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Astrocytic endothelin-1 overexpression impairs learning and memory ability in ischemic stroke via altered hippocampal neurogenesis and lipid metabolism

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Neural Regeneration Research 2024年第3期19卷 650-656页

作者： Jie Li Wen Jiang Yuefang Cai Zhenqiu Ning Yingying Zhou Chengyi Wang sookja Ki chung Yan Huang Jingbo Sun Minzhen Deng Lihua Zhou Xiao Cheng Guangzhou University of Traditional Chinese Medicine GuangzhouGuangdong ProvinceChina State Key Laboratory of Dampness Syndrome of Chinese Medicine The Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhouGuangdong ProvinceChina Guangdong Provincial Key Laboratory of Research on Emergency in TCM GuangzhouGuangdong ProvinceChina Department of Anesthesiology West China HospitalSichuan UniversityChengduSichuan ProvinceChina Department of Anatomy Sun Yat-Sen School of MedicineSun Yat-Sen UniversityShenzhenGuangdong ProvinceChina Faculty of Medicine Macao University of Science and TechnologyMacao Special Administration RegionChina

Vascular etiology is the second most prevalent cause of cognitive impairment ***-1,which is produced and secreted by endothelial cells and astrocytes,is implicated in the pathogenesis of ***,the way in which changes in astrocytic endothelin-1 lead to poststroke cognitive deficits following transient middle cerebral artery occlusion is not well ***,using mice in which astrocytic endothelin-1 was overexpressed,we found that the selective overexpression of endothelin-1 by astrocytic cells led to ischemic stroke-related dementia(1 hour of ischemia;7 days,28 days,or 3 months of reperfusion).We also revealed that astrocytic endothelin-1 overexpression contributed to the role of neural stem cell proliferation but impaired neurogenesis in the dentate gyrus of the hippocampus after middle cerebral artery *** proteome profiles and western blot analysis confirmed that levels of glial fibrillary acidic protein and peroxiredoxin 6,which were differentially expressed in the brain,were significantly increased in mice with astrocytic endothelin-1 overexpression in comparison with wild-type mice 28 days after ischemic ***,the levels of the enriched differentially expressed proteins were closely related to lipid metabolism,as indicated by Kyoto Encyclopedia of Genes and Genomes pathway *** chromatography-mass spectrometry nontargeted metabolite profiling of brain tissues showed that astrocytic endothelin-1 overexpression altered lipid metabolism products such as glycerol phosphatidylcholine,sphingomyelin,and phosphatidic ***,this study demonstrates that astrocytic endothelin-1 overexpression can impair hippocampal neurogenesis and that it is correlated with lipid metabolism in poststroke cognitive dysfunction.

关键词： astrocytic endothelin-1 dentate gyrus differentially expressed proteins hippocampus ischemic stroke learning and memory deficits lipid metabolism neural stem cells neurogenesis proliferation

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壮通饮通过Nrf2-SCL7A11/xCT-Gpx4通路调控铁死亡改善脑缺血再灌注损伤

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中山大学学报（医学科学版） 2024年第4期45卷 539-548页

作者：王成毅蔡粤芳宁振求邓敏贞孙景波 sookja kim.chung 李岩程骁广州中医药大学第二临床医学院广东广州510006 深圳市人民医院、南方科技大学第一附属医院、暨南大学第二临床医学院广东深圳518020 省部共建中医湿证国家重点实验室广东广州510120 广东省中医急症研究重点实验室广东广州510120 澳门科技大学医学院中国澳门999078 广西国际壮医医院广西南宁530201

【目的】探究壮通饮通过Nrf2-SCL7A11/xCT-Gpx4通路调控铁死亡对大脑中动脉栓塞模型小鼠脑缺血再灌注损伤的保护作用及其机制。【方法】将C57BL/6J小鼠随机分为假手术组(Sham)、模型组(MCAO)、低剂量壮通饮组(ZTY-L+MCAO),高剂量壮通饮... 详细信息

