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FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

Neural Regeneration Research 2025年第7期20卷 2068-2083页

作者： Jing Yao Yuan Li Xi Liu Wenping Liang Yu Li Liyong Wu Zhe Wang Weihong song The National Clinical Research Center for Geriatric Disease Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Department of Neurosurgery Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Pediatrics The Second Affiliated Hospital and Yuying Children’s HospitalKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceInstitute of AgingWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Oujiang Laboratory(Zhejiang Laboratory for Regenerative Medicine Visionand Brain Health)WenzhouZhejiang ProvinceChina

Alzheimer's disease is characterized by deposition of amyloid-β,which forms extracellular neuritic plaques,and accumulation of hyperphosphorylated tau,which aggregates to form intraneuronal neurofibrillary tangles,in the *** NLRP3 inflammasome may play a role in the transition from amyloid-βdeposition to tau phosphorylation and *** NLRP3 is primarily found in brain microglia,and tau is predominantly located in neurons,it has been suggested that NLRP3 expressed by microglia indirectly triggers tau phosphorylation by upregulating the expression of pro-inflammatory ***,we found that neurons also express NLRP3 in vitro and in vivo,and that neuronal NLRP3 regulates tau *** biochemical methods,we mapped the minimal NLRP3 promoter and identified FUBP3 as a transcription factor regulating NLRP3 expression in *** primary neurons and the neuroblastoma cell line Neuro2A,FUBP3 is required for endogenous NLRP3 expression and tau phosphorylation only when amyloid-βis *** the brains of aged wild-type mice and a mouse model of Alzheimer's disease,FUBP3 expression was markedly increased in cortical *** analysis suggested that FUBP3 plays a role in neuron-mediated immune *** also found that FUBP3 trimmed the 5′end of DNA fragments that it bound,implying that FUBP3 functions in stress-induced *** findings suggest that neuronal NLRP3 may be more directly involved in the amyloid-β-to–phospho-tau transition than microglial NLRP3,and that amyloid-βfundamentally alters the regulatory mechanism of NLRP3 expression in *** that FUBP3 was only expressed at low levels in young wild-type mice and was strongly upregulated in the brains of aged mice and Alzheimer's disease mice,FUBP3 could be a safe therapeutic target for preventing Alzheimer's disease progression.

关键词： 5′end trimming Alzheimer's disease amyloid-beta amyloid-β-dependent transcription FUBP3 inflammasome inflammation neuron NLRP3 tau transcription factor

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Pharmacological targeting cGAs/sTING/NF-κB axis by tryptanthrin induces microglia polarization toward M2 phenotype and promotes functional recovery in a mouse model of spinal cord injury

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Neural Regeneration Research 2025年第11期20卷 3287-3301页

作者： Ziwei Fan Mengxian Jia Jian Zhou Zhoule Zhu Yumin Wu Xiaowu Lin Yiming Qian Jiashu Lian Xin Hua Jianhong Dong Zheyu Fang Yuqing Liu sibing Chen Xiumin Xue Juanqing Yue Minyu Zhu Ying Wang Zhihui Huang Honglin Teng Department of Orthopedics(spine surgery) the First Affiliated Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina school of Pharmacy Hangzhou Normal UniversityHangzhouZhejiang ProvinceChina Department of Neurology The First Affiliated Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Pathology Affiliated Hangzhou First People’s HospitalSchool of MedicineWestlake UniversityHangzhouZhejiang ProvinceChina Department of Clinical Research Center Affiliated Hangzhou First People’s HospitalSchool of MedicineWestlake UniversityHangzhouZhejiang ProvinceChina

The M1/M2 phenotypic shift of microglia after spinal cord injury plays an important role in the regulation of neuroinflammation during the secondary injury phase of spinal cord *** of shifting microglia polarization from M1(neurotoxic and proinflammatory type)to M2(neuroprotective and anti-inflammatory type)after spinal cord injury appears to be *** possesses an anti-inflammatory biological ***,its roles and the underlying molecular mechanisms in spinal cord injury remain *** this study,we found that tryptanthrin inhibited microglia-derived inflammation by promoting polarization to the M2 phenotype in *** promoted M2 polarization through inactivating the cGAs/sTING/NF-κB ***,we found that targeting the cGAs/sTING/NF-κB pathway with tryptanthrin shifted microglia from the M1 to M2 phenotype after spinal cord injury,inhibited neuronal loss,and promoted tissue repair and functional recovery in a mouse model of spinal cord ***,using a conditional co-culture system,we found that microglia treated with tryptanthrin suppressed endoplasmic reticulum stress-related neuronal *** together,these results suggest that by targeting the cGAs/sTING/NF-κB axis,tryptanthrin attenuates microglia-derived neuroinflammation and promotes functional recovery after spinal cord injury through shifting microglia polarization to the M2 phenotype.

