CaMKⅡ)and synaptic associated protein(SynGAP)were detected in the hippocampal neurons by immunofluorescence staining and high content analysis(HCA)***,reverse transcription-polymerase chain reaction(RT-PCR)was used to detect the mRNA expression levels of SYN-α,NR2A,NR2B,PSD-95,CaMKⅡand *** in vivo experiments,except for those in the blank control group,all rats were treated within a single cage for chronic unpredictable stress-induced depression modeling and subjected to corresponding drug *** tests were used to detect depressive behavior and determine learning,memory and other cognitive abilities,whereas enzyme-linked immunosorbent assay(ELISA)was used to detect the CORT ***-Cox staining was used to observe changes in the syna

关键词： Compound Chai Jin Jie Yu Tablets(CJJYT) Depression SYN-α/NR Synaptic plasticity Cognition

Peripheral mitochondrial DNA as a neuroinflammatory biomarker for major depressive disorder

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Neural Regeneration Research 2025年第6期20卷 1541-1554页

作者： Jinmei Ye Cong Duan Jiaxin han Jinrong Chen Ning Sun yuan Li Tifei yuan Daihui Peng Division of Mood Disorder Shanghai Mental Health CenterShanghai Jiao Tong University School of MedicineShanghaiChina Department of Psychiatry First Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina shanghai Key Laboratory of Psychotic Disorders Brain Health InstituteNational Center for Mental DisordersShanghai Mental Health CenterShanghai Jiao Tong University School of MedicineShanghaiChina Co-Innovation Center of Neuroregeneration Nantong UniversityNantongJiangsu ProvinceChina

In the pathogenesis of major depressive disorder, chronic stress-related neuroinflammation hinders favorable prognosis and antidepressant response. Mitochondrial DNA may be an inflammatory trigger, after its release from stress-induced dysfunctional central nervous system mitochondria into peripheral circulation. This evidence supports the potential use of peripheral mitochondrial DNA as a neuroinflammatory biomarker for the diagnosis and treatment of major depressive disorder. Herein, we critically review the neuroinflammation theory in major depressive disorder, providing compelling evidence that mitochondrial DNA release acts as a critical biological substrate, and that it constitutes the neuroinflammatory disease pathway. After its release, mitochondrial DNA can be carried in the exosomes and transported to extracellular spaces in the central nervous system and peripheral circulation. Detectable exosomes render encaged mitochondrial DNA relatively stable. This mitochondrial DNA in peripheral circulation can thus be directly detected in clinical practice. These characteristics illustrate the potential for mitochondrial DNA to serve as an innovative clinical biomarker and molecular treatment target for major depressive disorder. This review also highlights the future potential value of clinical applications combining mitochondrial DNA with a panel of other biomarkers, to improve diagnostic precision in major depressive disorder.

关键词： biomarker cytokine exosomes inflammasome major depressive disorder microglia mitochondrial DNA mitochondrial dysfunction neuroinflammation Toll-like receptor

Computed tomography enterography-based radiomics for assessing mucosal healing in patients with small bowel Crohn's disease

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World Journal of Gastroenterology 2025年第3期31卷 62-72页

作者： Hao Ding yuan-yuan Fang Wen-Jie Fan Chen-Yu Zhang Shao-Fei Wang Jing Hu Wei han Qiao Mei Department of Gastroenterology The First Affiliated Hospital of Anhui Medical UniversityHefei 230022Anhui ProvinceChina Department of Radiation Oncology The First Affiliated Hospital of Anhui Medical UniversityHefei 230022Anhui ProvinceChina Department of Gastroenterology Suzhou First People's HospitalSuzhou 234099Anhui ProvinceChina