【目的】探究壮通饮通过Nrf2-SCL7A11/xCT-Gpx4通路调控铁死亡对大脑中动脉栓塞模型小鼠脑缺血再灌注损伤的保护作用及其机制。【方法】将C57BL/6J小鼠随机分为假手术组(Sham)、模型组(MCAO)、低剂量壮通饮组(ZTY-L+MCAO),高剂量壮通饮组(ZTY-H+MCAO),每组5只。其中MCAO组采用硅胶线栓法进行造模,小鼠大脑中动脉栓塞1h,拔出线栓再灌注72h后进行心脏灌注取脑,Sham组除了不插入线栓其余操作同MCAO组。采用Zea-Longa法对小鼠神经功能进行评分;采用TTC染色评估小鼠脑梗死体积;采用HE染色、尼氏染色评估脑损伤程度;采用普鲁士蓝染色评价三价铁离子蓄积水平;qPCR检测铁离子转运相关载体受体TfR1和DMT1、脂质过氧化相关基因ACSL4以及铁死亡标志物PTGS2 mRNA表达;ELISA试剂盒检测4-HNE的含量评估小鼠大脑脂质过氧化水平;Western-blot、免疫荧光检测小鼠脑组织中Nrf2、SCL7A11/xCT、Gpx4蛋白水平。【结果】①壮通饮改善了MCAO/R后小鼠神经功能(P<0.05)和大脑梗死体积(P<0.05)及缓解MCAO/R后大脑皮层细胞病理损伤。②壮通饮减弱了MCAO/R后小鼠大脑组织的三价铁离子蓄积状态;减少MCAO/R后小鼠大脑中与铁离子转运入细胞内相关载体TfR1和DMT1 mRNA的表达(P<0.001);下调MCAO/R后小鼠大脑脂质过氧化物4-HNE含量和组织脂质过氧化物酶ACSL4 mRNA表达(P<0.001);降低MCAO/R后小鼠大脑铁死亡标志物PTGS2 mRNA表达(P<0.001)。③壮通饮增加MCAO/R后Nrf2入核表达(P<0.001),以及增加xCT和Gpx4在神经元中的表达(P<0.001)。【结论】壮通饮能够改善MCAO/R小鼠神经功能和脑梗死体积,缓解大脑皮层细胞病理损伤,影响Nrf2-SCL7A11/xCT-Gpx4通路关键信号分子表达,所以壮通饮改善小鼠MCAO/R损伤的作用机制可能是通过Nrf2-SCL7A11/xCT-Gpx4通路调节铁死亡水平达到的。

关键词：缺血性脑卒中铁死亡壮通饮 Nrf2-SCL7A11/xCT-Gpx4通路机制研究

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Lycium barbarum polysaccharides related RAGE and Aβ levels in the retina of mice with acute ocular hypertension and promote maintenance of blood retinal barrier

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Neural Regeneration Research 2020年第12期15卷 2344-2352页

作者： Xue-Song Mi Qian Feng Amy Cheuk Yin Lo Raymond Chuen-chung Chang sookja kim.chung Kwok-Fai So Department of Ophthalmology the First Affiliated Hospital of Jinan UniversityGuangzhouGuangdong ProvinceChina Guangdong-Hong Kong-Macao Institute of CNS Regeneration Jinan UniversityGuangzhouGuangdong ProvinceChina Changsha Academician Expert Workstation Aier Eye Hospital GroupChangshaHunan ProvinceChina State Key Laboratory of Brain and Cognitive Sciences Hong Kong Special Administrative RegionChina Department of Ophthalmology The University of Hong KongHong Kong Special Administrative RegionChina Faculty of Medicine Macao University of Science and TechnologyMacao Special Administrative RegionChina School of Biomedical Science LKS Faculty of MedicineThe University of Hong KongHong Kong Special Administrative RegionChina

