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Inhibiting ShP2 reduces glycolysis, promotes microglial M1 polarization, and alleviates secondary inflammation following spinal cord injury in a mouse model

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Neural regeneration research 2025年第3期20卷 858-872页

作者： Xintian Ding Chun Chen heng Zhao Bin Dai Lei ye Tao Song Shuai huang Jia Wang Tao You Department of Orthopedics The First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Department of Orthopedics Provincial Hospital Affiliated to Anhui Medical UniversityHefeiAnhui ProvinceChina

reducing the secondary inflammatory response, which is partly mediated by microglia, is a key focus in the treatment of spinal cord injury. Src homology 2-containing protein tyrosine phosphatase 2(ShP2), encoded by PTPN11, is widely expressed in the human body and plays a role in inflammation through various mechanisms. Therefore, ShP2 is considered a potential target for the treatment of inflammation-related diseases. however, its role in secondary inflammation after spinal cord injury remains unclear. In this study, ShP2 was found to be abundantly expressed in microglia at the site of spinal cord injury. Inhibition of ShP2 expression using sirNA and ShP2 inhibitors attenuated the microglial inflammatory response in an in vitro lipopolysaccharide-induced model of inflammation. Notably, after treatment with ShP2 inhibitors, mice with spinal cord injury exhibited significantly improved hind limb locomotor function and reduced residual urine volume in the bladder. Subsequent in vitro experiments showed that, in microglia stimulated with lipopolysaccharide, inhibiting ShP2 expression promoted M2 polarization and inhibited M1 polarization. Finally, a co-culture experiment was conducted to assess the effect of microglia treated with ShP2 inhibitors on neuronal cells. The results demonstrated that inflammatory factors produced by microglia promoted neuronal apoptosis, while inhibiting ShP2 expression mitigated these effects. Collectively, our findings suggest that ShP2 enhances secondary inflammation and neuronal damage subsequent to spinal cord injury by modulating microglial phenotype. Therefore, inhibiting ShP2 alleviates the inflammatory response in mice with spinal cord injury and promotes functional recovery postinjury.

关键词： apoptosis glycolysis inflammatory response microglia neurons polarization spinal cord injury Src homology 2-containing protein tyrosine phosphatase 2

Overexpression of low-density lipoprotein receptor prevents neurotoxic polarization of astrocytes via inhibiting NLrP3 inflammasome activation in experimental ischemic stroke

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Neural regeneration research 2025年第2期20卷 491-502页

作者： Shuai Feng Juanji Li Tingting Liu Shiqi huang Xiangliang Chen Shen Liu Junshan Zhou hongdong Zhao ye hong Department of Neurology Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Neurology Nanjing Jinling HospitalAffiliated Hospital of Medical SchoolNanjing UniversityNanjingJiangsu ProvinceChina

Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion ***-density lipoprotein receptor,a classic cholesterol regulatory receptor,has been found to inhibit NLr family pyrin domain containing protein 3(NLrP3)inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s ***,little is known about the effects of low-density lipoprotein receptor on astrocytic activation in ischemic *** address this issue in the present study,we examined the mechanisms by which low-density lipoprotein receptor regulates astrocytic polarization in ischemic stroke ***,we examined low-density lipoprotein receptor expression in astrocytes via immunofluorescence staining and western blotting *** observed significant downregulation of low-density lipoprotein receptor following middle cerebral artery occlusion reperfusion and oxygen-glucose deprivation/***,we induced the astrocyte-specific overexpression of low-density lipoprotein receptor using astrocyte-specific adeno-associated ***-density lipoprotein receptor overexpression in astrocytes improved neurological outcomes in middle cerebral artery occlusion mice and reversed neurotoxic astrocytes to create a neuroprotective ***,we found that the overexpression of low-density lipoprotein receptor inhibited NLrP3 inflammasome activation in oxygen-glucose deprivation/reoxygenation injured astrocytes and that the addition of nigericin,an NLrP3 agonist,restored the neurotoxic astrocyte *** findings suggest that low-density lipoprotein receptor could inhibit the NLrP3-meidiated neurotoxic polarization of astrocytes and that increasing low-density lipoprotein receptor in astrocytes might represent a novel strategy for treating cerebral ischemic stroke.

