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Human-induced pluripotent stem cell-derived neural stem cell exosomes improve blood-brain barrier function after intracerebral hemorrhage by activating astrocytes via PI3K/AKT/MCP-1 axis

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Neural Regeneration Research 2025年第2期20卷 518-532页

作者： Conglin Wang Fangyuan Cheng Zhaoli Han Bo Yan Pan Liao Zhenyu Yin Xintong Ge Dai Li Rongrong Zhong Qiang Liu Fanglian Chen Ping Lei Department of Geriatrics Tianjin Medical University General HospitalTianjinChina School of Medicine Nankai UniversityTianjinChina Tianjin Neurological Institute TianjinChina

Cerebral edema caused by blood-brain barrier injury after intracerebral hemorrhage is an important factor leading to poor ***-induced pluripotent stem cell-derived neural stem cell exosomes(hiPSC-NSC-Exos)have shown potential for brain injury repair in central nervous system *** this study,we explored the impact of hiPSC-NSC-Exos on blood-brain barrier preservation and the underlying *** results indicated that intranasal delivery of hiPSC-NSC-Exos mitigated neurological deficits,enhanced blood-brain barrier integrity,and reduced leukocyte infiltration in a mouse model of intracerebral ***,hiPSC-NSC-Exos decreased immune cell infiltration,activated astrocytes,and decreased the secretion of inflammatory cytokines like monocyte chemoattractant protein-1,macrophage inflammatory protein-1α,and tumor necrosis factor-αpost-intracerebral hemorrhage,thereby improving the inflammatory *** sequencing indicated that hiPSC-NSC-Exo activated the PI3K/AKT signaling pathway in astrocytes and decreased monocyte chemoattractant protein-1 secretion,thereby improving blood-brain barrier *** with the PI3K/AKT inhibitor LY294002 or the monocyte chemoattractant protein-1 neutralizing agent C1142 abolished these *** summary,our findings suggest that hiPSC-NSC-Exos maintains blood-brain barrier integrity,in part by downregulating monocyte chemoattractant protein-1 secretion through activation of the PI3K/AKT signaling pathway in astrocytes.

关键词： AKT astrocyte blood-brain barrier cerebral edema exosomes human-induced pluripotent stem cells intracerebral hemorrhage neural stem cells neuroinflammation PI3K

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Cholesterol metabolism: physiological versus pathological aspects in intracerebral hemorrhage

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Neural Regeneration Research 2025年第4期20卷 1015-1030页

作者： Ruoyu Huang Qiuyu Pang Lexin Zheng Jiaxi Lin Hanxi Li Lingbo Wan Tao Wang Department of Forensic Science School of Basic Medicine and Biological SciencesSuzhou Medicine College of Soochow UniversitySuzhouJiangsu ProvinceChina

Cholesterol is an important component of plasma membranes and participates in many basic life functions,such as the maintenance of cell membrane stability,the synthesis of steroid hormones,and *** plays a key role in the establishment and maintenance of the central nervous *** brain contains 20%of the whole body’s cholesterol,80%of which is located within myelin.A huge number of processes(e.g.,the sterol regulatory element-binding protein pathway and liver X receptor pathway)participate in the regulation of cholesterol metabolism in the brain via mechanisms that include cholesterol biosynthesis,intracellular transport,and *** brain injuries or diseases involving crosstalk among the processes above can affect normal cholesterol metabolism to induce detrimental ***,we hypothesized that cholesterol-related molecules and pathways can serve as therapeutic targets for central nervous system *** hemorrhage is the most severe hemorrhagic stroke subtype,with high mortality and *** cholesterol levels are associated with the risk of intracerebral ***,secondary pathological changes after intracerebral hemorrhage are associated with cholesterol metabolism dysregulation,such as neuroinflammation,demyelination,and multiple types of programmed cell *** cholesterol accumulation in the brain has been found after intracerebral *** this paper,we review normal cholesterol metabolism in the central nervous system,the mechanisms known to participate in the disturbance of cholesterol metabolism after intracerebral hemorrhage,and the links between cholesterol metabolism and cell *** also review several possible and constructive therapeutic targets identified based on cholesterol metabolism to provide cholesterol-based perspectives and a reference for those interested in the treatment of intracerebral hemorrhage.