Our previous study verified the protective effects of Lycium barbarum polysaccharides(LBP)on retinal neurons and blood vessels in acute ocular hypertension(AOH)*** investigate the effect of LBP on the reactivity of retinal glial cells,an AOH mouse model was established in one eye by maintaining ocular hypertension of 90 mm Hg for 60 *** LBP solution(1 mg/kg)or phosphate-buffered saline was administrated to the mice by gavage daily,starting 7 days before the AOH insult and continuing until the mice were sacrificed for specimen collection on day 4 *** AOH insult,increased numbers of astrocytes and microglia were observed,together with decreased expression of the following glial cell biomarkers in the retinal ganglion cells of AOH mice:glial fibrillary acidic protein,glutamine synthetase,aquaporin-4,S-100 proteins,ionized calcium-binding adaptor molecule 1,amyloid precursor protein and receptor of advanced glycosylation *** intervention with LBP,the above changes were significantly ***,morphological remodeling of blood vessel-associated retinal astrocytes,marked by glial fibrillary acidic protein,was also *** results,taken together,suggest that LBP regulated the production of amyloid-βand expression of receptor of advanced glycosylation end-products,as well as mediating the activity of retinal glial cells,which may lead to the promotion of better maintenance of the blood-retinal barrier and improved neuronal survival in AOH *** study was approved by the Committee for the Use of Live Animals in Teaching and Research(approval ***-#1664-08).

关键词： astrocyte blood-retinal barrier glial cell Lycium barbarum microglia model plasticity remodel retina

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Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

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Science China(Life Sciences) 2015年第6期58卷 521-530页

作者： LIU Jin YEUNG Patrick Ka Kit CHENG Lu LO Amy Cheuk Yin chung Stephen Sum Man chung sookja kim Department of Anatomy Li Ka Shing Faculty of Medicine The University of Hong Kong Department of Ophthalmology Li Ka Shing Faculty of Medicine The University of Hong Kong Research Centre of Heart Brain Hormone and Healthy Aging Li Ka Shing Faculty of Medicine The University of Hong Kong Division of Science and Technology United International College Zhuhai 519085 China State Key Laboratory of Pharmaceutical Biotechnology The University of Hong Kong

Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac 1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion （tMCAO） was performed on Epacl-deficient （Epacl-/- ） mice, Epac2-deficient （Epac2-/-） mice, and their wild type counter-parts （Epacl＋/＋ and Epac2＋/＋）. Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neu-ronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 （AQP4）, glial fibrillary acidic protein （GFAP）, peroxiredoxin 6 （Prx6） were observed in ipsilateral retinae. Epac2 / ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2＋/＋. However, Epacl-/- ipsilateral retinae displayed similar pathology as those in Epacl＋/＋ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury.

关键词： Epac retina ischemia retinopathy

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Exacerbated VEGF up-regulation accompanies diabetes-aggravated hemorrhage in mice after experimental cerebral ischemia and delayed reperfusion

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Neural Regeneration Research 2022年第7期17卷 1566-1575页

作者： Angela Ka Wai Lai Tsz chung Ng Victor Ka Lok Hung Ka Cheung Tam Chi Wai Cheung sookja kim.chung Amy Cheuk Yin Lo Department of Ophthalmology Li Ka Shing Faculty of MedicineThe University of Hong KongHong Kong Special Administration RegionChina Department of Anesthesiology Laboratory and Clinical Research Institute for PainThe University of Hong KongHong Kong Special Administration RegionChina Macao University of Science and Technology TaipaMacao Special Administration RegionChinaSchool of Biomedical SciencesThe State Key Laboratory of Pharmaceutical BiotechnologyThe University of Hong KongHong Kong Special Administration RegionChina