关键词： inflammation ischemia/reperfusion injury ischemic stroke low-density lipoprotein receptor neuroprotective astrocytes neurotoxic astrocytes NLrP3 inflammasome polarization

Neuroprotective potential for mitigating ischemia-reperfusion-induced damage

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Neural regeneration research 2025年第8期20卷 2199-2217页

作者： Zi ye runqing Liu hangxing Wang Aizhen Zuo Cen Jin Nan Wang huiqi Sun Luqian Feng hua Yang The Clinical Medical College Guizhou Medical UniversityGuiyangGuizhou ProvinceChina Division of Infectious Diseases Department of Internal MedicinePeking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina School of Medical Imaging Guizhou Medical UniversityGuiyangGuizhou ProvinceChina Division of Gastroenterology First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina The Second Clinical Medical College Lanzhou UniversityLanzhouGansu ProvinceChina Department of Neurosurgery Affiliated Hospital of Guizhou Medical UniversityGuiyangGuizhou ProvinceChina

reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion *** studies have elucidated the neuroprotective role of the sirtuin protein family(Sirtuins)in modulating cerebral ischemia-reperfusion ***,the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional *** this review,the origin and research progress of Sirtuins are summarized,suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury,including inflammation,oxidative stress,blood-brain barrier damage,apoptosis,pyroptosis,and *** therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways,such as nuclear factor-kappa B signaling,oxidative stress mediated by adenosine monophosphate-activated protein kinase,and the forkhead box *** review also summarizes the potential of endogenous substances,such as rNA and hormones,drugs,dietary supplements,and emerging therapies that regulate Sirtuins *** review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk *** Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury,most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans,potentially influencing the efficacy of Sirtuinstargeting drug ***,this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.

关键词： apoptosis autophagy blood-brain barrier dietary supplements drug hormones inflammation neuroprotection oxidative stress prognosis pyroptosis reperfusion injury risk factors rNA therapeutics

An Unprecedented Efficiency with Approaching 21%Enabled by Additive‑Assisted Layer‑by‑Layer Processing in Organic Solar Cells

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Nano-Micro Letters 2025年第2期17卷 372-375页

作者： Shuai Xu Youdi Zhang Yanna Sun Pei Cheng Zhaoyang Yao Ning Li Long ye Lijian Zuo Ke Gao Key Laboratory of Advanced Green Functional Materials College of ChemistryChangchun Normal UniversityChangchun 130032People’s Republic of China Shandong Provincial Key Laboratory for Science of Material Creation and Energy Conversion School of Chemistry and Chemical EngineeringShandong UniversityQingdao 266237People’s Republic of China College of Polymer Science and Engineering Sichuan UniversityChengdu 610065People’s Republic of China State Key Laboratory and Institute of Elemento‑Organic Chemistry Centre of Nanoscale Science and Technology and Key Laboratory of Functional Polymer MaterialsRenewable Energy Conversion and Storage Center(RECAST)College of ChemistryNankai UniversityTianjin 300071People’s Republic of China Institute of Polymer Optoelectronic Materials and Devices State Key Laboratory of Luminescent Materials and Devices South China University of TechnologyGuangzhou 510640People’s Republic of China Tianjin Key Laboratory of Molecular Optoelectronic Sciences School of Materials Science and EngineeringTianjin UniversityTianjin 300350People’s Republic of China State Key Laboratory of Silicon Materials MOE Key Laboratory of Macromolecular Synthesis and FunctionalizationDepartment of Polymer Science and EngineeringZhejiang UniversityHangzhou 310027People’s Republic of China

recently published in Joule,Feng Liu and colleagues from Shanghai Jiaotong University reported a record-breaking 20.8%power conversion efficiency in organic solar cells(OSCs)with an interpenetrating fibril network active layer morphology,featuring a bulk p-in structure and proper vertical segregation achieved through additive-assisted layer-by-layer *** optimized hierarchical gradient fibrillar morphology and optical management synergistically facilitates exciton diffusion,reduces recombination losses,and enhances light capture *** approach not only offers a solution to achieving high-efficiency devices but also demonstrates the potential for commercial applications of OSCs.