关键词： cell death cholesterol metabolism intracerebral hemorrhage myelination therapeutic target

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Biocompatible custom ceria nanoparticles against reactive oxygen species resolve acute inflammatory reaction after intracerebral hemorrhage

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Nano Research 2017年第8期10卷 2743-2760页

作者： Dong-Wan Kang Chi Kyung Kim Han-Gil Jeong Min Soh Taeho Kim In-Young Choi SeuI-Ki Ki Do Yeon Kim Wookjin Yang Taeghwan Hyeon Seung-Hoon Lee Laboratory of Innovative Nanobiotechnology Biomedical Research Institute Seoul National University Hospital Seoul 03080 Republic of Korea Department of Neurology Seoul National University Hospital Seou103080 Republic of Korea Department of Neurology Korea University Guro Hospital and Korea University College of Medicine Seou108308 Republic of Korea Center for Nanoparticle Research Institute for Basic Science (IBS) Seoul 151-742 Republic of Korea School of Chemical and Biological Engineering and Institute of Chemical Processes Seoul National University Seoul 151-742 Republic of Korea

intracerebral hemorrhage （ICH） is a devastating subtype of stroke with a high mortality rate, for which there currently is no effective treatment. A perihematomal edema caused by an intense inflammatory reaction is more deleterious than the hematoma itself and can result in neurological deterioration and death. Ceria nanoparticles （CeNPs） are potent free radical scavengers with potential for biomedical applications. As oxidative stress plays a major role in post-ICH inflammation, we hypothesized that CeNPs might protect against ICH. To test this hypothesis, core CeNPs were synthesized using a modified reverse micelle method and covered with phospholipid-polyethylene glycol （PEG） to achieve biocompatibility. We investigated whether our custom-made biocompatible CeNPs have protective effects against ICH. The CeNPs reduced oxidative stress, hemin-induced cytotoxicity, and inflammation in vitro. In a rodent ICH model, intravenously administered CeNPs were mainly distributed in the hemorrhagic hemisphere, suggesting that they could diffuse through the damaged blood-brain barrier. Moreover, CeNPs attenuated microglia/macrophage recruitment around the hemorrhagic lesion and inflammatory protein expression. Finally, CeNP treatment reduced the brain edema by 68.4% as compared to the control. These results reveal the great potential of CeNPs as a novel therapeutic agent for patients with ICH.

关键词： ceria nanoparticles intracerebral hemorrhage free radical injury anti-inflammation neuroprotective agents biomedical application

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Customized lipid-coated magnetic mesoporous silica nanoparticle doped with ceria nanoparticles for theragnosis of intracerebral hemorrhage

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Nano Research 2018年第7期11卷 3582-3592页

作者： Bong Geun Cha Han-Gil Jeong Dong-Wan Kang Myong-Joo Nam Chi Kyung Kim Do Yeon Kim In-Young Choi Seul Ki Ki Song I Kim Ju hee Han Jaeyun Kim Seung-Hoon Lee School of Chemical Engineering Sungkyunkwan University Suwon 16419 Republic of Korea Department of Laboratory of Innovative Nanobiotechnology Biomedical Research Institute Seoul National University Hospital 101 Daehak-ra Jongno-gu Seou103080 Republic of Korea Department of Neurology Seoul National University Hospital 101 Daehak-ro Jongno-gu Seou103080 Republic of Korea Department of Neurology Korea University Guro Hospital and Korea University College of Medicine Seoul 08308 Republic of Korea Department of Health Sdences and Technology Samsung Advanced Institute for Health Science & Technology (SAIHST) Sungkyunkwan University Suwon 16419 Republic of Korea Biomedical Institute for Convergence at SKKU (BICS) Sungkyunkwan University Suwon 16419 Republic of Korea

intracerebral hemorrhage （ICH）, caused by the sudden rupture of an artery within the brain, is a devastating subtype of stroke, which currently has no effective treatment. Intense inflammatory reactions that occur in the peri-hematomal area after ICH are more deleterious than the hematoma itself, resulting in subsequent brain edema and neurologic deterioration. Thus, we developed lipid-coated magnetic mesoporous silica nanoparticles doped with ceria nanoparticles （CeNPs）, abbreviated as LMCs, which have both potent anti-inflammatory therapeutic effects via scavenging reactive oxygen species and help in increasing the efficacy of magnetic resonance imaging enhancement in the peri-hematomal area. LMCs consist of mesoporous silica nanopartide-supported lipid bilayers, which are loaded with large amounts of CeNPs for scavenging of reactive oxygen species, and iron oxide nanoparticles for magnetic resonance imaging contrast. LMCs loaded with CeNPs exhibited strong anti-oxidative and anti-inflammatory activities in vitro. In the rodent ICH model, intracerebraUy injected LMCs reached the peri-hematomal area and were engulfed by macrophages, which were clearly visualized by magnetic resonance imaging of the brain. Moreover, LMCs reduced inflammatory macrophage infiltration, and thus significantly reduced brain edema. Finally, LMC treatment markedly improved neurologic outcomes of the animals with ICH. Thus, LMC is the first nanobiomaterial that successfully showed theragnostic effects in ICH.

