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Neural Regeneration Research 2025年第5期20卷 1403-1404页

作者： Oliver Kann Lennart Soder Babak Khodaie Institute of physiology and pathophysiology Heidelberg UniversityHeidelbergGermany Interdisciplinary Center for Neurosciences(IZN) Heidelberg UniversityHeidelbergGermany

The metabolite lactate (L-lactate) can be generated and released by diverse brain cells,including neurons,astrocytes,and oligodendrocytes (Kann,2023;Rae et al.,2024).Lactate production usually requires the degradation of glucose (D-glucose)-and glycogen in astrocytes-to pyruvate by glycolysis and subsequent conversion of pyruvate to lactate by the enzyme lactate dehydrogenase(Figure 1A;Dienel,2019;Rae et al.,2024).

关键词： consequences Figure restoration

New insights on the role of chondroitin sulfate proteoglycans in neural stem cell–mediated repair in spinal cord injury

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Neural Regeneration Research 2025年第6期20卷 1699-1700页

作者： Seyed Mojtaba Hosseini Soheila Karimi-Abdolrezaee department of physiology and pathophysiology Spinal Cord Research CentreRady Faculty of Health SciencesUniversity of ManitobaWinnipegMBCanada Manitoba Multiple Sclerosis Research Center WinnipegMBCanada Children Hospital Research Institute of Manitoba WinnipegMBCanada

Extensive neurodegeneration is a hallmark of traumatic spinal cord injury (SCI) that underlies permanent sensorimotor and autonomic impairments (Alizadeh et al.,2019).Following the primary impact,the spinal cord undergoes a cascade of secondary injury mechanisms that are driven by disruption of the blood-spinal cord ba rrier,vascula r inju ry,glial reactivity,neu roinfla mmation,oxidative stress,lipid peroxidation,and glutamate excitotoxicity that culminate in neuronal and oligodendroglial cell death,demyelination,and axonal damage(Alizadeh et al.,2019).To achieve a meaningful functional recovery after SCI,regeneration of new neurons and oligodendrocytes and their successful growth and integration within the neural network are critical steps for reconstructing the damaged spinal cord tissue (Fischer et al.,2020).

关键词： peroxidation Fischer injury

Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

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Acta Pharmacologica Sinica 2006年第3期27卷 299-306页

作者： Sheng-ying WU~(2,6) Chun-shui PAN~3 Bin GENG~3 Jing ZHAO~3 Fang YU~3 Yong-zheng PANG~3 Chao-shu TANG~4 Yong-fen QI~(3,4,5) ~2Institute of Cardiovascular Disease,Peking University First Hospital.Beijing 100034 ~3department of physiology and pathophysiology,Peking University Health Science Center,Beijing 100083,China,~4Key Laboratory of Molecular Cardiovascular Science,Ministry of Education,Beijing 100083,China 2Institute of Cardiovascular Disease Peking University First Hospital Beijing 100034 China 3department of physiology and pathophysiology Peking University Health Science Center Beijing 100083 China 3department of physiology and pathophysiology Peking University Health Science Center Beijing 100083 China 3department of physiology and pathophysiology Peking University Health Science Center Beijing 100083 China 3department of physiology and pathophysiology Peking University Health Science Center Beijing 100083 China 3department of physiology and pathophysiology Peking University Health Science Center Beijing 100083 China 4Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing 100083 China 4Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing 100083 China

Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in ***:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain *** calcium content,45Ca2+accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were ***:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified *** calcium content,45Ca2+accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with *** expression of the OPNgene was upregulated(P34.8%,40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group,respectively(P3.9%,37.8 % and 46.2% lower in the aorta in the high-dosage NariS group than in theVDN group,respectively(P<0.01).The expression of the OPN gene ***:The production of H,S,and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

关键词： hydrogen sulfide cystathionine-lyase vascular calcification mRNA

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

Reevaluating the cause of laminopathy in Alzheimer’s disease

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Neural Regeneration Research 2023年第10期18卷 2200-2201页

作者： Md Imamul Islam Eftekhar Eftekharpour department of physiology and pathophysiology University of ManitobaWinnipegMBCanada

Alzheimer’s disease (AD) is the most common form of dementia and is diagnosed clinically by cognitive deficits,and anatomically by accumulation of extracellular amyloid plaques and intracellular neurofib rilla ry ta ngles (NFT) containing hyperphosphorylated *** the past three decades of AD resea rch,the"a myloid hypothesis"gained the most attention as the main player inneurodegeneration.

