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High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

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Neural Regeneration Research 2025年第9期20卷 2611-2623页

作者： Mengshi Yang Miao Bai Yuan Zhuang Shenghua Lu Qianqian Ge Hao Li Yu Deng Hongbin Wu Xiaojian Xu Fei Niu Xinlong Dong Bin Zhang Baiyun Liu Beijing Tiantan Hospital Capital Medical UniversityBeijingChina department of Neurology The First Hospital of Tsinghua UniversityBeijingChina department of Neurotrauma and Beijing Key Laboratory of Central Nervous System Injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina department of critical care Medicine Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Center for Nerve Injury and Repair Beijing Institute of Brain DisordersChina National Clinical Research Center for Neurological DiseasesBeijingChina

Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently *** potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet *** the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of *** vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial ***,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were ***-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of *** Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our ***-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain *** dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in *** receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain ***,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is th

关键词： apoptosis BV2 microglia dexamethasone glucocorticoid receptor glucocorticoids innate immune system microglial polarization neuroinflammation primary microglia traumatic brain injury

Spatial transcriptomics combined with single-nucleus RNA sequencing reveals glial cell heterogeneity in the human spinal cord

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Neural Regeneration Research 2025年第11期20卷 3302-3316页

作者： Yali Chen Yiyong Wei Jin Liu Tao Zhu Cheng Zhou Donghang Zhang department of Anesthesiology West China HospitalSichuan UniversityChengduSichuan ProvinceChina Laboratory of Anesthesia and critical care Medicine National-Local Joint Engineering Research Center of Translational Medicine of AnesthesiologyWest China HospitalSichuan UniversityChengduSichuan ProvinceChina department of Anesthesiology Longgang District Maternity&Child Healthcare Hospital of Shenzhen City(Longgang Maternity and Child Institute of Shantou University Medical College)ShenzhenGuangdong ProvinceChina department of Anesthesiology Affiliated Hospital of Zunyi Medical UniversityZunyiGuizhou ProvinceChina

Glial cells play crucial roles in regulating physiological and pathological functions,including sensation,the response to infection and acute injury,and chronic neurodegenerative *** cells include astrocytes,microglia,and oligodendrocytes in the central nervous system,and satellite glial cells and Schwann cells in the peripheral nervous *** the greater understanding of glial cell types and functional heterogeneity achieved through single-cell and single-nucleus RNA sequencing in animal models,few studies have investigated the transcriptomic profiles of glial cells in the human spinal ***,we used high-throughput single-nucleus RNA sequencing and spatial transcriptomics to map the cellular and molecular heterogeneity of astrocytes,microglia,and oligodendrocytes in the human spinal *** explore the conservation and divergence across species,we compared these findings with those from *** the human spinal cord,astrocytes,microglia,and oligodendrocytes were each divided into six distinct transcriptomic *** the mouse spinal cord,astrocytes,microglia,and oligodendrocytes were divided into five,four,and five distinct transcriptomic subclusters,*** comparative results revealed substantial heterogeneity in all glial cell types between humans and ***,we detected sex differences in gene expression in human spinal cord glial ***,in all astrocyte subtypes,the levels of NEAT1 and CHI3L1 were higher in males than in females,whereas the levels of CST3 were lower in males than in *** all microglial subtypes,all differentially expressed genes were located on the sex *** addition to sex-specific gene differences,the levels of MT-ND4,MT2A,MT-ATP6,MT-CO3,MT-ND2,MT-ND3,and MT-CO_(2) in all spinal cord oligodendrocyte subtypes were higher in females than in ***,the present dataset extensively characterizes glial cell heterogeneity and offers a valuable resource for explo

关键词： astrocyte glial cell human microglia oligodendrocyte sex differentiation single-nucleus RNA sequencing spatial transcriptomics species variation spinal cord

EZH2-dependent myelination following sciatic nerve injury

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Neural Regeneration Research 2025年第8期20卷 2382-2394页

作者： Hui Zhu Li Mu Xi Xu Tianyi Huang Ying Wang Siyuan Xu Yiting Wang Wencong Wang Zhiping Wang Hongkui Wang Chengbin Xue Research Center of Clinical Medicine Affiliated Hospital of Nantong UniversityKey Laboratory of Neuroregeneration of Jiangsu and Ministry of EducationCo-innovation Center of NeuroregenerationNMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology ProductsNantong UniversityNantongJiangsu ProvinceChina medical School of Nantong University NantongJiangsu ProvinceChina department of Neurology Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina department of Rehabilitation Medicine Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina department of critical care Medicine Nantong Fourth People’s HospitalNantongJiangsu ProvinceChina