关键词： cGAs/sTING functional recovery microglia neuroinflammation neuroprotection nuclear factor-κB polarization spinal cord injury tryptanthrin

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Integration of perioperative features and intragraft TCF7L2 expression to predict lipid metabolic disorder in liver transplant recipients

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science China Life sciences 2025年第1期 297-299页

作者： Junbin Zhou Rongli Wei Guanghan Fan Zhengxing Lian Xuanyu Zhang Linsong Tang Zhetuo Qi Haiyang Xie shusen Zheng Qiang Wei Xiao Xu Department of Hepatobiliary and Pancreatic surgery People's Hospital of LishuiAffiliated Lishui Hospital of Wenzhou Medical UniversityThe First Affiliated Hospital of Lishui University NHFPC Key Laboratory of Combined Multi-Organ Transplantation Key Laboratory of Integrated Oncology and Intelligent Medicine of Zhejiang Province Department of Hepatobiliary and Pancreatic SurgeryHangzhou First People's Hospital Department of Hepatobiliary and Pancreatic surgery The First Affiliated HospitalZhejiang University School of Medicine Department of Urology The Second Affiliated HospitalZhejiang University School of Medicine Department of Hepatobiliary and Pancreatic surgery Department of Liver TransplantationShulan (Hangzhou) Hospital Hangzhou medical College Zhejiang university school of Medicine

Dear Editor, Liver transplantation(LT) is the only curative therapy for patients with endstage liver disease(He et al., 2023; Ling et al., 2022). Post-transplant hypertriglyceridemia(PTHT), which has an incidence of up to 32.8% in 6 months after LT, is one of the major post-transplant complications(Toshima et al., 2020).

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Chlorogenic acid alleviates hypoxic-ischemic brain injury in neonatal mice

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Neural Regeneration Research 2023年第3期18卷 568-576页

作者： Lu-Yao Li Qi Wang Lu Deng Zhen Lin Jing-Jing Lin Xin-Ye Wang Tian-Yang shen Yi-Hui Zheng Wei Lin Pei-Jun Li Xiao-Qin Fu Zhen-Lang Lin Department of Pharmacy The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Neonatology The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Geriatrics The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Orthopedics The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Neurology The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina

Recent studies have shown that chlorogenic acid(CGA),which is present in coffee,has protective effects on the nervous ***,its role in neonatal hypoxic-ischemic brain injury remains *** this study,we established a newborn mouse model of hypoxic-ischemic brain injury using a modified Rice-Vannucci method and performed intraperitoneal injection of *** found that CGA intervention effectively reduced the volume of cerebral infarct,alleviated cerebral edema,restored brain tissue structure after injury,and promoted axon growth in injured brain ***,CGA pretreatment alleviated oxygen-glucose deprivation damage of primary neurons and promoted neuron *** addition,changes in ferroptosis-related proteins caused by hypoxic-ischemic brain injury were partially reversed by ***,CGA intervention upregulated the expression of the key ferroptosis factor glutathione peroxidase 4 and its upstream glutamate/cystine antiporter related factors sLC7A11 and *** summary,our findings reveal that CGA alleviates hypoxic-ischemic brain injury in neonatal mice by reducing ferroptosis,providing new ideas for the treatment of neonatal hypoxic-ischemic brain injury.

关键词： chlorogenic acid ferroptosis glutathione peroxidase 4 lipid peroxidation neonatal hypoxic-ischemic brain injury neurons neuroprotection oxidative stress oxygen-glucose deprivation system Xc^(-)

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Reperfusion after hypoxia-ischemia exacerbates brain injury with compensatory activation of the antiferroptosis system:based on a novel rat model

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Neural Regeneration Research 2023年第10期18卷 2229-2236页

作者： Tian-Lei Zhang Zhi-Wei Zhang Wei Lin Xin-Ru Lin Ke-Xin Lin Ming-Chu Fang Jiang-Hu Zhu Xiao-Ling Guo Zhen-Lang Lin Department of Pediatrics the Second School of Medicinethe Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina second Clinical medical College Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Key Laboratory of children Genitourinary Diseases of wenzhou the Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Key Laboratory of Perinatal Medicine of wenzhou the Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina Basic medical Research Center the Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhouZhejiang ProvinceChina

