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

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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CNKSR2 interactome analysis indicates its association with the centrosome/microtubule system

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Neural Regeneration Research 2025年第8期20卷 2420-2432页

作者： Lin Yin Yalan Xu Jie Mu Yu Leng Lei Ma Yu Zheng Ruizhi Li Yin Wang Peifeng Li Hai Zhu Dong Wang Jing Li Institute for Translational medicine The Affiliated Hospital of Qingdao UniversityMedical CollegeQingdao UniversityQingdaoShandong ProvinceChina School of Basic medicine Qingdao UniversityQingdaoShandong ProvinceChina college of Life Sciences and School of PharmacyMedical CollegeQingdao UniversityQingdaoShandong ProvinceChina Department of Urology Qingdao Municipal Hospital Affiliated to Qingdao UniversityQingdaoShandong ProvinceChina

The protein connector enhancer of kinase suppressor of Ras 2(CNKSR2),present in both the postsynaptic density and cytoplasm of neurons,is a scaffolding protein with several protein-binding *** of the CNKSR2 gene have been implicated in neurodevelopmental disorders,particularly intellectual disability,although the precise mechanism involved has not yet been fully *** has demonstrated that CNKSR2 plays a role in facilitating the localization of postsynaptic density protein complexes to the membrane,thereby influencing synaptic signaling and the morphogenesis of dendritic ***,the function of CNKSR2 in the cytoplasm remains to be *** this study,we used immunoprecipitation and high-resolution liquid chromatography-mass spectrometry to identify the interactors of *** a combination of bioinformatic analysis and cytological experiments,we found that the CNKSR2 interactors were significantly enriched in the proteome of the *** also showed that CNKSR2 interacted with the microtubule protein DYNC1H1 and with the centrosome marker *** colocalization analysis confirmed the centrosomal localization of *** we downregulated CNKSR2 expression in mouse neuroblastoma cells(Neuro 2A),we observed significant changes in the expression of numerous centrosomal *** manipulation also affected centrosome-related functions,including cell size and shape,cell proliferation,and ***,we found that CNKSR2 interactors were highly enriched in de novo variants associated with intellectual disability and autism spectrum *** findings establish a connection between CNKSR2 and the centrosome,and offer new insights into the underlying mechanisms of neurodevelopmental disorders.

关键词： autism spectrum disorder centrosome CNKSR2 intellectual disability interactome mass spectrometry microtubule neurodevelopmental disease protein complexes protein-protein interactions

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Resolving the developmental mechanisms of cardiac microthrombosis of SARS-CoV-2 based on single-cell transcriptome analysis

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Science China Life Sciences 2025年第1期 103-115页

作者： Xizi Luo Nan Zhang Yuntao Liu Beibei Du Xuan Wang Tianxu Zhao Bingqiang Liu Shishun Zhao Jiazhang Qiu Guoqing Wang State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases Key Laboratory for Zoonosis Research of the Ministry of EducationCollege of Basic MedicineJilin University State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases Key Laboratory for Zoonosis Research of the Ministry of EducationCollege of Veterinary MedicineJilin University college of Mathematics Jilin University Bioinformatic Lab School of MathematicsShandong University Department of Cardiology China-Japan Union HospitalJilin University

The coronavirus disease 2019（COVID-19） outbreak caused by the severe acute respiratory syndrome coronavirus-2（SARS-CoV-2） developed into a global health emergency. Systemic microthrombus caused by SARS-CoV-2 infection is a common complication in patients with COVID-19. Cardiac microthrombosis as a complication of SARS-CoV-2 infection is the primary cause of cardiac injury and death in patietns with severe COVID-19. In this study, we performed single-cell sequencing analysis of the right ventricular free wall tissue from healthy donors,patients who died during the hypercoagulable period of characteristic coagulation abnormality（CAC）, and patients who died during the fibrinolytic period of CAC. We collected 61,187 cells enriched in 24 immune cell subsets and 13 cardiac-resident cell subsets. We found that in the course of SARS-CoV-2 infected heart microthrombus, MYO1EhighRASGEF1Bhighmonocyte-derived macrophages promoted hyperactivation of the immune system and initiated the extrinsic coagulation pathway by activating chemokines CCL3, CCL5. This series of events is the main cause of cardiac microthrombi following SARS-CoV-2 infection. In a SARS-CoV-2 infected heart microthrombus, excessive immune activation is accompanied by an increase in cellular iron content, which in turn promotes oxidative stress and intensifies intercellular competition. This induces cells to alter their metabolic environment, resulting in increased sugar uptake via the glycosaminoglycan synthesis pathway. In addition, high levels of reactive oxygen species generated by elevated iron levels promote increased endogenous malondialdehyde synthesis in a subpopulation of cardiac endothelial cells. This exacerbates endothelial cell dysfunction and exacerbates the coagulopathy process.

