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Intravitreal slow-release dexamethasone alleviates traumatic proliferative vitreoretinopathy by inhibiting persistent inflammation and Müller cell gliosis in rabbits

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International Journal of Ophthalmology(English edition) 2023年第1期16卷 22-32页

作者： Yi-Ming Zhao Rong-Sha Sun Fang Duan Fang-Yu Wang Yu-Jie Li Xiao-Bing Qian Jie-Ting Zeng Yao Yang Xiao-Feng Lin State Key Laboratory of Ophthalmology Zhongshan Ophthalmic CenterSun Yat-sen UniversityGuangdong Provincial Key Laboratory of Ophthalmology and Visual ScienceGuangzhou 510060Guangdong ProvinceChina Xi’an People’s Hospital(Xi’an Fourth Hospital) Shaanxi Eye HospitalXi’an 710004Shaanxi ProvinceChina

AIM:To evaluate the effects of intravitreal slow-release dexamethasone on traumatic proliferative vitreoretinopathy(PVR)and Müller cell gliosis and preliminarily explored the possible inflammatory mechanism in a rabbit model induced by penetrating ocular ***:Traumatic PVR was induced in the right eyes of pigmented rabbits by performing an 8-mm circumferential scleral incision placed 2.5 mm behind the limbus,followed by treatment with a slow-release dexamethasone implant(Ozurdex)or sham *** eyes were used as normal *** intraocular pressure(IOP)was monitored using an iCare *** severity was evaluated via anatomical and histopathological examinations every week for 6wk;specific inflammatory cytokine and proliferative marker levels were measured by quantitative real-time polymerase chain reaction,Western blot,protein chip analysis,or immunofluorescence ***:During the observation period,PVR severity gradually *** Müller cell gliosis was observed in the peripheral retina near the wound and in the whole retina of PVR *** significantly alleviated PVR development and Müller cell ***-traumatic inflammation fluctuated and was *** interleukin-1β(IL-1β)mRNA level was significantly upregulated,peaking on day 3 and increasing again on day 21 after *** expression of nod-like receptor family pyrin domain containing 3(NLRP3)showed a similar trend that began earlier than that of IL-1β*** suppressed the expression of IL-1β,NLRP3,and phosphorylated nuclear factor-kappa B(NF-κB).The average IOP after treatment was within normal ***:The present study demonstrates chronic and fluctuating inflammation in a traumatic PVR rabbit model over *** treatment significantly inhibites inflammatory cytokines expression and Müller cell gliosis,and thus alleviates PVR *** study highlights the important role of IL-1β,and Ozurdex inhibites inflammation pres

关键词： ocular trauma proliferative vitreoretinopathy gliosis Ozurdex inflammation rabbit

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Neuroprotective effect of Paeoniae Radix Rubra on hippocampal CA1 region of mice induced by transient focal cerebral ischemia via anti-gliosis and anti-oxidant activity

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Chinese Herbal Medicines 2019年第1期11卷 86-91页

作者： Xiao-lu Zhu Bing-chun Yan Cheng Tang Guo-wei Qiu Yao Wu Jie Wang Ping Bo Department of Traditional Chinese and Western Medicine Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases Yangzhou University Medical Center Yangzhou University Department of Neurology Affiliated Hospital Yangzhou University Jiangsu Key Laboratory of Zoonosis Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and ZoonosesYangzhou University

Objective: Stroke is the second leading cause of death worldwide. This study aimed to investigate the neuroprotective effect of Paeoniae Radix Rubra(PRR) on ischemic stroke of ***: The focal ischemic stroke model was produced via middle cerebral artery occlusion. The experimental mice were divided into four groups: vehicle-sham group, PRR-sham group, vehicle-ischemia group, and PRR-treated ischemia group. The cerebral infarction volume was detected with TTC *** number of neurons in the hippocampal CA1 of the ischemic side, and the activation of astrocytes and microglia were observed via immunohistochemical staining. Western blotting was used to determine the expression changes of SOD1, SOD2, and Catalase protein levels in the ***: PRR significantly reduced the cerebral infarct volume induced by ischemic injury and inhibited the astrocytes and microglia activation in the hippocampal CA1 region. The decreased levels of SOD1,SOD2, and Catalase that was induced by ischemic reperfusion were simultaneously improved after PRR ***: PRR improved neuronal injuries that were induced by transient cerebral ischemia via inhibiting gliosis and elevating anti-oxidants.