Demyelination and remyelination have been major focal points in the study of peripheral nerve regeneration following peripheral nerve ***,the gene regulatory network of regenerated myelin differs from that of native *** of enhancer of zeste homolog 2(EZH2)hinders the differentiation,maturation,and myelination of Schwann cells in *** further determine the role of EZH2 in myelination and recovery post-peripheral nerve injury,conditional knockout mice lacking Ezh2 in Schwann cells(Ezh2^(fl/fl);Dhh-Cre and Ezh2^(fl/fl);Mpz-Cre)were *** results show that a significant proportion of axons in the sciatic nerve of Ezh2-depleted mice remain *** highlights the crucial role of Ezh2 in initiating Schwann cell ***,we observed that 21 days after inducing a sciatic nerve crush injury in these mice,most axons had remyelinated at the injury site in the control nerve,while Ezh2^(fl/fl);Mpz-Cre mice had significantly fewer remyelinated axons compared with their wild-type *** suggests that the absence of Ezh2 in Schwann cells impairs myelin formation and *** conclusion,EZH2 has emerged as a pivotal regulatory factor in the process of demyelination and myelin regeneration following peripheral nerve *** EZH2 activity during these processes may offer a promising therapeutic target for the treatment of peripheral nerve injuries.

关键词： demyelination EZH2 myelination peripheral nerve injury PRC2 remyelination Schwann cells sciatic nerve crush sciatic nerve transection

Procalcitionin as a diagnostic marker to distinguish upper and lower gastrointestinal perforation

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World Journal of Gastroenterology 2017年第24期23卷 4422-4427页

作者： Yang Gao Kai-Jiang Yu Kai Kang Hai-Tao Liu Xing Zhang Rui Huang Jing-Dong Qu Si-Cong Wang Rui-Jin Liu Yan-Song Liu Hong-Liang Wang department of critical care Medicine the Second Affiliated Hospital of Harbin Medical University department of critical care Medicine the Cancer Hospital of Harbin Medical University Institute of critical care Medicine in Sino Russian medical Research Center of Harbin medical University department of critical care Medicine the First Affiliated Hospital of Harbin Medical University

AIM To assess the accuracy of serum procalcitionin(PCT)as a diagnostic marker in verifying upper and lower gastrointestinal perforation(GIP).METHODS This retrospective study included 46 patients from the surgical intensive care unit(ICU)of the Second Affiliated Hospital of Harbin medical University who were confirmed to have GIP between June 2013 and December *** and clinical patient data were recorded on admission to *** were divided into upper(n=19)and lower(n=27)GIP groups according to the perforation site(above or below Treitz ligament).PCT and WBC count was obtained before laparotomy and then compared between ***,the diagnostic accuracy of PCT was *** Patients with lower GIP exhibited significantly higher APACHE II score,SOFA score and serum PCT level than patients with upper GIP(P=0.017,0.004,and0.001,respectively).There was a significant positive correlation between serum PCT level and APACHE II score or SOFA score(r=0.715 and r=0.611,respectively),while there was a significant negative correlation between serum PCT level and prognosis(r=-0.414).WBC count was not significantly different between the two groups,and WBC count showed no significant correlation with serum PCT level,APACHE II score,SOFA score or *** area under the receiver operating characteristic curve of PCT level to distinguish upper or lower GIP was *** with a serum PCT level above 17.94 ng/d L had a high likelihood of lower GIP,with a sensitivity of 100%and a specificity of 42.1%.CONCLUSION Serum PCT level is a reliable and accurate diagnostic marker in identifying upper or lower GIP before laparotomy.