Hypoxic-ischemic encephalopathy,which predisposes to neonatal death and neurological sequelae,has a high morbidity,but there is still a lack of effective prevention and treatment in clinical *** better understand the pathophysiological mechanism underlying hypoxic-ischemic encephalopathy,in this study we compared hypoxic-ischemic reperfusion brain injury and simple hypoxic-ischemic brain injury in neonatal ***,based on the conventional RiceVannucci model of hypoxic-ischemic encephalopathy,we established a rat model of hypoxic-ischemic reperfusion brain injury by creating a common carotid artery muscle *** we performed tandem mass tag-based proteomic analysis to identify differentially expressed proteins between the hypoxic-ischemic reperfusion brain injury model and the conventional Rice-Vannucci model and found that the majority were mitochondrial *** also performed transmission electron microscopy and found typical characteristics of ferroptosis,including mitochondrial shrinkage,ruptured mitochondrial membranes,and reduced or absent mitochondrial ***,both rat models showed high levels of glial fibrillary acidic protein and low levels of myelin basic protein,which are biological indicators of hypoxic-ischemic brain injury and indicate similar degrees of ***,we found that ferroptosis-related Ferritin(Fth1)and glutathione peroxidase 4 were expressed at higher levels in the brain tissue of rats with hypoxic-ischemic reperfusion brain injury than in rats with simple hypoxic-ischemic brain *** on these results,it appears that the rat model of hypoxic-ischemic reperfusion brain injury is more closely related to the pathophysiology of clinical *** not only aggravates hypoxic-ischemic brain injury but also activates the anti-ferroptosis system.

关键词： ferroptosis hypoxic-ischemic brain injury hypoxic-ischemic encephalopathy hypoxic-ischemic reperfusion brain injury mitochondria model proteomic analysis reperfusion Rice-Vannucci transmission electron microscopy

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De novo brain arteriovenous malformation formation and development:A case report

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World Journal of Clinical Cases 2022年第18期10卷 6277-6282页

作者： Huan Huang Xue Wang An-Na Guo Wei Li Ren-Hua Duan Jun-Hao Fang Bo Yin Dan-Dong Li Department of Radiology The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina Department of Neurosurgery The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical UniversityWenzhou 325000Zhejiang ProvinceChina

BACKGROUnd Brain arteriovenous malformation(AVM),an aberrant vascular development during the intrauterine period,is traditionally considered a congenital *** reports of cases of de novo AVM formation in children and adults have challenged the traditional view of its congenital *** sUMMARY In this report,we have presented the case of a child with a de novo brain *** resonance imaging and magnetic resonance angiography of the brain showed no AVM at the age of 5 years and 2 *** AVM was first detected in this child at the age of 7 years and 4 *** brain AVM was significantly advanced,and hemorrhage was seen for the first time at the age of 12 years and 8 *** was further progression in the AVM,and hemorrhage occurred again at the age of 13 years and 5 *** analysis of this patient revealed a mutation in the NOTCH2(***473 Val)*** In short,our case has once again confirmed the view that brain AVM is an acquired disease and is the result of the interaction of genes,environment,and molecules.

关键词： De novo arteriovenous malformation Angiogenesis Hemorrhage NOTCH2 Case report

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Human cytomegalovirus-encoded Us28 may act as a tumor promoter in colorectal cancer

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World Journal of Gastroenterology 2016年第9期22卷 2789-2798页

作者： Zhen-Zhai Cai Jian-Gang Xu Yu-Hui Zhou Ji-Hang Zheng Ke-Zhi Lin shu-Zhi Zheng Meng-si Ye Yun He Chang-Bao Liu Zhan-Xiong Xue Department of Gastroenterology The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University Department of surgical Oncology Wenzhou Central Hospital Department of General surgery The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University Department of Pathology Wenzhou Medical University