关键词： cerebral ischemia/reperfusion gliosis neuroprotective oxidative stress Paeoniae Radix Rubra

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Müller cells are activated in response to retinal outer nuclear layer degeneration in rats subjected to simulated weightlessness conditions

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Neural Regeneration Research 2025年第7期20卷 2116-2128页

作者： Yuxue Mu Ning Zhang Dongyu Wei Guoqing Yang Lilingxuan Yao Xinyue Xu Yang Li Junhui Xue Zuoming Zhang Tao Chen Aerospace Clinical Medical Center School of Aerospace MedicineAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Aviation Medicine Xijing HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Emergency Medicine Wuhan No.1 HospitalWuhanHubei ProvinceChina Third Regiment School of Basic MedicineAir Force Medical UniversityXi’anShaanxi ProvinceChina Fourth Regiment School of Basic MedicineAir Force Medical UniversityXi’anShaanxi ProvinceChina

A microgravity environment has been shown to cause ocular damage and affect visual acuity,but the underlying mechanisms remain ***,we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under *** 4 weeks of tail suspension,there were no notable alterations in retinal function and morphology,while after 8 weeks of tail suspension,significant reductions in retinal function were observed,and the outer nuclear layer was thinner,with abundant apoptotic *** investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina,proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail *** results showed that the expression levels of fibroblast growth factor 2(also known as basic fibroblast growth factor)and glial fibrillary acidic protein,which are closely related to Müller cell activation,were significantly *** addition,Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks,respectively,of simulated *** findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.

关键词： glial fibrous acidic protein gliosis Müller cells nerve growth factor neural differentiation neurodegeneration proteomic retinal degeneration retinal outer nuclear layer simulated weightlessness

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Neuroimaging of inflammation in alcohol use disorder: a review

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Science China(Information Sciences) 2020年第7期63卷 19-37页

作者： Dana E.FELDMAN Katherine L.MCPHERSON Catherine L.BIESECKER Corinde E.WIERS Peter MANZA Nora D.VOLKOW Gene-Jack WANG National Institute on Alcohol Abuse and Alcoholism National Institute on Drug Abuse

Alcohol use disorder(AUD) is a global health concern associated with several *** health problems related to AUD, such as cognitive deficits, have been linked to *** use has been associated with changes in neuroimmune activity, although current literature has yielded mixed results. For example, markers of gliosis, including translocator protein 18-kDa(TSPO), proinflammatory cytokines, glutamate(Glu), and myo-inositol(mI), are disrupted in the alcohol-dependent brain. Further, neuroinflammatory-related phenomena including membrane turnover, blood brain barrier(BBB) permeability, and adenosine release have also shown alterations in AUD. However, current literature remains inconclusive about the directionality of these changes. Both in vivo and in vitro studies have provided insight on the relationship between alcohol use and neuroinflammatory processes, suggesting considerable treatment potential for alcohol use disorder and its inflammatory comorbidities. Here, we review current neuroimaging literature assessing the impacts of alcohol use on neuroimmune activity in the brain.

关键词： acetate adenosine alcohol use disorder blood brain barrier choline gliosis glutamate myoinositol neuroimaging neuroinflammation

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Neurovascular unit in diabetic retinopathy:pathophysiological roles and potential therapeutical targets

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Eye and Vision 2021年第3期8卷 135-153页

作者： Shen Nian Amy C.Y.Lo Yajing Mi Kai Ren Di Yang Department of Pathology Xi’an Medical UniversityXi’anShaanxi ProvinceChina Department of Ophthalmology LKS Faculty of MedicineThe University of Hong KongHong KongHong Kong Institute of Basic Medicine Science Xi’an Medical UniversityXi’anShaanxi ProvinceChina Department of Biochemistry and Molecular Biology Xi’an Medical UniversityXi’anShaanxi ProvinceChina Department of Ophthalmology First Affiliated Hospital of Kunming Medical UniversityKunming Medical UniversityKunmingYunnan ProvinceChina

Diabetic retinopathy(DR),one of the common complications of diabetes,is the leading cause of visual loss in working-age individuals in many industrialized *** has been traditionally regarded as a purely microvascular disease in the ***,an increasing number of studies have shown that DR is a complex neurovascular disorder that affects not only vascular structure but also neural tissue of the *** of neural retina could precede microvascular abnormalities in the DR,leading to microvascular ***,disruption of interactions among neurons,vascular cells,glia and local immune cells,which collectively form the neurovascular unit,is considered to be associated with the progression of DR early on in the ***,it makes sense to develop new therapeutic strategies to prevent or reverse retinal neurodegeneration,neuroinflammation and impaired cell-cell interactions of the neurovascular unit in early stage ***,we present current perspectives on the pathophysiology of DR as a neurovascular disease,especially at the early *** novel treatments for preventing or reversing neurovascular injuries in DR are discussed as well.