关键词： magnetic mesoporous silica nanoparticle ceria nanoparticles intracerebral hemorrhage reactive oxygen species therapeutics imaging

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Mitophagy in intracerebral hemorrhage:a new target for therapeutic intervention

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Neural Regeneration Research 2024年第2期19卷 316-323页

作者： Yiyang Chen Wenxuan Tang Xinqi Huang Yumei An Jiawen Li Shengye Yuan Haiyan Shan Mingyang Zhang Institute of Forensic Sciences Suzhou Medical CollegeSoochow UniversitySuzhouJiangsu ProvinceChina Shanghai Key Lab of Forensic Medicine Key Lab of Forensic ScienceMinistry of Justice(Academy of Forensic Science)ShanghaiChina Department of Obstetrics and Gynecology The Affiliated Suzhou Hospital of Nanjing Medical UniversitySuzhouJiangsu ProvinceChina

intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe ***,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke *** studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral ***,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged *** markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral *** review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral *** conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.

关键词： intracerebral hemorrhage mitochondrial dysfunction mitophagy neuroinflammation neuroprotection reactive oxygen species secondary brain injury therapeutic target

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Acute hyperglycemia together with hematoma of high-glucose blood exacerbates neurological injury in a rat model of intracerebral hemorrhage

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Neuroscience Bulletin 2014年第1期30卷 90-98页

作者： Rong-Yi Liu Jun-Jun Wang Xia Qiu Ji-Min Wu Department of Neurology Second Affiliated Hospital College of Medicine Zhejiang University Department of Neurology Zhejiang Hospital

Recent evidence suggests that admission hypergly- cemia has deleterious effects on the survival and functional outcome of patients with intracerebral hemorrhage （ICH）. In this study, we first induced acute hyperglycemia in male adult Sprague-Dawley rats by intraperitoneal injection of 50% glucose （6 mL/kg）, and created the ICH model thereafter by delivering autologous whole blood or homologous normal- glucose blood into the right basal ganglia. Twenty- four hours later, we assessed the neurological injury, evaluated the hematoma and brain water content, and investigated autophagy. We found elevations of neurological deficit scores, brain water content, and microtubule-associated protein light chain-3 （LC3） and beclin-1 protein levels, and decreased SQSTM1/ p62 levels after ICH with normal-glucose blood （without hyperglycemia）. Acute hyperglycemia with ICH of high-glucose blood hematoma was associated with significantly increased forelimb-use asymmetry test scores, brain water content and SQSTM1/p62 protein levels, and evident decreases in the ratio of LC3-11/LC3-1 and beclin-1 protein levels. On the other hand, acute hyperglycemia and ICH with normal- glucose blood hematoma only slightly increased the neurological deficit scores and brain water content （P 〉0.05）. In conclusion, the autophagy pathway was activated after ICH, and acute hyperglycemia with hematoma of high-glucose blood exacerbates the neurological injury, and reduces autophagy around the hematoma.

关键词： intracerebral hemorrhage hyperglycemia autophagy

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Fingolimod alters inflammatory mediators and vascular permeability in intracerebral hemorrhage

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Neuroscience Bulletin 2015年第6期31卷 755-762页

作者： Yu-Jing Li Guo-Qiang Chang Yuanchu Liu Ye Gong Chunsheng Yang Kristofer Wood Fu-Dong Shi Ying Fu Yaping Yan Department of Neurology Tianjin Neurological InstituteTianjin Medical University General Hospital Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest ChinaCollege of Life SciencesShaanxi Normal University Department of Neurology Barrow Neurological InstituteSt. Joseph's Hospital and Medical Center

intracerebral hemorrhage （ICH） leads to high rates of death and disability. The pronounced inflammatory reactions that rapidly follow ICH contribute to disease progression. Our recent clinical trial demonstrated that oral administration of an immune modulator fingolimod restrained secondary injury derived from initial hematoma, but the mechanisms remain unknown. In this study, we aim to investigate the effects of fingolimod on inflammatory mediators and vascular permeability in the clinical trial of oral fingolimod for intracerebral hemorrhage （ICH）. The results showed that fingolimod decreased the numbers of circulating CD4~ T, CD8~ T, CD19~ B, NK, and NKT cells and they recovered quickly after the drug＇ was stopped. The plasma ICAM level was decreased and IL-10 was increased by fingolimod. Interestingly, fingolimod protected vascular permeability as indicated by a decreased plasma level of MMP9 and the reduced rT1%. In conclusion, modulation of systemic inflammation by fingolimod demonstrates that it is an effective therapeutic agent for ICH. Fingolimod may prevent perihematomal edema enlargement by protecting vascular permeability.