关键词： Organic solar cells Additive-assisted layer-by-layer processing Three-dimensional fibril morphology Bulk p-i-n structure Optical management

The complex roles of m^(6)A modifications in neural stem cell proliferation, differentiation, and self-renewal and implications for memory and neurodegenerative diseases

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Neural regeneration research 2025年第6期20卷 1582-1598页

作者： Yanxi Li Jing Xue Yuejia Ma Ke ye Xue Zhao Fangliang Ge Feifei Zheng Lulu Liu Xu Gao Dayong Wang Qing Xia Department of Biochemistry and Molecular Biology College of Basic Medical SciencesHarbin Medical UniversityHarbinHeilongjiang ProvinceChina College of Basic Medical Sciences Harbin Medical UniversityHarbinHeilongjiang ProvinceChina Basic Medical Institute Heilongjiang Academy of Medical SciencesHarbinHeilongjiang ProvinceChina Key Laboratory of heilongjiang Province for Genetically Modified Animals Harbin Medical UniversityHarbinHeilongjiang ProvinceChina Translational Medicine research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbinHeilongjiang ProvinceChina Dongzhimen hospital Beijing University of Chinese MedicineBeijingChina

N6-methyladenosine(m^(6)A), the most prevalent and conserved rNA modification in eukaryotic cells, profoundly influences virtually all aspects of mrNA metabolism. mrNA plays crucial roles in neural stem cell genesis and neural regeneration, where it is highly concentrated and actively involved in these processes. Changes in m^(6)A modification levels and the expression levels of related enzymatic proteins can lead to neurological dysfunction and contribute to the development of neurological diseases. Furthermore, the proliferation and differentiation of neural stem cells, as well as nerve regeneration, are intimately linked to memory function and neurodegenerative diseases. This paper presents a comprehensive review of the roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, as well as its implications in memory and neurodegenerative diseases. m^(6)A has demonstrated divergent effects on the proliferation and differentiation of neural stem cells. These observed contradictions may arise from the time-specific nature of m^(6)A and its differential impact on neural stem cells across various stages of development. Similarly, the diverse effects of m^(6)A on distinct types of memory could be attributed to the involvement of specific brain regions in memory formation and recall. Inconsistencies in m^(6)A levels across different models of neurodegenerative disease, particularly Alzheimer's disease and Parkinson's disease, suggest that these disparities are linked to variations in the affected brain regions. Notably, the opposing changes in m^(6)A levels observed in Parkinson's disease models exposed to manganese compared to normal Parkinson's disease models further underscore the complexity of m^(6)A's role in neurodegenerative processes. The roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, and its implications in memory and neurodegenerative diseases, appear contradictory. These inconsistencies may be a

关键词： Alzheimer's disease cell self-renewal central nervous system memory microglia nerve regeneration neurodegenerative diseases neurogenesis rNA methylation

The compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4h-pyran-4-one alleviates neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease

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Neural regeneration research 2025年第11期20卷 3330-3344页

作者： Xueyan Liu Wei Wu Xuejuan Li Chengyan Wang Ke Chai Fanru Yuan huijuan Zheng Yuxing Yao Chenlu Li Zu-Cheng ye Daijun Zha Department of Medicinal Chemistry School of PharmacyFujian Medical UniversityFuzhouFujian ProvinceChina Fujian Provincial Key Laboratory of Brain Aging and Neurodegenerative Diseases School of Basic Medical SciencesFujian Medical UniversityFuzhouFujian ProvinceChina Institute of Laboratory Animal Center Fujian Medical UniversityFuzhouFujian ProvinceChina Department of Neurosurgery Neurosurgery Research InstituteThe First Affiliated HospitalFujian Medical UniversityFuzhouFujian ProvinceChina Department of hyperbaric Oxygen National Regional Medical CenterBinhai Campus of the First Affiliated HospitalFujian Medical UniversityFuzhouFujian ProvinceChina

Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4h-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregation,and alleviates scopolamine-induced cognitive impairment,similar to the phase Ⅲ clinical drug *** this study,we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced *** results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment,promoted fibrillar amyloid-β clearance from the hippocampus and cortex,suppressed oxidative stress,and inhibited activation of microglia and astrocytes.D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein ***,we demonstrated that exogenous fibrillar amyloid-βintroduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain,and this increase was blocked by *** the role of D30 in clearing amyloid-β,inhibiting neuroinflammation,protecting synapses,and improving cognition,this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.