BACKGROUND Mucosal healing(MH)is the major therapeutic target for Crohn's disease(CD).As the most commonly involved intestinal segment,small bowel(SB)assessment is crucial for CD ***,it poses a significant challenge due to its limited accessibility through conventional endoscopic *** To establish a noninvasive radiomic model based on computed tomography enterography(CTE)for MH assessment in SBCD *** Seventy-three patients diagnosed with SBCD were included and divided into a training cohort(n=55)and a test cohort(n=18).Radiomic features were obtained from CTE images to establish a radiomic *** demographics were analysed to establish a clinical model.A radiomic-clinical nomogram was constructed by combining significant clinical and radiomic *** diagnostic efficacy and clinical benefit were evaluated via receiver operating characteristic(ROC)curve analysis and decision curve analysis(DCA),*** Of the 73 patients enrolled,25 patients achieved *** radiomic-clinical nomogram had an area under the ROC curve of 0.961(95%confidence interval:0.886-1.000)in the training cohort and 0.958(0.877-1.000)in the test cohort and provided superior clinical benefit to either the clinical or radiomic models alone,as demonstrated by *** These results indicate that the CTE-based radiomic-clinical nomogram is a promising imaging biomarker for MH and serves as a potential noninvasive alternative to enteroscopy for MH assessment in SBCD patients.

关键词： Crohn’s disease Computed tomography enterography Mucosal healing Nomogram Radiomics

FK506 contributes to peripheral nerve regeneration by inhibiting neuroinflammatory responses and promoting neuron survival

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Neural Regeneration Research 2025年第7期20卷 2108-2115页

作者： Yuhui Kou Zongxue Jin Yusong yuan Bo Ma Wenyong Xie Na han Department of Trauma and Orthopedics Peking University People’s HospitalBeijingChina National Center for Trauma Medicine Peking University People’s HospitalBeijingChina Key Laboratory of Trauma and Neural Regeneration(Peking University) Ministry of EducationBeijingChina Trauma Medicine Center Peking University People’s HospitalBeijingChina Department of Orthopedics China-Japan Friendship HospitalBeijingChina

FK506(Tacrolimus)is a systemic immunosuppressant approved by the *** and Drug ***506 has been shown to promote peripheral nerve regeneration,however,its precise mechanism of action and its pathways remain *** this study,we established a rat model of sciatic nerve injury and found that FK506 improved the morphology of the injured sciatic nerve,increased the numbers of motor and sensory neurons,reduced inflammatory responses,markedly improved the conduction function of the injured nerve,and promoted motor function *** findings suggest that FK506 promotes peripheral nerve structure recovery and functional regeneration by reducing the intensity of inflammation after neuronal injury and increasing the number of surviving neurons.

关键词： FK506 inflammation motor neurons nerve regeneration neuron peripheral nerve injury sensory neurons

盐诱导激酶在中枢神经系统疾病中的作用机制研究进展

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中国新药杂志 2023年第21期32卷 2164-2172页

作者：任廷婷邹蔓姝韩远山王华王宇红湖南中医药大学科技创新中心长沙410208 抑郁类疾病中医药防治湖南省重点实验室长沙410007 湖南中医药大学第一附属医院长沙410208

盐诱导激酶(salt-inducible kinases,SIKs)属于腺苷酸活化激酶(AMP-activated protein kinase,AMPK)家族,主要调控环磷酸苷效应元件结合蛋白(cAMP-response element binding protein,CREB)转录共激活因子(CREB-regulated transcription coactivators,CRTCs)的胞核-胞质分布,对CRTC-CREB复合物的合成起到调节作用,从而间接影响CREB目的基因的转录与表达,影响多种生理过程,例如能量代谢、细胞周期进程和细胞凋亡。过去对SIKs的相关研究主要集中在外周系统疾病,包括肿瘤、高血压和糖异生等。近年来越来越多的研究开始探索SIKs和中枢神经系统疾病的关联性,如抑郁症、睡眠障碍、癫痫和阿尔茨海默病等都存在SIKs水平异常的情况,这提示SIKs信号失调参与这些疾病的病理过程,SIKs具有成为此类疾病新治疗靶点的潜力。本文就SIKs在抑郁症、睡眠障碍及其他神经系统疾病中的作用和调控机制进行综述。

关键词：盐诱导激酶 CREB转录共激活因子抑郁症睡眠障碍中枢神经系统疾病

逍遥抗癌解郁方通过调控COX通路对乳腺癌并发抑郁模型小鼠的治疗作用及机制研究

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中国中药杂志 2023年第14期48卷 3874-3881页

作者：何璎邹蔓姝任廷婷李萍刘洋韩远山湖南中医药大学第一附属医院湖南长沙410007 湖南中医药大学科技创新中心湖南长沙410208 抑郁类疾病中医药防治湖南省重点实验室湖南长沙410208

