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3,6-dichlorobenzo[b]thiophene-2-carboxylic acid alleviates ulcerative colitis by suppressing mammalian target of rapamycin complex 1 activation and regulating intestinal microbiota

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World Journal of Gastroenterology 2022年第46期28卷 6522-6536页

作者： Qiong-Zi He Peng Wei Jun-Zhi Zhang tong-tong liu Kun-Qun Shi Huan-Huan liu Jing-Wei Zhang Shi-Jia liu Affiliated Hospital of Nanjing University of Chinese Medicine Jiangsu Province Hospital of Chinese MedicineNanjing 210029Jiangsu ProvinceChina College of The First Clinical Medicine Nanjing University of Chinese MedicineNanjing 210023Jiangsu ProvinceChina School of Life Science and Technology China Pharmaceutical UniversityNanjing 211198Jiangsu ProvinceChina

BACKGROUND 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid(BT2)is a benzothiophene carboxylate derivative that can suppress the catabolism of branched-chain amino acid(BCAA)-associated mammalian target of rapamycin complex 1(mTORC1)*** studies have demonstrated the therapeutic effects of BT2 on arthritis,liver cancer,and kidney ***,the effects of BT2 on ulcerative colitis(UC)are *** To investigate the anti-UC effects of BT2 and the underlying *** Mouse UC models were created through the administration of 3.5%dextran sodium sulfate(DSS)for 7 *** mice in the treated groups were administered salazosulfapyridine(300 mg/kg)or BT2(20 mg/kg)orally from day 1 to day *** the end of the study,all of the mice were sacrificed,and colon tissues were removed for hematoxylin and eosin staining,immunoblot analyses,and immunohistochemical *** levels were measured by flow *** contents of BCAAs including valine,leucine,and isoleucine,in mouse serum were detected by liquid chromatography-tandem mass spectrometry,and the abundance of intestinal flora was analyzed by 16S ribosomal DNA *** Our results revealed that BT2 significantly ameliorated the inflammatory symptoms and pathological damage induced by DSS in ***2 also reduced the production of the proinflammatory cytokines interleukin 6(IL-6),IL-9,and IL-2 and increased the anti-inflammatory cytokine IL-10 *** addition,BT2 notably improved BCAA catabolism and suppressed mTORC1 activation and cyclooxygenase-2 expression in the colon tissues of UC ***,highthroughput sequencing revealed that BT2 restored the gut microbial abundance and diversity in mice with *** with the DSS group,BT2 treatment increased the ratio of Firmicutes to Bacteroidetes and decreased the abundance of Enterobacteriaceae and *** Our results indicated that BT2 significantly ameliorated DSS-induced UC and that the late

关键词： 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid Ulcerative colitis Mechanistic target of rapamycin complex 1 Intestinal flora Dextran sodium sulfate Cyclooxygenase-2

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Prognostic and clinicopathological value of Twist expression in esophageal cancer:A meta-analysis

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World Journal of Gastrointestinal Oncology 2022年第9期14卷 1874-1886页

作者： Wen-Peng Song Su-Yan Wang Si-Cheng Zhou Dong-Sheng Wu Jia-Yu Xie tong-tong liu Xiu-Zhu Wu Guo-Wei Che Lung Cancer Center West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina Frontiers Science Center for Disease-related Molecular Network West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina West China School of Medicine Sichuan UniversityChengdu 610041Sichuan ProvinceChina Laboratory Experiments in Microbiology Shuang Liu Center for Disease Control and PreventionChengdu 610041Sichuan ProvinceChina West China School of Public Health&West China Fourth Hospital Sichuan UniversityChengdu 610041Sichuan ProvinceChina