关键词： Procalcitionin White blood cell count Gastrointestinal perforation Sepsis APACHE II score SOFA score

Interleukin-17 inhibits development of malignant pleural effusion via interleukin-9-dependent mechanism

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Science China(Life Sciences) 2016年第12期59卷 1297-1304页

作者： Yong Lu Hua Lin Kan Zhai Xiaojuan Wang Qiong Zhou Huanzhong Shi department of Respiratory and critical care Medicine Beijing Chaoyang Hospital Capital Medical University department of Respiratory and critical care Medicine Union Hospital Tongji Medical College Huazhong University of Science and Technology

Th17 and Th9 cells have been demonstrated to possess immune regulatory functions in malignant pleural effusion （MPE）. However, whether IL-17 can affect differentiation and function of Th9 cells in MPE remains unknown. The objective of the present study was to explore the impact of IL-17 on the in vivo differentiation of Th9 cells in relation to Th2 cells in a murine model of MPE, and to explore whether IL-17 inhibits MPE formation via IL-9-dependent mechanism. It was found that Th9 and Th2 cells were decreased in MPE from 1L-17-/- mice as compared with wild type mice. IL-17 deficiency inhibited Th9 and Th2 cell differentiation via suppressing transcription faclLors IRF4 and GATA-3, respectively. IL-17 deficiency enhanced MPE formation by promoting angiogenesis and proliferation of pleurai tumors, and thus accelerated the death of mice bearing MPE. The in vivo administration of anti-IL-9 neutralizing mAb accelerated the death of WT mice; whereas administration of exoge- nous IL-9 improved the survival of IL-17-/- mice. Our data provide the first definitive evidence that IL-17 promotes the differ- entiation of Th9 and Th2 cells in MPE. Our findings also demonstrate that IL-17 inhibits the formation of MPE and improves the survival of mice bearing MPE via an IL-9-dependent mechanism.

关键词： malignant pleural effusion interleukin 17 Th9 cells

Inflammasome links traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease

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Neural Regeneration Research 2025年第6期20卷 1644-1664页

作者： Gabriela Seplovich Yazan Bouchi Juan Pablo de Rivero Vaccari Jennifer C.Munoz Pareja Andrew Reisner Laura Blackwell Yehia Mechref Kevin K.Wang J.Adrian Tyndall Binu Tharakan Firas Kobeissy department of Surgery Morehouse School of MedicineAtlantaGAUSA department of Neurobiology Center for NeurotraumaMultiomics&Biomarkers(CNMB)Neuroscience InstituteMorehouse School of MedicineAtlantaGAUSA department of Neurological Surgery and the Miami Project to Cure Paralysis University of Miami Miller School of MedicineMiamiFLUSA Division of Pediatric critical care Department of PediatricsUniversity of Miami Miller School of MedicineMiamiFLUSA department of Pediatrics Emory UniversityAtlantaGAUSA department of Neurosurgery Children’s Healthcare of AtlantaAtlantaGAUSA department of Chemistry and Biochemistry Texas Tech UniversityLubbockTXUSA Morehouse School of Medicine AtlantaGAUSA

Traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease are three distinct neurological disorders that share common pathophysiological mechanisms involving neuroinflammation. One sequela of neuroinflammation includes the pathologic hyperphosphorylation of tau protein, an endogenous microtubule-associated protein that protects the integrity of neuronal cytoskeletons. Tau hyperphosphorylation results in protein misfolding and subsequent accumulation of tau tangles forming neurotoxic aggregates. These misfolded proteins are characteristic of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease and can lead to downstream neuroinflammatory processes, including assembly and activation of the inflammasome complex. Inflammasomes refer to a family of multimeric protein units that, upon activation, release a cascade of signaling molecules resulting in caspase-induced cell death and inflammation mediated by the release of interleukin-1β cytokine. One specific inflammasome, the NOD-like receptor protein 3, has been proposed to be a key regulator of tau phosphorylation where it has been shown that prolonged NOD-like receptor protein 3 activation acts as a causal factor in pathological tau accumulation and spreading. This review begins by describing the epidemiology and pathophysiology of traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease. Next, we highlight neuroinflammation as an overriding theme and discuss the role of the NOD-like receptor protein 3 inflammasome in the formation of tau deposits and how such tauopathic entities spread throughout the brain. We then propose a novel framework linking traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer's disease as inflammasomedependent pathologies that exist along a temporal continuum. Finally, we discuss potential therapeutic targets that may intercept this pathway and ultimately minimize long-term neurological decline.