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Altered 3D genome reorganization mediates precocious myeloid differentiation of aged hematopoietic stem cells in inflammation

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Science China Life Sciences 2025年

作者： Xinyu Cui Yu Dong Qiang Zhan Yixin Huang Qianshu Zhu Zihao Zhang Guang Yang Liping Wang Shijun Shen Jia Zhao Zhiyi Lin Jiatong Sun Zhongqu Su Yihan Xiao Chuyu Zhang Yuwei Liang Lu Shen Lichen Ji Xuguang Zhang Jiqing Yin Hong Wang Zhiyang Chen Zhenyu Ju Cizhong Jiang Rongrong Le Shaorong Gao Clinical and Translational Research Center of Shanghai First Maternity & Infant Hospital Frontier Science Center for Stem Cells School of Life Sciences and Technology Tongji University Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education Orthopaedic Department of Tongji Hospital School of Life Sciences and Technology Tongji University Key Laboratory of Regenerative medicine of Ministry of Education Institute of Aging and Regenerative Medicine Department of Developmental & Regenerative Medicine College of Life Science and Technology Jinan University shandong Key Laboratory of Animal Bioengineering and Disease Prevention College of Animal Science and Technology Shandong Agricultural University Department of Joint Surgery Shanghai East Hospital Tongji University School of Medicine Shanghai Institute of Nutrition and Health Chinese Academy of Sciences

Inflammation is a driving force of hematopoietic stem cells(HSCs) aging, causing irreversible exhaustion of functional HSCs. However, the underlying mechanism of HSCs erosion by inflammatory insult remains poorly understood. Here, we find that transient LPS exposure primes aged HSCs to undergo accelerated differentiation at the expense of self-renewal, leading to depletion of HSCs. Meanwhile, the central regulator nuclear factor kappa B(NF-κB) mediating functional impairment by inflammation insult induces differential transcriptional response in aged HSCs compared with young HSCs, with precocious activation of myeloid lineage genes. Altered compartmentalization and chromatin loop formation are associated with aging-related differential transcriptional response in HSCs upon lipopolysaccharide(LPS)stimulation. Mechanistically, enhancer and promoter regions of myeloid lineage genes in aged HSCs are more accessible and display more rapid and prominent CTCF occupancy upon LPS stimulation. Our study provides comprehensive resources for the three-dimensional(3D)genome structure of HSCs and sheds light into the ordered genome organization and the associated transcriptome signature underlying HSCs aging.

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Anti-inflammatory mechanism of rhein in treating asthma based on network pharmacology

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Journal of Traditional Chinese medicine 2022年第2期42卷 296-303页

作者： FENG Junfang CHEN Ou WANG Yibiao Department of Pediatrics the Second HospitalCheeloo College of MedicineShandong UniversityJinan 250033China School of Nursing Cheeloo College of MedicineShandong UniversityJinan 250012China

OBJECTIVE:To predict the anti-inflammatory targets and related pathways of rhein in the treatment of asthma by using network pharmacology,and to further explore its potential mechanism in ***:The corresponding targets of rhein were obtained from the Traditional Chinese medicine Systems Pharmacology Database and Analysis Platform(TCMSP),and the rhein-target network was constructed with Cytoscape 3.7.1 *** Genbank and Drugbank databases were used to collect and screen asthma targets,and the rhein-target-disease interaction network was constructed.A target protein-protein interaction(PPI)network was constructed using the STRING database to screen key ***,Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis was used to identify biological processes and signaling *** anti-asthmatic effects of rhein were tested in vitro,and the expression levels of proteins in the mitogen-activated protein kinase/nuclear factor kappa-B(MAPK/NF-κB)signaling pathway were assessed by western blot ***:Altogether,83 targets of rhein were screened in the relevant databases,989 targets of asthma were obtained in the National Center for Biotechnology Information(NCBI)GENE *** network analysis and KEGG pathway enrichment analysis predicted that rhein could regulate the epidermal active growth factor receptor(EGFR),mitogen-activated protein kinase 14(MAPK14),tumour necrosis factor receptor superfamily member 1A(TNFRSF1A),receptor tyrosineprotein kinase erb B-2(ERBB2),and other signaling ***,we selected the MAPK signaling pathway to determine the anti-inflammatory effects of ***,further in vitro experiments demonstrated that rhein was shown to inhibit HBE cells ***:The anti-inflammatory mechanism of rhein in the treatment of asthma may be related to EGFR,MAPK14,TNFRSF1A and ERBB2 as well as their signaling *** prevent the exacerbation of asthma,instead of targeting a