BACKGROUND Twist is a repressor of E-cadherin transcription that induces epithelial-mesenchymal transition and cancer ***,the prognostic value of Twist expression in patients with esophageal cancer remains *** To investigate the prognostic and clinicopathological value of Twist expression in esophageal *** Published literature in databases such as EMBASE,Web of Science,PubMed,China National Knowledge Infrastructure,Wanfang,and VIP databases was searched for eligible *** with esophageal cancer whose tumor tissues underwent immunohistochemistry to detect the expression of Twist were *** meta-analysis was conducted using Stata version *** hazard ratio(HR) and relative ratio(RR) with their 95 % CI were *** was estimated by I^(2) *** Eleven articles published between 2009 and 2021 fulfilled the selection *** pooled HR for overall survival was 1.88(95%CI:1.32-2.69,I^(2)=68.6%),and the pooled HR for disease-free survival/relapse-free survival/progression-free survival was 1.84(95 % CI:1.12-3.02,I^(2)=67.1%),suggesting that high Twist expression is associated with poor prognosis in esophageal cancer *** addition,overexpression of Twist was correlated with T stage(T3+T4 vs T1+T2,RR=1.38,95 % CI:1.14-1.67),lymph node metastasis(yes vs no,RR=1.34,95 % CI:1.11-1.60),distant metastasis(yes vs no,RR=1.18,95 % CI:1.02-1.35),tumor,node and metastasis(TNM) stage(Ⅲ+Ⅳ vs Ⅰ+Ⅱ,RR=1.35,95 % CI:1.14-1.60),and clinical stage(Ⅲ+Ⅳ vs Ⅰ+Ⅱ,RR=1.58,95 % CI:1.34-1.87).However,no correlation between Twist expression and age,gender,tumor location,differentiation,or venous invasion was *** High expression of Twist is associated with poor esophageal cancer ***,Twist overexpression is correlated with T stage,lymph node metastasis,distant metastasis,TNM stage,and clinical stage,which indicates that Twist might accelerate esophageal cancer progression

关键词： Twist Esophageal cancer Prognosis Epithelial-mesenchymal transition Metastasis Meta-analysis

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Role of reactive oxygen species in the antiproliferative effects of metavanadate on human prostate cancer DU145 cells

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Journal of Chinese Pharmaceutical Sciences 2012年第1期21卷 57-61页

作者： tong-tong liu Yan-Jun liu Xiao-Gai Yang Department of Chemical Biology School of Pharmaceutical SciencesPeking University Health Science CenterBeijing 100191

In the present study, the effects of metavanadate on the human prostate cancer cell line DU145 and the underlying mechanism were investigated. The results showed that metavanadate can cause cell cycle arrest at G2/M phase which was evidenced by cell cycle analysis and the increased phosphorylation of Cdc2 at its inactive Tyr-15 site. In addition, the results showed that metavanadate can induce reactive oxygen species （ROS） elevation and decrease the level of Cdc25C. This process can be rescued by an antioxidant, N-acetyl cysteine. In conclusion, the results demonstrate that metavanadate can inhibit cell proliferation via cell cycle arrest at G2/M phase in DU145 ceils. Metavanadate-induced ROS formation may play an important role in this process by mediating the degradation of Cdc25C.

关键词： Metavanadate G2/M cell cycle arrest Cdc25C Reactive oxygen species

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产前超声诊断胎儿右位主动脉弓并右位动脉导管

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中国介入影像与治疗学 2017年第1期14卷 35-38页

作者：罗欢佟彤易艳刘涛熊奕深圳市福田区第二人民医院超声科广东深圳518049 暨南大学第二临床医学院深圳市人民医院超声科广东深圳518020

目的探讨产前超声诊断胎儿右位主动脉弓并右位动脉导管的价值。方法回顾分析11胎右位主动脉弓并右位动脉导管的胎儿超声心动图特征,重点观察三血管气管切面主动脉弓与肺动脉动脉导管的连接形态、主动脉弓和动脉导管与气管的位置关系。... 详细信息

目的探讨产前超声诊断胎儿右位主动脉弓并右位动脉导管的价值。方法回顾分析11胎右位主动脉弓并右位动脉导管的胎儿超声心动图特征,重点观察三血管气管切面主动脉弓与肺动脉动脉导管的连接形态、主动脉弓和动脉导管与气管的位置关系。结果右位主动脉弓并右位动脉导管时,主动脉弓和动脉导管均位于气管的右侧,呈反向的"V"型连接,即主动脉弓和动脉导管仍呈"V"型连接,但位于气管的右侧。所有11胎右位主动脉弓并右位导管胎儿均不伴迷走左锁骨下动脉,未形成血管环。结论胎儿右位主动脉弓并右位导管的诊断切面为三血管气管切面,但不表现为右位主动脉弓并左位导管时特征性的"U"型连接,诊断的关键在于仔细观察主动脉弓和动脉导管与气管的位置关系。

关键词：心血管畸形胎儿超声心动描记术主动脉弓综合征

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Boosting hydrocarbon conversion via Cu-doping induced oxygen vacancies on CeO2 in CO2 electroreduction

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Journal of Energy Chemistry 2025年第1期100卷 66-76页