关键词： Diabetic retinopathy Neurovascular unit Neurodegeneration gliosis Inflammation treatment

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Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

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Neural Regeneration Research 2017年第12期12卷 2007-2013页

作者： Hyun-Jin Tae Il Jun Kang Tae-Kyeong Lee Jeong Hwi Cho Jae-Chul Lee Myoung Cheol Shin Yoon Sung Kim Jun Hwi Cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah Lee Yang Hee Kim Moo-Ho Won Young Joo Lee Bio-Safety Research Institute College of Veterinary Medicine Chonbuk National University Iksan South Korea Department of Food Science and Nutrition Hallym University Chuncheon South Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Samcheok Medical Center Samcheok South Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon South Korea Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon South Korea Department of Obstetrics and Gynecology School of Medicine Kangwon National University Chuncheon South Korea Department of Surgery School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Seoul South Korea

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

关键词： nerve regeneration post-cardiac arrest syndrome normothermia neuronal damage gliosis tumor necrosis factor-alpha neural regeneration

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Amelioration of Alzheimer's disease pathology and cognitive deficits by immunomodulatory agents in animal models of Alzheimer's disease

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Neural Regeneration Research 2019年第7期14卷 1158-1176页

作者： Bridget Martinez Philip V.Peplow Department of Molecular & Cellular Biology University of California Department of Medicine St.Georges University School of Medicine Department of Physics and Engineering Los Alamos National Laboratory Department of Anatomy University of Otago

The most common age-related neurodegenerative disease is Alzheimer's disease(AD) characterized by aggregated amyloid-β(Aβ) peptides in extracellular plaques and aggregated hyperphosphorylated tau protein in intraneuronal neurofibrillary tangles,together with loss of cholinergic neurons,synaptic alterations,and chronic inflammation within the *** lead to progressive impairment of cognitive *** is evidence of innate immune activation in AD with ***-activated microglia(M1 state) secrete inflammatory and neurotoxic mediators,and peripheral immune cells are recruited to inflammation sites in the *** few drugs approved by the US FDA for the treatment of AD improve symptoms but do not change the course of disease progression and may cause some undesirable *** of active and passive immunotherapy targeting Aβ in AD animal model trials had limited success in clinical *** with immunomodulatory/anti-inflammatory agents early in the disease process,while not preventive,is able to inhibit the inflammatory consequences of both Aβ and tau *** studies described in this review have identified several agents with immunomodulatory properties that alleviated AD pathology and cognitive impairment in animal models of *** majority of the animal studies reviewed had used transgenic models of early-onset *** effort needs to be given to creat models of late-onset *** effects of a combinational therapy involving two or more of the tested pharmaceutical agents,or one of these agents given in conjunction with one of the cell-based therapies,in an aged animal model of AD would warrant investigation.

关键词： Alzheimer’s disease neuropathology cognitive deficits behavioral deficits immunomodulatory agents animal models amyloid deposits gliosis

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Epidural electrical stimulation for spinal cord injury

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Neural Regeneration Research 2021年第12期16卷 2367-2375页

作者： Elliot H.Choi Sandra Gattas Nolan J.Brown John D.Hong Joshua N.Limbo Alvin Y.Chan Michael Y.Oh Department of Pharmacology School of MedicineCase Western Reserve UniversityClevelandOHUSA Department of Ophthalmology Gavin Herbert Eye InstituteSchool of MedicineUniversity of CaliforniaIrvineCAUSA Department of Neurosurgery University of CaliforniaIrvineCAUSA

A long-standing goal of spinal cord injury research is to develop effective repair strategies,which can restore motor and sensory functions to near-normal *** advances in clinical management of spinal cord injury have significantly improved the prognosis,survival rate and quality of life in patients with spinal cord *** addition,a significant progress in basic science research has unraveled the underlying cellular and molecular events of spinal cord *** efforts enabled the development of pharmacologic agents,biomaterials and stem-cell based *** these efforts,there is still no standard care to regenerate axons or restore function of silent axons in the injured spinal *** challenges led to an increased focus on another therapeutic approach,namely *** multiple animal models of spinal cord injury,epidural electrical stimulation of the spinal cord has demonstrated a recovery of motor *** evidence regarding the efficacy of epidural electrical stimulation has further expanded the potential of epidural electrical stimulation for treating patients with spinal cord ***,most clinical studies were conducted on a very small number of patients with a wide range of spinal cord ***,subsequent studies are essential to evaluate the therapeutic potential of epidural electrical stimulation for spinal cord injury and to optimize stimulation ***,we discuss cellular and molecular events that continue to damage the injured spinal cord and impede neurological recovery following spinal cord *** also discuss and summarize the animal and human studies that evaluated epidural electrical stimulation in spinal cord injury.