关键词： asthma rhein anti-inflammatory agents pharmacology drug development

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Glucocorticoid receptor modulates myeloid-derived suppressor cell function via mitochondrial metabolism in immune thrombocytopenia

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Cellular & Molecular Immunology 2022年第7期19卷 764-776页

作者： Yu Hou Jie Xie Shuwen Wang Daqi Li Lingjun Wang Haoyi Wang Xiaofei Ni Shaoqiu Leng Guosheng Li Ming Hou Jun Peng Department of Hematology Qilu HospitalCheeloo College of MedicineShandong UniversityJinanChina shandong Provincial Key Laboratory of Immunohematology Qilu HospitalCheeloo College of MedicineShandong UniversityJinanChina Jinan Central Hospital Cheeloo College of MedicineShandong UniversityJinanChina Leading Research Group of Scientific Innovation Department of Science and Technology of Shandong ProvinceQilu HospitalCheeloo College of MedicineShandong UniversityJinanChina Advanced Medical Research Institute Shandong UniversityJinanChina

Myeloid-derived suppressor cells(MDSCs)are a heterogeneous population of immature cells and natural inhibitors of adaptive *** metabolic changes in MDSCs exert a direct immunological influence on their suppressive *** previous study demonstrated that high-dose dexamethasone(HD-DXM)corrected the functional impairment of MDSCs in immune thrombocytopenia(ITP);however,the MDSC population was not restored in nonresponders,and the mechanism remained *** this study,altered mitochondrial physiology and reduced mitochondrial gene transcription were detected in MDSCs from HD-DXM nonresponders,accompanied by decreased levels of carnitine palmitoyltransferase-1(CPT-1),a rate-limiting enzyme in fatty acid oxidation(FAO).Blockade of FAO with a CPT-1 inhibitor abolished the immunosuppressive function of MDSCs in HD-DXM *** also report that MDSCs from ITP patients had lower expression of the glucocorticoid receptor(GR),which can translocate into mitochondria to regulate the transcription of mitochondrial DNA(mtDNA)as well as the level of oxidative *** was confirmed that the expression of CPT-1 and mtDNA-encoded genes was downregulated in GR-siRNA-treated murine ***,by establishing murine models of active and passive ITP via adoptive transfer of DXM-modulated MDSCs,we confirmed that GR-silenced MDSCs failed to alleviate thrombocytopenia in mice with *** conclusion,our study indicated that impaired aerobic metabolism in MDSCs participates in the pathogenesis of glucocorticoid resistance in ITP and that intact control of MDSC metabolism by GR contributes to the homeostatic regulation of immunosuppressive cell function.

关键词： immune thrombocytopenia myeloid-derived suppressor cell HD-DXM glucocorticoid receptor

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Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

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Neural Regeneration Research 2025年第5期20卷 1445-1454页

作者： Meifeng Zheng Borui Zhang Sonata S Y Yau Kwok-Fai So Li Zhang Haining Ou Department of Rehabilitation medicine Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Department of Rehabilitation medicine The Fifth Clinical College of Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Key Laboratory of CNS Regeneration(Ministry of Education) Guangdong-Hong Kong-Macao Institute of CNS RegenerationJinan UniversityGuangzhouGuangdong ProvinceChina Department of Rehabilitation Sciences The Hong Kong Polytechnic UniversityHong Kong Special Administrative RegionChina State Key Laboratory of Brain and Cognitive Science Li Ka Shing Faculty of MedicineThe University of Hong KongHong Kong Special Administrative RegionChina Center for Exercise and Brain Science School of PsychologyShanghai University of SportShanghaiChina Neuroscience and Neurorehabilitation Institute University of Health and Rehabilitation SciencesQingdaoShandong ProvinceChina

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug *** exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after *** this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral *** also examined the role of exercise-induced circulating factors in these *** mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery *** found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory *** analysis showed that circulating adiponectin plays a critical role in these preventive effects of *** activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise *** summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

关键词： adiponectin cerebral ischemia exercise pre-conditioning hippocampus memory function middle cerebral artery occlusion prefrontal cortex synaptic proteins treadmill exercise

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Diagnostic value of amygdala volume on structural magnetic resonance imaging in Alzheimer’s disease

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World Journal of Clinical Cases 2021年第18期9卷 4627-4636页

作者： De-Wei Wang Shou-Luan Ding Xian-Li Bian Shi-Yue Zhou Hui Yang Ping Wang Department of Neurology The Second HospitalCheeloo College of MedicineShandong UniversityJinan 250033Shandong ProvinceChina Center for Evidence-Based medicine Institute of Medical SciencesThe Second HospitalCheeloo College of MedicineShandong UniversityJinan 250033Shandong ProvinceChina cheeloo college of medicine Shandong UniversityJinan 250012Shandong ProvinceChina