AIM: To assess human cytomegalovirus-encoded Us28 gene function in colorectal cancer(CRC) ***: Immunohistochemical analysis was performed to determine Us28 expression in 103 CRC patient samples and 98 corresponding adjacent noncancerous samples. Patient data were compared by age, sex, tumor location, histological grade, Dukes' stage, and overall mean survival time. In addition, the Us28 gene was transiently transfected into the CRC LOVO cell line, and cell proliferation was assessed using a cell counting kit-8 assay. Cell cycle analysis by flow cytometry and a cell invasion transwell assay were also carried ***: Us28 levels were clearly higher in CRC tissues(38.8%) than in adjacent noncancerous samples(7.1%)(P = 0.000). Interestingly, elevated Us28 amounts in CRC tissues were significantly associated with histological grade, metastasis, Dukes' stage, and overall survival(all P s28 expression was not significantly correlated with age, sex or tumor location. In addition, multivariate Coxregression data revealed Us28 level as an independent CRC prognostic marker(P = 0.000). LOVO cells successfully transfected with the Us28 gene exhibited higher viability, greater chemotherapy resistance, accelerated cell cycle progression, and increased invasion ***: Us28 expression is predictive of poor prognosis and may promote CRC.

关键词： Human cytomegalovirus Us28 Colorectal cancer Prognosis Proliferation Invasion

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Carbon Chain Length Determines Inhibitory Potency of Perfluoroalkyl sulfonic Acids on Human Placental 3β-Hydroxysteroid Dehydrogenase 1:screening,structure-Activity Relationship,and In silico Analysis

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Biomedical and Environmental sciences 2023年第11期36卷 1015-1027页

作者： TANG Lu Ming MAO Bai Ping ZHANG Bing Ru LI Jing Jing TANG Yun Bing LI Hui Tao GE Ren shan Department of Emergency Medicine The Second Affiliated Hospital and Yuying Children Hospital of Wenzhou Medical UniversityWenzhou 325000ZhejiangChina Department of Anesthesiology The Second Affiliated Hospital and Yuying Children Hospital of Wenzhou Medical UniversityWenzhou 325000ZhejiangChina Department of Obstetrics and Gynecology The Second Affiliated Hospital and Yuying Children Hospital of Wenzhou Medical UniversityWenzhou 325000ZhejiangChina Key Laboratory of structural Malformations in children of Zhejiang Province Wenzhou 325000ZhejiangChina

Objective This study aimed to compare 9 perfluoroalkyl sulfonic acids(PFsA)with carbon chain lengths(C4–C12)to inhibit human placental 3β-hydroxysteroid dehydrogenase 1(3β-HsD1),aromatase,and rat 3β-HsD4 *** Human and rat placental 3β-HsDs activities were determined by converting pregnenolone to progesterone and progesterone secretion in JEG-3 cells was determined using HPLC/Ms–Ms,and human aromatase activity was determined by *** PFsA inhibited human 3β-HsD1 structure-dependently in the order:perfluorooctanesulfonic acid(PFOs,half-maximum inhibitory concentration,IC50:9.03±4.83μmol/L)>perfluorodecanesulfonic acid(PFDs,42.52±8.99μmol/L)>perfluoroheptanesulfonic acid(PFHps,112.6±29.39μmol/L)>perfluorobutanesulfonic acid(PFBs)=perfluoropentanesulfonic acid(PFPs)=perfluorohexanesulfonic acid(PFHxs)=perfluorododecanesulfonic acid(PFDos)(ineffective at 100μmol/L).6:2FTs(1H,1H,2H,2H-perfluorooctanesulfonic acid)and 8:2FTs(1H,1H,2H,2H-perfluorodecanesulfonic acid)did not inhibit human 3β-*** and PFHps are mixed inhibitors,whereas PFDs is a competitive ***,1–10μmol/L PFOs and PFDs significantly reduced progesterone biosynthesis in JEG-3 *** analysis revealed that PFsA binds to the steroid-binding site of human 3β-HsD1 in a carbon chain length-dependent *** 100μmol/L PFsA solutions did not affect rat 3β-HsD4 and human placental aromatase *** Carbon chain length determines inhibitory potency of PFsA on human placental 3β-HsD1 in a V-shaped transition at PFOs(C8),with inhibitory potency of PFOs>PFDs>PFHps>PFBs=PFPs=PFHxs=PFDos=6:2FTs=8:2FTs.