Reperfusion therapy is the preferred treatment for ischemic stroke,but is hindered by its short treatment window,especially in patients with diabetes whose reperfusion after prolonged ischemia is often accompanied by exacerbated *** mechanisms underlying exacerbated hemorrhage are not fully *** study aimed to identify this mechanism by inducing prolonged 2-hour transient intraluminal middle cerebral artery occlusion in diabetic Ins2Akita/+mice to mimic patients with diabetes undergoing delayed mechanical *** results showed that at as early as 2 hours after reperfusion,Ins2Akita/+mice exhibited rapid development of neurological deficits,increased infarct and hemorrhagic transformation,together with exacerbated down-regulation of tight-junction protein ZO-1 and upregulation of blood-brain barrier-disrupting matrix metallopeptidase 2 and matrix metallopeptidase 9 when compared with normoglycemic Ins2+/+*** indicated that diabetes led to the rapid compromise of vessel integrity immediately after reperfusion,and consequently earlier death and further aggravation of hemorrhagic transformation 22 hours after *** observation was associated with earlier and stronger up-regulation of pro-angiogenic vascular endothelial growth factor(VEGF)and its downstream phospho-Erk1/2 at 2 hours after reperfusion,which was suggestive of premature angiogenesis induced by early VEGF up-regulation,resulting in rapid vessel disintegration in diabetic *** reticulum stress-related pro-apoptotic C/EBP homologous protein was overexpressed in challenged Ins2Akita/+mice,which suggests that the exacerbated VEGF up-regulation may be caused by overwhelming endoplasmic reticulum stress under diabetic *** conclusion,the results mimicked complications in patients with diabetes undergoing delayed mechanical thrombectomy,and diabetes-induced accelerated VEGF up-regulation is likely to underlie exacerbated hemorrhagic transformat

关键词： blood-brain barrier brain injury diabetes mellitus hemorrhagic transformation infarct ischemia/reperfusion injury middle cerebral artery occlusion mouse model stroke vascular endothelial growth factor

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Molecular basis for diabetes-associated metabolic defect in the nervous tissue

Molecular basis for diabetes-associated metabolic defect in ...

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中国解剖学会2015年年会

作者： sookja kim.chung Department of Anatomy University of Hong Kong

＜正＞Mouse genome has been manipulated to understand the pathogenesis of human diseases by employing the state-of-art technology,i.e.,conventional,conditional and inducible transgenic and knockout mouse *** genetically manipulated mouse models are powerful reagents for understanding the genes’function and their role in complex disease *** have

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Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells

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Neural Regeneration Research 2017年第6期12卷 945-952页

作者： Jiang Lu Xue-qin Yao Xin Luo Yu Wang sookja kim.chung He-xin Tang Chi Wai Cheung Xian-yu Wang Chen Meng Qing Li Anesthesiology Research Institute of Hubei University of Medicine Department of Anesthesiology Taihe Hospital Hubei University of Medicine Department of Anesthesiology Li Ka Shing Faculty of Medicine The University of Hong Kong Laboratory and Clinical Research Institute for Pain Li Ka Shing Faculty of Medicine The University of Hong Kong Department of Anatomy Li Ka Shing Faculty of Medicine The University of Hong Kong

Monosialoganglioside 1（GM1） is the main ganglioside subtype and has neuroprotective properties in the central nervous system. In this study, we aimed to determine whether GM1 alleviates neurotoxicity induced by moderate and high concentrations of propofol combined with remifentanil in the immature central nervous system. Hippocampal neural stem cells were isolated from newborn Sprague-Dawley rats and treated with remifentanil（5, 10, 20 ng/m L） and propofol（1.0, 2.5, 5.0 μg/m L）, and/or GM1（12.5, 25, 50 μg/m L）. GM1 reversed combined propofol and remifentanil-induced decreases in the percentage of 5-bromodeoxyuridine（＋） cells and also reversed the increase in apoptotic cell percentage during neural stem cell proliferation and differentiation. However, GM1 with combined propofol and remifentanil did not affect β-tubulin（＋） or glial fibrillary acidic protein（＋） cell percentage during neural stem cell differentiation. In conclusion, we show that GM1 alleviates the damaging effects of propofol combined with remifentanil at moderate and high exposure concentrations in neural stem cells in vitro, and exerts protective effects on the immature central nervous system.