关键词： Alzheimer's disease caspase-1 chronic traumatic encephalopathy inflammasomes neurodegeneration neuroinflammation NLRP1 NLRP3 pyroptosis tauopathy traumatic brain injury

HSA-MIR-203/MyD88 axis mediates the protective effect of hispidulin on LPS-induced apoptosis in a human renal tubular epithelial line,HK-2

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BIOCELL 2022年第1期46卷 149-158页

作者： SICONG WANG RUIJIN LIU QIUYUAN HAN KAIJIANG YU department of critical care Medicine The Second Affiliated Hospital of Harbin Medical UniversityHarbin150001China department of critical care Medicine The Cancer Hospital of Harbin Medical UniversityHarbin150081China department of critical care Medicine The First Affiliated Hospital of Harbin Medical UniversityHarbin150001China

Acute kidney injury(AKI),commonly occurring as complications of sepsis,cardiac surgery,and liver or kidney transplantation,is a critical care *** is well known that lipopolysaccharide(LPS)shock is a common triggering factor for *** study is aimed to examine the effect of flavonoid compound hispidulin on LPS-induced *** this,renal tubular epithelial cell HK-2 was treated with LPS to establish an in vitro model of *** effect of hispidulin on HK-2 cell viability was examined using CCK-8 *** apoptosis was determined by TUNEL and flow *** marker proteins were determined by using western *** levels of pro-inflammatory cytokines were determined by ELISA assay and *** translocation of NF-κB was determined by western *** effect of MyD88 on the cytoprotective activities of hispidulin was examined by overexpressing MyD88 in HK-2 *** results showed that hispidulin was not able to produce a cytotoxic effect on HK-2 cells at tested ***,hispidulin could protect HK-2 cells from LPS-induced cell *** results also showed that hispidulin was able to attenuate LPS-induced HK-2 cell *** addition,LPS led to an inflammatory response in HK-2 cells,evidenced by NF-κB p65 activation as well as increased expression and release of inflammatory cytokine IL-6 and TNF-α,which could be reversed by pretreatment with *** MyD88 was found to significantly dampen the cytoprotective activities of hispidulin against LPS *** importantly,MyD88 was identified as a direct target of hsa-miR-203,and hispidulin was found to regulate the expression of MyD88 via upregulating *** results showed that hispidulin attenuates LPS-induced HK-2 damage via regulating hsa-miR-203/MyD88 axis.

关键词： Hispidulin LPS HK-2 hsa-miR-203 MyD88

Hepatic organ protection:From basic science to clinical practice

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World Journal of Gastroenterology 2010年第48期16卷 6044-6045页

作者： Rene Schmidt department of Anesthesiology and critical care Medicine Freiburg University Medical Center

Hepatic ischemia and reperfusion (I/R) injury during liver surgery is still the main cause of postoperative liver failure and the subsequent rise of mortality in these patients. During the last few years, a multitude of underlying mechanisms have been extensively characterized and many different protective approaches have been evaluated under experimental conditions. Some of them have already found their way into small sized clinical trials. In this Topic Highlight series of articles, we present recent insights into promising protective concepts including the regulation and optimization of hepatic blood flow, molecular mechanisms of preconditioning and pharmacological approaches with the aim of limiting hepatic I/R injury. Leading international experts present the latest experimental evidence in their fields stressing clinically relevant ideas, which are now on the edge of entering clinical practice.

关键词： Heme oxygenase-1 Hepatectomy Hepatic organ protection Ischemia/reperfusion injury Liver blood flow Liver transplantation Preconditioning

Eosinophils in asthma

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Chinese medical Journal 2004年第5期117卷 792-794页

作者：施焕中 department of Pulmonary and critical care Medicine

The contribution of eosinophils to host-defense and inflammatory responses has undergone periodic reevalu-ations. Thirty years ago, eosinophil was considered as a principal effector cell in host-defense against parasites. Furthermore, the actions of eosinophil enzymes, like histaminase, were thought to suppress mast cell-released allergic mediators. Asthma is a chronic inflammatory condition of the airways that is characterized by a prominent eosinophilic inflammatory infiltration into the bronchial mucosa. Activated eosinophils secrete granular basic proteins that damage the bronchial epithelium and membrane-derived lipid mediators, which contract smooth muscle, increase mucous secretion, and cause vasodilation. The correlation between eosinophil numbers and disease severity supports the hypothesis that the eosinophil is the central effector cell in ongoing airway inflammation in asthma. However, it would be unwise to totally overestimate eosinophil\' s potential in the development of asthma unless we have effective and selective methods of depleting the cells from the tissues.

关键词： IL SCH Eosinophils in asthma