关键词： 3β-hydroxysteroid dehydrogenase 1 Docking analysis Perfluorooctanesulfonic acid Progesterone structure-activityrelationship

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GW842166X Alleviates Osteoarthritis by Repressing LPs-mediated Chondrocyte Catabolism in Mice

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Current medical science 2022年第5期42卷 1046-1054页

作者： Wan-ran HUANG Jun-xue TU Ai-qing QIAO Li-jia CHEN Department of Pharmacy The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou325000China

Objective To explore the role and underlying mechanism of GW842166X on osteoarthritis and osteoarthritis-associated abnormal *** The extracted mouse chondrocytes were treated with GW842166X followed by lipopolysaccharide(LPs).The chondrocytes were divided into the control group,LPs group,LPs+50 nmol/L GW842166X group,and LPs+100 nmol/L GW842166X *** cytotoxicity of GW842166X was tested using the CCK-8 *** blot,RT-qPCR,and ELIsA were applied to evaluate the expression of the inflammatory biomarkers in mouse *** expression of extracellular matrix molecules was detected by the Western blot,RT-qPCR,and ***,the activity of NF-κB was checked by the Western blot and *** mouse Hulth models were generated to examine the in vivo effects of GW842166X on *** and eosin staining,safranin O/fast green staining,and immunohistochemistry were applied to detect the histological *** GW842166X below 200µmol/L had no cytotoxicity on the mouse ***-induced high expression of TGF-β1,IL-10,TNF-α,and IL-6 was significantly reduced by *** addition,GW842166X upregulated the expression of aggrecan and collagen type III,which was downregulated after the LPs *** upregulated expression of ADAMTs-5 and MMP-13 by LPs stimulation was dropped in response to the GW842166X ***,LPs decreased the IκBαexpression in the cytoplasm and increased the nuclear p65 ***,these changes were reversed by the GW842166X ***,the damages in the knees caused by the Hulth surgery in mice were restored by *** GW842166X impeded the LPs-mediated catabolism in mouse chondrocytes,thereby inhibiting the progression of osteoarthritis.

关键词： GW842166X lipopolysaccharide osteoarthritis chondrocyte catabolism cartilage extracellular matrix

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2-(2-Benzofuranyl)-2-imidazoline treatment within 5 hours after cerebral ischemia/reperfusion protects the brain

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Neural Regeneration Research 2018年第12期13卷 2111-2118页

作者： Zheng Zhang Jin-Long Yang Lin-Lei Zhang Zhen-Zhen Chen Jia-Ou Chen Yun-Gang Cao Man Qu Xin-Da Lin Xun-Ming Ji Zhao Han Department of Neurology the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Department of Neurology the First Affiliated Hospital of Wenzhou Medical University Department of Neurosurgery Xuanwu Hospital Capital Medical University Department of Neurology Shan Xian Central Hospital Department of children Rehabilitation the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University China-America Institute of Neuroscience Xuanwu Hospital Capital Medical University

We previously demonstrated that administering 2-（2-benzofuranyl）-2-imidazolin（2-BFI）, an imidazoline I2 receptor agonist, immediately after ischemia onset can protect the brain from ischemic insult. However, immediate administration after stroke is difficult to realize in the clinic. Thus, the therapeutic time window of 2-BFI should be determined. sprague-Dawley rats provided by wenzhou medical university in China received right middle cerebral artery occlusion for 120 minutes, and were treated with 2-BFI（3 mg/kg） through the caudal vein at 0, 1, 3, 5, 7, and 9 hours after reperfusion. Neurological function was assessed using the Longa＇s method. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride assay. Morphological changes in the cortical penumbra were observed by hematoxylin-eosin staining under transmission electron microscopy. The apoptosis levels in the ipsilateral cortex were examined with terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling（TUNEL） assay. The protein expression of Bcl-2 and BAX was detected using immunohistochemistry. We found the following： Treatment with 2-BFI within 5 hours after reperfusion obviously improved neurological function. Administering 2-BFI within 9 hours after ischemia/reperfusion decreased infarct volume and alleviated apoptosis. 2-BFI administration at different time points after reperfusion alleviated the pathological damage of the ischemic penumbra and reduced the number of apoptotic neurons, but the protective effect was more obvious when administered within 5 hours. Administration of 2-BFI within 5 hours after reperfusion remarkably increased Bcl-2 expression and decreased BAX expression. To conclude, 2-BFI shows potent neuroprotective effects when administered within 5 hours after reperfusion, seemingly by up-regulating Bcl-2 and down-regulating BAX expression. The time window provided clinical potential for ischemic stroke by 2-BFI.

关键词： nerve regeneration ischemia/reperfusion 2-(2-benzofuranyl)-2-imidazoline neuroprotection time window apoptosis Bcl-2 BAX neural regeneration

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