关键词： fingolimod inflammatory mediator vascular permeability intracerebral hemorrhage

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Ion Channel Dysregulation Following intracerebral hemorrhage

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Neuroscience Bulletin 2024年第3期40卷 401-414页

作者： Xiangyu Zhang Yan Zhang Qiuyang Su Yang Liu Zhe Li V.Wee Yong Mengzhou Xue Department of Cerebrovascular Diseases The Second Afliated Hospital of Zhengzhou UniversityZhengzhou 450000China Academy of Medical Science Zhengzhou UniversityZhengzhou 450000China Hotchkiss Brain Institute and Department of Clinical Neurosciences University of CalgaryCalgaryAB T2N 1N4Canada

Injury to the brain after intracerebral hemorrhage(ICH)results from numerous complex cellular *** present,effective therapy for ICH is limited and a better understanding of the mechanisms of brain injury is necessary to improve *** is increasing evidence that ion channel dysregulation occurs at multiple stages in primary and secondary brain injury following *** channels such as TWIK-related K+channel 1,sulfonylurea 1 transient receptor potential melastatin 4 and glutamate-gated channels affect ion homeostasis in *** in turn participate in the formation of brain edema,disruption of the blood-brain barrier,and the generation of *** this review,we summarize the interaction between ions and ion channels,the effects of ion channel dysregulation,and we discuss some therapeutics based on ion-channel modulation following ICH.

关键词： intracerebral hemorrhage Ion dyshomeostasis Sulfonylurea 1 transient receptor potential melastatin 4 TWIK-related K+channel 1 N-methyl-Daspartate receptor Transient receptor potential vanilloid 4

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Combined Transplantation of Neural Stem Cells and Olfactory Ensheathing Cells Improves the Motor Function of Rats with intracerebral hemorrhage

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Biomedical and Environmental Sciences 2010年第1期23卷 62-67页

作者： ZHOU-PING TANG XUE-WEI XIE YUAN-HONG SHI NA LIU SuI-QIANG ZHU ZAI-WANG LI YUN CHEN Department of Neurology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei China

Objective To investigate the effects of combined transplantation of neural stem cells （NSC） and olfactory ensheathing cells （OEC） on the motor function of rats with intracerebral hemorrhage. Methods In three days after a rat model of caudate nucleus hemorrhage was established, NSCs and OEC, NSC, OEC （from embryos of Wistar rats） or normal saline were injected into bematomas of rats in combined transplantation group, NSC group, OEC group, and control group, respectively. Damage of neural function was scored before and in 3, 7, 14, 30 days after operation. Tissue after transplantation was observed by immunocytochemistry staining. Results The scores for the NSC, OEC and co-transplantation groups were significantly lower in 14 and 30 days after operation than in 3 days after operation （P〈0.05）. The scores for the NSC and OEC groups were significantly lower than those for the control group only in 30 days after operation （P〈0.05）, while the difference for the NSC-OEC group was significant in 14 days after operation （P〈0.05）. Immunocytochemistry staining revealed that the transplanted OEC and NSC could survive, migrate and differentiate into neurons, astrocytes, and oligodendrocytes. The number of neural precursor cells was greater in the NSC and combined transplantation groups than in the control group. The number of neurons differentiated from NSC was significantly greater in the co-transplantation group than in the NSC group. Conclusion Co-transplantation of NSC and OEC can promote the repair of injured tissue and improve the motor fimction of rats with intracerebral hemorrhage.

关键词： Stem cell Olfactory bulb Cell transplantation intracerebral hemorrhage Motor function

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Pharmacological Activation of RXR-a Promotes Hematoma Absorption via a PPAR-y-dependent Pathway After intracerebral hemorrhage

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Neuroscience Bulletin 2021年第10期37卷 1412-1426页

作者： Chaoran Xu Huaijun Chen Shengjun Zhou Chenjun Sun Xiaolong Xia Yucong Peng Jianfeng Zhuang Xiongjie Fu Hanhai Zeng Hang Zhou Yang Cao Qian Yu Yin Li Libin Hu Guoyang Zhou Feng Yan Gao Chen Jianru Li Department of Neurosurgery The Second Affiliated Hospital of Zhejiang University School of MedicineHangzhou 310052China

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage(ICH).This study sought to determine the role of retinoid X receptor-ot(RXR-a)in the context of hematoma absorption after *** results showed that pharmacologically activating RXR-a with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ***-ot was expressed in microglia/macro-phages,neurons,and ***,bexarotene promoted the nuclear translocation of RXR-a and PPAR-y,as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the Ml into the M2 ***,all the beneficial effects of RXR-a in ICH were reversed by the PPAR-y inhibitor *** conclusion,the pharmacological activation of RXR-a confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-y-related *** data support the notion that RXR-ot might be a promising therapeutic target for ICH.

关键词： intracerebral hemorrhage RXR-a PPAR-y Polarization Phagocytosis Neuroinflammation

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