关键词： central nervous system chondroitin sulfate proteoglycans epidural electrical stimulation glial scar gliosis neural activity neuromodulation oligodendrocyte spinal cord injury

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Retinal regeneration requires dynamic Notch signaling

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Neural Regeneration Research 2022年第6期17卷 1199-1209页

作者： Leah J.Campbell Jaclyn L.Levendusky Shannon A.Steines David R.Hyde Department of Biological Sciences Center for Zebrafish ResearchCenter for Stem Cells and Regenerative MedicineUniversity of Notre DameNotre DameINUSA

Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal *** signaling,which is a fundamental mechanism known to drive cell-cell communication,is required to maintain Müller glia in a quiescent state in the undamaged retina,and repression of Notch signaling is necessary for Müller glia to reenter the cell *** dynamic regulation of Notch signaling following retinal damage also directs proliferation and neurogenesis of the Müller glia-derived progenitor cells in a robust regeneration *** contrast,mammalian Müller glia respond to retinal damage by entering a prolonged gliotic state that leads to additional neuronal death and permanent vision *** the dynamic regulation of Notch signaling in the zebrafish retina may aid efforts to stimulate Müller glia reprogramming for regeneration of the diseased human *** findings identified DeltaB and Notch3 as the ligand-receptor pair that serves as the principal regulators of zebrafish Müller glia *** addition,multi-omics datasets and functional studies indicate that additional Notch receptors,ligands,and target genes regulate cell proliferation and neurogenesis during the regeneration time ***,our understanding of Notch signaling during retinal regeneration is *** fully appreciate the complex regulation of Notch signaling that is required for successful retinal regeneration,investigation of additional aspects of the pathway,such as post-translational modification of the receptors,ligand endocytosis,and interactions with other fundamental pathways is *** we review various modes of Notch signaling regulation in the context of the vertebrate retina to put recent research in perspective and to identify open areas of inquiry.

关键词： differentiation gliosis Müller glia neuronal progenitor cell Notch signaling proliferation quiescence retinal development retinal regeneration zebrafish

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Targeting tau in Alzheimer's disease:from mechanisms to clinical therapy

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Neural Regeneration Research 2024年第7期19卷 1489-1498页

作者： Jinwang Ye Huali Wan Sihua Chen Gong-Ping Liu Shenzhen Key Laboratory of Marine Biotechnology and Ecology College of Life Sciences and OceanographyShenzhen UniversityShenzhenGuangdong ProvinceChina Department of Laboratory Medicine Guangdong Provincial People’s Hospital(Guangdong Academy of Medical Sciences)Southern Medical UniversityGuangzhouGuangdong ProvinceChina Co-innovation Center of Neurodegeneration Nantong UniversityNantongJiangsu ProvinceChina Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina

Alzheimer’s disease is the most prevalent neurodegenerative disease affecting older *** features of Alzheimer’s disease include extra cellular aggregation of amyloid-βplaques and the accumulation of neurofibrillary tangles,fo rmed by tau protein,in the *** there are amyloid-β-ta rgeting therapies for the treatment of Alzheimer’s disease,these therapies are costly and exhibit potential negative side *** evidence suggests significant involvement of tau protein in Alzheimer’s disease-related *** an important microtubule-associated protein,tau plays an important role in maintaining the stability of neuronal microtubules and promoting axonal *** fact,clinical studies have shown that abnormal phosphorylation of tau protein occurs before accumulation of amyloid-βin the *** therapeutic strategies targeting tau protein have begun to emerge,and are considered possible methods to prevent and treat Alzheimer’s ***,abnormalities in post-translational modifications of the tau protein,including aberrant phosphorylation,ubiquitination,small ubiquitin-like modifier(SUMO)ylation,acetylation,and truncation,contribute to its microtubule dissociation,misfolding,and subcellular *** causes mitochondrial damage,synaptic impairments,gliosis,and neuroinflammation,eventually leading to neurodegeneration and cognitive *** review summarizes the recent findings on the underlying mechanisms of tau protein in the onset and progression of Alzheimer’s disease and discusses tau-targeted treatment of Alzheimer’s disease.

关键词： acetylation Alzheimer’s disease cognitive deficits gliosis mitochondria damage neuroinflammation phosphorylation synaptic impairments tau tau immunotherapy

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