作者： Lei Xue tong Shi Chenhui Han Heng Zhang Fenrong liu Haorun Li Yan Wang Xiaojun Gu Shanghong Zeng Inner Mongolia Key Laboratory of Chemistry and Physics of Rare Earth Materials School of Chemistry and Chemical Engineering Inner Mongolia University State Key Laboratory of Coal Conversion Institute of Coal Chemistry Chinese Academy of Sciences Institute of Catalysis Department of Chemistry Zhejiang University National Key Laboratory of Baiyunobo Rare Earth Resource Research and Comprehensive Utilization Baotou Research Institute of Rare Earths

Conversion of CO2back to hydrocarbons is the most direct way of closing the“carbon cycle”,and its significance is further enlarged if this process is driven by renewable energies such as ***,precisely controlling the product selectivity towards hydrocarbons against the competitive hydrogen evolution remains challenging,especially for Cu-based ***,we report a novel defect engineering strategy,by which Cu-doping-induced oxygen vacancies on CeO2nanorods were effectively created,with adjustable vacancy/Cu *** resulting optimum catalyst shows up to 79% catalytic current density to hydrocarbons （excluding CO）,with 49% faradaic efficiency to *** and density functional theory unveil that the ratio between oxygen vacancy and Cu affects significantly the formation of*CHO and activation of H2O,which leads to the following deep hydrogenation to *** findings may spur new insights for designing and developing more controllable chemical process relevant to CO2utilization.

关键词： Oxygen vacancy Hydrocarbon production Reaction mechanism

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Targeting Epac2 and GluA3-containing AMPARs:a novel therapeutic strategy for Alzheimer's disease

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Neural Regeneration Research 2025年第11期20卷 3223-3224页

作者： tong Zhang Martina Schmidt Department of Molecular Pharmacology Groningen Research Institute of PharmacyUniversity of GroningenGroningenThe Netherlands School of Pharmacy Tianjin Medical UniversityTianjinChina

Alzheimer's disease(AD)is a neurodegenerative disease that manifests progressive decline in memory and *** the early stage of AD,memory retrieval is impaired preceding memory acquisition and consolidation(Roy et al.,2016).Prior to the onset of symptoms,pathological amyloid-β(Aβ)plagues and tau protein tangles accumulate in extracellular and intracellular spaces,respectively,leading to *** these hallmark pathologies,Aβ is proposed to be the primary etiology by triggering a cascade of pathogenic events,including neuroinflammation,oxidative stress,tau hyperphosphorylation,synaptic/neuronal dysfunction,and neuronal death(Zhang et al.,2023b).

关键词： Alzheimer impaired Aβ

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Apolipoprotein E elicits targetdirected miRNA degradation to maintain neuronal integrity

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Neural Regeneration Research 2025年第9期20卷 2577-2578页

作者： Jiazi Tan Chin-tong Ong Temasek Life Sciences Laboratory National University of SingaporeSingapore Department of Biological Sciences National University of SingaporeSingapore

Apolipoprotein E has diverse functions in neurons:Apolipoprotein E(ApoE)is a glycoprotein that primarily regulates lipid metabolism and transport in the central nervous *** are three predominant human ApoE protein isoforms with cysteine and arginine substitutions at amino acid positions 112 and 158 that impact their lipidation and related functions(Flowers and Rebeck,2020).ApoE2 is characterized by Cys112 and Cys158,ApoE3 by Cys112 and Arg158,whereas ApoE4 contains Arg112 and Arg158.

关键词： metabolism glycoprotein maintain

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Exosomes originating from neural stem cells undergoing necroptosis participate in cellular communication by inducing TSC2 upregulation of recipient cells following spinal cord injury

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Neural Regeneration Research 2025年第11期20卷 3273-3286页

作者： Shiming Li Jianfeng Li Guoliang Chen Tao Lin Penghui Zhang Kuileung tong Ningning Chen Shaoyu liu Shenzhen Key Laboratory of Bone Tissue Repair and Translational Research Department of Orthopedic SurgeryThe Seventh Affiliated HospitalSun Yat-sen UniversityShenzhenGuangdong ProvinceChina Department of Orthopedic Surgery The First Affiliated Hospital of Jinan UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedics and Traumatology Zhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedic Surgery The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Department of Orthopedic Surgery The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina

We previously demonstrated that inhibiting neural stem cells necroptosis enhances functional recovery after spinal cord *** exosomes are recognized as playing a pivotal role in neural stem cells exocrine function,their precise function in spinal cord injury remains *** investigate the role of exosomes generated following neural stem cells necroptosis after spinal cord injury,we conducted singlecell RNA sequencing and validated that neural stem cells originate from ependymal cells and undergo necroptosis in response to spinal cord ***,we established an in vitro necroptosis model using neural stem cells isolated from embryonic mice aged 16-17 days and extracted *** results showed that necroptosis did not significantly impact the fundamental characteristics or number of *** sequencing of exosomes in necroptosis group identified 108 differentially expressed messenger RNAs,104 long non-coding RNAs,720 circular RNAs,and 14 microRNAs compared with the control *** of a competing endogenous RNA network identified the following hub genes:tuberous sclerosis 2(Tsc2),solute carrier family 16 member 3(Slc16a3),and forkhead box protein P1(Foxp1).Notably,a significant elevation in TSC2 expression was observed in spinal cord tissues following spinal cord ***2-positive cells were localized around SRY-box transcription factor 2-positive cells within the injury ***,in vitro analysis revealed increased TSC2 expression in exosomal receptor cells compared with other *** assessment of cellular communication following spinal cord injury showed that Tsc2 was involved in ependymal cellular communication at 1 and 3 days post-injury through the epidermal growth factor and midkine signaling *** addition,Slc16a3 participated in cellular communication in ependymal cells at 7 days post-injury via the vascular endothelial growth factor and macrophage migration inhibitory factor signaling

关键词： cellular communication competing endogenous RNA exosomes Foxp1 necroptosis neural stem cells Slc16a3 spinal cord injury transcriptome sequencing Tsc2

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Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

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Neural Regeneration Research 2025年第6期20卷 1776-1788页

作者： Zige Jiang Dexiang liu Tingting Li Chengcheng Gai Danqing Xin Yijing Zhao Yan Song Yahong Cheng tong Li Zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurosurgery Surgery Qingdao Municipal HospitalQingdaoShandong ProvinceChina

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

关键词： apoptosis cystathionine-β-synthase nuclear factor erythroid 2-related factor 2 Huntington's disease hydrogen sulfide mitochondrion neuroplasticity oxidative stress quinolinic acid reactive oxygen species

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Nanomaterials-mediated lysosomal regulation:a robust protein-clearance approach for the treatment of Alzheimer’s disease

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Neural Regeneration Research 2025年第2期20卷 424-439页

作者： Mengqi Hao Jianjian Chu Tinglin Zhang tong Yin Yuankai Gu Wendanqi Liang Wenbo Ji Jianhua Zhuang Yan liu Jie Gao You Yin Department of Neurology Second Affiliated Hospital of Naval Medical University(Shanghai Changzheng Hospital)ShanghaiChina School of Health Science and Engineering University of Shanghai for Science and TechnologyShanghaiChina Changhai Clinical Research Unit Shanghai Changhai HospitalNaval Medical UniversityShanghaiChina Department of Clinical Pharmacy Xinhua HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Department of Neurology Shanghai East HospitalSchool of MedicineTongji UniversityShanghaiChina

Alzheimer’s disease is a debilitating,progressive neurodegenerative disorder characterized by the progressive accumulation of abnormal proteins,including amyloid plaques and intracellular tau tangles,primarily within the ***,crucial intracellular organelles responsible for protein degradation,play a key role in maintaining cellular *** studies have suggested a link between the dysregulation of the lysosomal system and pathogenesis of neurodegenerative diseases,including Alzheimer’s *** the normal physiological function of lysosomes hold the potential to reduce the pathological burden and improve the symptoms of Alzheimer’s ***,the efficacy of drugs in treating Alzheimer’s disease is limited,with major challenges in drug delivery efficiency and ***,nanomaterials have gained widespread use in Alzheimer’s disease drug research owing to their favorable physical and chemical *** review aims to provide a comprehensive overview of recent advances in using nanomaterials(polymeric nanomaterials,nanoemulsions,and carbon-based nanomaterials)to enhance lysosomal function in treating Alzheimer’s *** review also explores new concepts and potential therapeutic strategies for Alzheimer’s disease through the integration of nanomaterials and modulation of lysosomal *** conclusion,this review emphasizes the potential of nanomaterials in modulating lysosomal function to improve the pathological features of Alzheimer’s *** application of nanotechnology to the development of Alzheimer’s disease drugs brings new ideas and approaches for future treatment of this disease.

关键词： Alzheimer’s disease autophagy dysfunction lysosomal acidification lysosomal system nanomaterials neurodegenerative diseases

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