研究逍遥抗癌解郁方对乳腺癌并发抑郁模型小鼠海马小胶质细胞和神经元损伤的干预作用及其机制。采用腋下接种4T1乳腺癌细胞联合皮下注射皮质酮(30 mg·kg^(-1))的方法构建乳腺癌并发抑郁小鼠模型,将造模成功的小鼠随机分为模型组,阳性药... 详细信息

研究逍遥抗癌解郁方对乳腺癌并发抑郁模型小鼠海马小胶质细胞和神经元损伤的干预作用及其机制。采用腋下接种4T1乳腺癌细胞联合皮下注射皮质酮(30 mg·kg^(-1))的方法构建乳腺癌并发抑郁小鼠模型,将造模成功的小鼠随机分为模型组,阳性药组[卡培他滨(60 mg·kg^(-1))+氟西汀(19.5 mg·kg^(-1))],逍遥抗癌解郁方组(19.5 g·kg^(-1)),每组6只,另取6只正常小鼠作为正常组。各给药组灌胃相应药物,正常组和模型组给予等体积蒸馏水,每日1次,连续给药21 d。采用糖水消耗实验、旷场实验和新奇摄食实验评价小鼠抑郁行为;苏木素-伊红(hematoxylin eosin,HE)染色和抑瘤率评价腋下肿瘤变化情况;实时荧光定量PCR(quantitative real-time PCR,qRT-PCR)法检测小鼠海马白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-18(interleukin-18,IL-18)、环氧酶-2(cyclooxyganese-2,COX-2)、前列腺素受体(glutamyl-prolyl-tRNA synthetase,EPRs)mRNA表达;免疫组化检测海马IL-1β、IL-18、COX-2、EPRs蛋白的相对表达量,免疫荧光检测海马小胶质细胞活化标志分子CD11b的平均荧光强度;尼氏染色观察海马神经元形态变化;透射电镜观察海马神经元的超微形态变化。结果显示,与正常组比较,模型组小鼠糖水消耗、矿场总活动数均显著降低(P<0.05,P<0.01),新奇摄食实验首次摄食时间显著上升(P<0.01),抑郁样行为显著;海马中IL-1β、IL-18、COX-2、EPRs表达显著升高(P<0.05,P<0.01),海马小胶质细胞活化,神经元明显损伤。与模型组相比,阳性药和逍遥抗癌解郁方给药后小鼠抑郁行为均明显改善;海马IL-1β、IL-18、COX-2、EPRs含量均明显降低,海马小胶质细胞激活和神经元损伤情况得以缓解;阳性药抑瘤率为40.32%,逍遥抗癌解郁方抑瘤率为48.83%,肿瘤生长速度都慢于模型组。综上所述,逍遥抗癌解郁方可能通过COX信号通路的激活改善乳腺癌并发抑郁症模型小鼠海马小胶质细胞激活和神经元损伤。

关键词：逍遥抗癌解郁方乳腺癌并发抑郁症 COX信号通路小胶质细胞海马神经元

左归降糖解郁方对糖尿病并发抑郁症大鼠血糖血脂的影响

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中草药 2014年第11期45卷 1602-1606页

作者：王宇红杨蕙尹玲桃柴上韩远山张秀丽谭元生湖南省中药粉体与创新药物省部共建国家重点实验室培育基地湖南长沙410007 湖南中医药大学第一附属医院湖南长沙410007 湖南省中医药研究院杨永华名老中医药专家传承工作室湖南长沙410007

目的研究左归降糖解郁方对糖尿病并发抑郁症大鼠血糖、血脂的影响。方法采用ig高脂乳剂、iv链脲佐菌素(STZ,38 mg/kg)和慢性应激联合的方法制备糖尿病并发抑郁症大鼠模型,并随机分为5组:模型组,阳性药(二甲双胍0.18 g/kg+百忧解1.8 mg/... 详细信息