关键词： Alzheimer amyloid gained

Zinc dysregulation in cancers and its potential as a therapeutic target

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Cancer Biology & Medicine 2020年第3期17卷 612-625页

作者： Jie Wang Huanhuan Zhao Zhelong Xu Xinxin Cheng department of physiology and pathophysiology Tianjin Medical UniversityTianjin 300070China

Zinc is an essential element and serves as a structural or catalytic component in many *** families of transporters are involved in maintaining cellular zinc homeostasis:the ZIP(SLC39A)family that facilitates zinc influx into the cytoplasm,and the ZnT(SLC30A)family that facilitates zinc efflux from the *** dyshomeostasis caused by the dysfunction of zinc transporters can contribute to the initiation or progression of various cancers,including prostate cancer,breast cancer,and pancreatic *** addition,intracellular zinc fluctuations lead to the disturbance of certain signaling pathways involved in the malignant properties of cancer *** review briefly summarizes our current understanding of zinc dyshomeostasis in cancer,and discusses the potential roles of zinc or zinc transporters in cancer therapy.

关键词： Cancer cancer therapy zinc homeostasis zinc transporter

p38 MAPK mediates cardiovascular and behavioral responses induced by central IL-1β and footshock in conscious rats

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Acta Pharmacologica Sinica 2004年第3期25卷 12-16页

作者： Rui-mao ZHENG,Chang-jiang ZOU,Shi-gong ZHU2 department of physiology and pathophysiology,Health Science Center,Peking University,Beijing 100083,China department of physiology and pathophysiology Health Science Center Peking University Beijing 100083 China

AIM: To investigate the roles of p38 mitogen-activated protein kinase (p38 MAPK) in the cardiovascular and behavioral responses induced by intracerebral ventricular injection (icv) of interleukin-1β (IL-1β) or footshock. METHODS: We examined the effects of p38 MAPK on mean artery blood pressure (mABP), heart rate (HR), and motor activity (MA) during central administration of IL-1β, or footshock after icv SB203580 (a specific inhibitor of the p38 MAPK) with Cardiovascular and Behavior Telemetry System in conscious SD rats. RESULTS: (1) IL-1β (icv) or footshock remarkably rise the mABP, and the maximal changes are (7.8±1.8) and (12.3±3.5) mmHg, respectively, which was abrogated by the pretreatment with p38 inhibitor SB203580 intracerebroventricularly. (2) Compared with icv saline group, the motor activity was significantly decreased in SB203580 group with maximal changes (-7.6±1.1) counts/min after footshock. CONCLUSION: p38 MAPK plays an important role in the pres- sor response induced by central administration of IL-1β or footshock and change of motor activity after footshock in conscious rats.

关键词： mitogen-activated protein kinase p38 interleukin-1 blood pressure motor activity

Effects of RNA interference-induced tryptase down-regulation in P815 cells on IL-6 and TNF-α release of endothelial cells

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2008年第8期9卷 656-661页

作者： Yi-feng JIANG Feng-di ZHAO Xiao-bo LI Yan-xia NING Xiu-ling ZHI Rui-zhe QIAN Lian-hua YIN department of physiology and pathophysiology Shanghai Medical College Fudan University Shanghai 200032 China

Objective： To explore the effects of down-regulated tryptase expression in mast cells on the synthesis and release of interleukin-6 （IL-6） and tumor necrosis factor-alpha （TNF-α） of vascular endothelial cells. Methods： Tryptase-siRNA （small-interfering RNA） vector was constructed to inhibit tryptase expression in P815 cells. The medium of P815 cells treated by the tryptase-siRNA （RNAi-P815 group） or pure vector （P815 group） was collected and used to culture bEnd.3 cells. The messenger RNAs （mRNAs） of IL-6 and TNF-α in bEnd.3 cells and their protein levels in the medium were measured by reverse transcription polymerase chain reaction （RT-PCR） and enzyme-linked immunosorbent assay （ELISA）, respectively. Results： IL-6 and TNF-α mRNAs in bEnd.3 cells cultured in RNAi-P815-conditioned medium decreased significantly compared to those in P815-conditioned medium. Consistently, lL-6 and TNF-α protein levels in the medium of bEnd.3 of RNAi-P815 group were lower than those of P815 group. Conclusion： Reduced tryptase expression significantly inhibited the synthesis and release of IL-6 and TNF-α in vascular endothelial cells. RNA interference targeting tryptase expression may be a new anti-inflammatory strategy for vascular diseases.