关键词： Alzheimer's disease amyloid-β astrocyte cognitive impairment D30 dendritic spines galectin-3 microglia neuroinflammation neuron

Life-Cycle Bearing Capacity for Pre-Stressed T-beams Based on Full-Scale Destructive Test

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Structural Durability & health Monitoring 2025年第1期19卷 145-166页

作者： Yushan ye Tao Gao Liankun Wang Junjie Ma Yingchun Cai heng Liu Xiaoge Liu China Construction Seventh Engineering Division Corp. Ltd.Zhengzhou450004China School of Water Conservancy and Transportation Zhengzhou UniversityZhengzhou450001China

To investigate the evolution of load-bearing characteristics of pre-stressed beams throughout their service life and to provide a basis for accurately assessing the actual working state of damaged pre-stressed concrete T-beams,destructive tests were conducted on full-scale pre-stressed concrete *** on the measurement and ana-lysis of beam deﬂection,strain,and crack development under various loading levels during the research tests,combined with the veriﬁcation coefﬁcient indicators speciﬁed in the codes,the veriﬁcation coefﬁcients of bridges at different stages of damage can be *** results indicate that the T-beams experience complete,incom-plete linear,and non-linear stages during the destructive test *** the complete linear elastic stage,both the deﬂection and bottom strain veriﬁcation coefﬁcients comply with the speciﬁcations,indicating a good structural load-bearing capacity no longer adheres to the code’s *** the non-linear stage,both coefﬁcients exhi-bit a sharp increase,resulting in a further decrease in the structure’s load-bearing *** to the pro-visions of the current code,the beam can be in the incomplete linear stage when both values fall within the code’s speciﬁed *** strain veriﬁcation coefﬁcient sourced from the compression zone at the bottom of theﬂange is not recommended for assessing the bridge’s load-bearing capacity.

关键词： Pre-stressed T-beams whole process destructive test bearing capacity veriﬁcation coefﬁcient

Neuroinflammation as a therapeutic target in huntington's disease

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Neural regeneration research 2025年第3期20卷 817-818页

作者： Andrea Kwakowsky Thulani h.Palpagama Center for Brain research and Department of Anatomy and Medical Imaging Faculty of Medical and Health SciencesUniversity of AucklandAucklandNew Zealand Pharmacology and Therapeutics School of MedicineGalway Neuroscience CentreUniversity of GalwayGalwayIreland

In 1872, George huntington presented his essay “On Chorea” to the Meigs and Mason Academy of Medicine and, in doing so, detailed a disease that would later bear his name. huntington's disease(hD) is a genetic, neurodegenerative disease that manifests as the loss of motor control,cognitive impairment,and mood and psychiatric changes in paents.

关键词： huntington inflammation Medicine

Glial response in the midcingulate cortex in huntington’s disease

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Neural regeneration research 2025年第1期20卷 207-208页

作者： Thulani h.Palpagama Andrea Kwakowsky Center for Brain research and Department of Anatomy and Medical Imaging Faculty of Medical and Health SciencesUniversity of AucklandAucklandNew Zealand Pharmacology and Therapeutics School of MedicineGalway Neuroscience CenterUniversity of GalwayGalwayIreland

huntington’s disease(hD)is a genetic disease characterized by the progressive degeneration of the striatum and *** can present with a variety of symptoms that can broadly be classified into motor symptoms,inclusive of choreatic movements and rigidity,mood and psychiatric symptoms,such as depression and apathy,and cognitive symptoms,such as cognitive *** causal mutation underlying hD results from an expansion of a CAG repeat sequence on the IT15 gene,resulting in the formation and accumulation of a mutant huntingtin protein.

关键词： huntington degeneration cortex