目的研究左归降糖解郁方对糖尿病并发抑郁症大鼠血糖、血脂的影响。方法采用ig高脂乳剂、iv链脲佐菌素(STZ,38 mg/kg)和慢性应激联合的方法制备糖尿病并发抑郁症大鼠模型,并随机分为5组:模型组,阳性药(二甲双胍0.18 g/kg+百忧解1.8 mg/kg)组,左归降糖解郁方高、中、低剂量(20.53、10.26、5.13 g/kg)组,同时以正常大鼠为对照组。各组造模同时ig给药,共4周;生化法检测各组大鼠血糖、糖化血红蛋白水平、胰岛素抵抗及血脂水平,ELISA法测定大鼠血浆皮质酮水平,HE染色观察大鼠肾上腺的病理改变。结果与对照组比较,模型组大鼠血糖、糖化血红蛋白、低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)、三酰甘油(TG)和血浆皮质酮水平显著升高,高密度脂蛋白胆固醇(HDL-C)水平显著降低(P<0.05),具有明显的胰岛素抵抗。给予左归降糖解郁方干预后,大鼠血糖、糖化血红蛋白、TC、TG、LDL-C水平显著降低,HDL-C水平显著升高,胰岛素抵抗程度减轻,血浆皮质酮水平明显降低(P<0.05、0.01),肾上腺损伤程度减轻。结论左归降糖解郁方可改善糖尿病并发抑郁症大鼠的血糖、血脂异常,该作用可能与其保护肾上腺,降低循环系统皮质酮水平有关。

关键词：左归降糖解郁方糖尿病并发抑郁症血糖血脂皮质酮胰岛素抵抗

左归降糖解郁方对自噬介导的糖尿病并发抑郁症大鼠海马神经血管单元中神经元损伤的保护作用及其机制

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中草药 2019年第10期50卷 2420-2427页

作者：刘检刘林唐林韩远山杨蕙凌佳龙红萍蔺晓源王宇红湖南中医药大学第一附属医院湖南长沙410007 湖南中医药大学湖南省中药粉体与创新药物省部共建国家重点实验室培育基地湖南长沙410208 湖南中医药大学科技创新中心湖南长沙410208

目的探讨左归降糖解郁方(ZGF)对自噬介导的糖尿病并发抑郁症(diabetes mellitus with depression,DD)大鼠海马神经血管单元(neurovascularunit,NVU)中神经元的保护作用及其机制。方法原代分离、纯化和培养SD大鼠海马神经元、星形胶质细... 详细信息

目的探讨左归降糖解郁方(ZGF)对自噬介导的糖尿病并发抑郁症(diabetes mellitus with depression,DD)大鼠海马神经血管单元(neurovascularunit,NVU)中神经元的保护作用及其机制。方法原代分离、纯化和培养SD大鼠海马神经元、星形胶质细胞及脑微血管内皮细胞,构建海马NVU体外共培养体系,并进行免疫细胞化学染色鉴定。采用高糖(150mmol/L)联合皮质酮(200μmol/L)干预制备海马NVU细胞模型,实验设对照组、模型组、空白血清对照组和ZGF含药血清组。采用Furo-3/AM染色法检测海马NVU神经元细胞内钙水平,高内涵细胞成像分析技术(high content analysis,HCA)检测海马NVU神经元细胞内自噬标志物自噬相关蛋白1(Beclin-1)、人微管相关蛋白轻链3II(LC3-II)及谷氨酸受体2(Glu R2)/Ca2+/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路关键蛋白的表达,TUNEL染色法观察各组海马神经元细胞凋亡。结果与对照组比较,模型组及空白血清对照组海马NVU神经元细胞内钙水平显著升高,自噬标志物Beclin-1、LC3-II蛋白表达水平显著升高,Glu R2、m TOR蛋白表达水平显著降低,AMP依赖的蛋白激酶(AMPK)蛋白表达水平显著升高,且细胞凋亡明显增多;与模型组比较,ZGF含药血清组海马NVU神经元细胞内钙水平明显降低,自噬标志物Beclin-1、LC3-II蛋白表达水平降低,GluR2/Ca2+/mTOR信号通路中Glu R2、m TOR蛋白表达水平升高,AMPK蛋白表达水平降低,同时细胞凋亡显著减少。结论 ZGF对自噬介导的DD大鼠海马NVU神经元细胞损伤具有明显的保护作用,其作用机制与调控GluR2/Ca2+/mTOR信号通路及细胞凋亡有关。

关键词：左归降糖解郁方糖尿病并发抑郁症神经血管单元海马神经元自噬凋亡 GluR2/Ca^2+/mTOR信号通路