BACKGROUND The main clinical manifestation of Alzheimer’s disease(AD)is memory loss,which can be accompanied by neuropsychiatric symptoms at different stages of the *** is closely related to emotion and *** To evaluate the diagnostic value of amygdala on structural magnetic resonance imaging(sMRI)for *** In this study,22 patients with AD and 26 controls were *** amygdala volumes were measured by sMRI and analyzed using an automatic analysis *** The bilateral amygdala volumes of AD patients were significantly lower than those of the controls and were positively correlated with the hippocampal *** operating characteristic curve analyses showed that the sensitivity of the left and right amygdala volumes in diagnosing AD was 80.8%and 88.5%,*** analyses showed that amygdala atrophy was more serious in AD patients with neuropsychiatric symptoms,which mainly included irritability(22.73%),sleep difficulties(22.73%),apathy(18.18%),and hallucination(13.64%).CONCLUSION Amygdala volumes measured by sMRI can be used to diagnose AD,and amygdala atrophy is more serious in patients with neuropsychiatric symptoms.

关键词： Alzheimer’s disease Amygdala Structural magnetic resonance imaging Neuropsychiatric symptoms

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Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SHSY5Y cells induced by Aβ_(25-35)

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BIOCELL 2022年第2期46卷 471-478页

作者： XINWEI WU GUOYONG JIA HONGNA YANG CONGCONG SUN YING LIU ZENGYAN DIAO Department of Geriatrics Qilu HospitalCheeloo College of MedicineShandong UniversityJinanChina Department of Neurology Qilu HospitalCheeloo College of MedicineShandong UniversityJinanChina Department of Critical-Care medicine Qilu HospitalCheeloo College of MedicineShandong UniversityJinanChina

A progressive neurodegenerative disease,Alzheimer’s disease(AD).Studies suggest that highly expressed protein isoaspartate methyltransferase 1(PCMT1)in brain *** the current study,we explored the effects of neural stem cell-conditioned medium(NSC-CDM)on the PCMT1/MST1 pathway to alleviate Aβ_(25-35)-induced damage in SH-SY5Y *** data suggested that Aβ_(25-35) markedly inhibited cell ***-CDM or Neural stem cell-complete medium(NSC-CPM)had a suppression effect on toxicity when treatment with Aβ_(25-35),with a greater effect observed with NSC-CDM.Aβ_(25-35)+NSC-CDM group exhibited an increase in PCMT1 ***-PCMT1 markedly decreased cell proliferation and suppressed the protective role of NSC-CDM through the induction of apoptosis and improved p-MST1 *** of PCMT1 reversed the Aβ_(25-35)-induced decrease in cell proliferation and *** summary,our findings suggest that NSC-CDM corrects the Aβ_(25-35)-induced damage to cells by improving PCMT1 expressions,which in turn reduces phosphorylation of MST1.

关键词： Neural stem cell conditioned medium Protein isoaspartate methyltransferase 1 MST1 Amyloidβ_(25-35) Apoptosis

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Adsorption of glycine at the anatase TiO_(2)/water interface: Effects of Ca^(2+) ions

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Journal of Environmental Sciences 2023年第6期128卷 26-34页

作者： Yanli Yang Jiaqi Liu Mengyao Zhu Shengping Dou Lei Ding School of Public Health Cheeloo College of MedicineShandong UniversityChina Environment Research Institute Shandong UniversityQingdao 266237China

Adsorption reactions of amino acids(AAs)on TiO_(2) nanoparticles(NPs)play an important role in the available nutrients in soils and *** pH effects on glycine adsorption have been studied,but little is known about its coadsorption with Ca^(2+)at the molecular *** attenuated total reflectance Fourier transform infrared(ATR-FTIR)flow-cell measurements and density functional theory(DFT)calculationswere used to determine the surface complex and corresponding dynamic adsorption/desorption *** structures of glycine adsorbed onto TiO_(2) were closely associated with its dissolved species in the solution *** presence of Ca^(2+)exerted different influences on glycine adsorption within pH 4−11,thus affecting its migration rate in soils and *** mononuclear bidentate complex at pH 4−7,involving the COO−moiety of zwitterionic glycine,remained unchanged in the absence and presence of Ca^(2+).At pH 11,the mononuclear bidentate complex with deprotonated NH2 can be removed from the TiO_(2) surface upon coadsorption with Ca^(2+).The bonding strength of glycine on TiO_(2) was much weaker than that of the Ca-bridged ternary surface *** adsorption was inhibited at pH 4 but was enhanced at pH 7 and 11.

关键词： Amino acid Coadsorption with Ca^(2+) Dynamic process ATR-FTIR spectroscopy DFT calculations

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