关键词： Tryptase RNA interference lnterleukin-6 (IL-6) Tumor necrosis factor-alpha (TNF-α) Endothelial cells

Systematical identification of regulatory GPCRs by single-cell trajectory inference reveals the role of ADGRD1 and GPR39 in adipogenesis

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Science China Life Sciences 2025年

作者： Chuan Ye Xuemei Wang Jun Lin Chenyang Wu Yuhua Gao Chenghao Guo Yunxi Liao Ziyan Rao Shaodong Huang Weixuan Chen Ying Huang Jinpeng Sun Dongyu Zhao Changtao Jiang Center of Basic Medical Research Institute of Medical Innovation and ResearchPeking University Third Hospital department of physiology and pathophysiology School of Basic Medical SciencesPeking University department of Biomedical Informatics School of Basic Medical SciencesPeking University State Key Laboratory of Vascular Homeostasis and Remodeling Peking University Center for Obesity and Metabolic Disease Research School of Basic Medical SciencesPeking University State Key Laboratory of Female Fertility Promotion Center for Reproductive MedicineDepartment of Obstetrics and GynecologyPeking University Third Hospital National Clinical Research Center for Obstetrics and Gynecology Peking University Third Hospital department of Endocrinology and Metabolism Peking University Third Hospital Key Laboratory Experimental Teratology of the Ministry of Education Department of Biochemistry and Molecular BiologySchool of Basic Medical SciencesCheeloo College of MedicineShandong University department of Immunology School of Basic Medical SciencesPeking University

Adipogenesis is the healthy expansion of white adipose tissue (WAT),serving as a compensatory response to maintain metabolic homeostasis in the presence of excess energy in the ***,the identification of novel regulatory molecules in adipogenesis,specifically membrane receptors such as G protein-coupled receptors (GPCRs),holds significant clinical *** receptors can serve as viable targets for pharmaceuticals,offering potential for restoring metabolic homeostasis in individuals with *** utilized trajectory inference methods to analyze three distinct single-nucleus sequencing (sNuc-seq) datasets of adipose tissue and systematically identified GPCRs with the potential to regulate *** verification in primary adipose progenitor cells (APCs) of mice,we discovered that ADGRD1 promoted the differentiation of APCs,while GPR39 inhibits this *** the obese mouse model induced by a high-fat diet(HFD),both gain-of-function and loss-of-function studies validated that ADGRD1 promoted adipogenesis,thereby improving metabolic homeostasis,while GPR39 inhibited adipogenesis,leading to metabolic ***,through the analysis of 2,400 ChIP-seq data and 1,204 bulk RNA-seq data,we found that the transcription factors (TFs) MEF2D and TCF12 regulated the expression of ADGRD1and GPR39,*** study revealed the regulatory role of GPCRs in adipogenesis,providing novel targets for clinical intervention of metabolic dysfunction in obese patients.

关键词：

The 2016 Albert Lasker Basic Medical Research Award: Oxygen sensing—a mysterious process essential for survival

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Science China(Life Sciences) 2016年第11期59卷 1195-1197页

作者： Ziru Li Weizhen Zhang department of physiology and pathophysiology Peking University Health Science Center

The 2016 Albert Lasker Basic Medical Research Award honors three physician-scientists： William G. Kaelin, Jr. from Harvard Medical School, Peter J. Ratcliffe from Uni- versity of Oxford and Gregg L. Semenza, from Johns Hopkins University School of Medicine, for their discovery of the pathway by which cells from human and most animals sense and adapt to changes in oxygen availability, a process essential for survival. The Lasker Award is widely considered as America＇s mosLt prestigious honor in the biomedical field. For 71 years,

关键词： HIF gene a mysterious process essential for survival Oxygen sensing The 2016 Albert Lasker Basic Medical Research Award Basic