关键词： propofol alleviate tubulin anesthesia moderate newborn protective fibrillary glial aimed

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Reducing host aldose reductase activity promotes neuronal differentiation of transplanted neural stem cells at spinal cord injury sites and facilitates locomotion recovery

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Neural Regeneration Research 2022年第8期17卷 1814-1820页

作者： Kun Zhang Wen-Can Lu Ming Zhang Qian Zhang Pan-Pan Xian Fang-Fang Liu Zhi-Yang Chen chung sookja kim Sheng-Xi Wu Hui-Ren Tao Ya-Zhou Wang Department of Neurobiology and Institute of Neurosciences School of Basic MedicineFourth Military Medical UniversityXi’anShaanxi ProvinceChina Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration Tongji UniversityShanghaiChina Department of Spine Surgery Shenzhen University General HospitalShenzhenGuangdong ProvinceChina Department of Neurology Hainan Hospital of Chinese PLA General HospitalSanyaHainan ProvinceChina Department of Anesthesiology Tangdu HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina Faculty of Medicine Macao University of Science and TechnologyMacao Special Administrative RegionChina

Neural stem cell(NSC)transplantation is a promising strategy for replacing lost neurons following spinal cord ***,the survival and differentiation of transplanted NSCs is limited,possibly owing to the neurotoxic inflammatory *** of the important role of glucose metabolism in M1/M2 polarization of microglia/macrophages,we hypothesized that altering the phenotype of microglia/macrophages by regulating the activity of aldose reductase(AR),a key enzyme in the polyol pathway of glucose metabolism,would provide a more beneficial microenvironment for NSC survival and ***,we reveal that inhibition of host AR promoted the polarization of microglia/macrophages toward the M2 phenotype in lesioned spinal cord injuries.M2 macrophages promoted the differentiation of NSCs into neurons in *** of NSCs into injured spinal cords either deficient in AR or treated with the AR inhibitor sorbinil promoted the survival and neuronal differentiation of NSCs at the injured spinal cord site and contributed to locomotor functional *** findings suggest that inhibition of host AR activity is beneficial in enhancing the survival and neuronal differentiation of transplanted NSCs and shows potential as a treatment of spinal cord injury.

关键词： aldose reductase functional recovery inflammation macrophage microglia neural stem cell transplantation neuronal differentiation polarization spinal cord injury

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葡萄糖对小鼠胚胎干细胞生长的影响

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中国临床药理学与治疗学 2009年第7期14卷 760-765页

作者：李华 Amy Lam 吴浩佳郝敏 sookja kim.chung 香港大学李嘉诚医学院解剖系大连医科大学药学院药理教研室

目的:目前小鼠胚胎干细胞(mouse embry-onic stem cells,mESC)常规应用高浓度葡萄糖(25 mmol/L)培养基培养,但是在应用干细胞向糖尿病胰岛beta细胞分化的研究中发现,慢性高糖培养可促进干细胞的凋亡、降低细胞分化的效率及分化后胰岛bet... 详细信息

目的:目前小鼠胚胎干细胞(mouse embry-onic stem cells,mESC)常规应用高浓度葡萄糖(25 mmol/L)培养基培养,但是在应用干细胞向糖尿病胰岛beta细胞分化的研究中发现,慢性高糖培养可促进干细胞的凋亡、降低细胞分化的效率及分化后胰岛beta细胞对葡萄糖的反应性,因此本研究拟选择合适的较低浓度的葡萄糖以优化胚胎干细胞的培养基、提高胚胎干细胞的生长、分化效率。方法:mESC传代4或12 h后,将传统的25 mmol/L葡萄糖培养基分别换为5、10、15、25 mmol/L葡萄糖培养基培养,均用碱性磷酸酶(AP)染色计数细胞集落形成情况、台盼兰染色测定细胞数目,MTT法测定细胞活力及用4’,6-联脒-2-苯基吲哚(4’,6-diamidino-2-phenylindole,DAPI)染色检测细胞凋亡情况。结果:mESC传代4 h后即调换葡萄糖浓度:(1)各葡萄糖浓度组(5、10、15 mmol/L)与25 mmol/L组相比,集落形成明显减少。(2)各葡萄糖浓度组与25 mmol/L组相比,mESC增殖及细胞活力均受到不同程度明显影响。mESC传代12 h后调换葡萄糖浓度:(1)各葡萄糖浓度组(5、10、15 mmol/L)与25 mmol/L组相比,集落形成无明显变化,且AP染色呈强阳性。(2)15 mmol/L葡萄糖组对mESC增殖及细胞活力均无明显影响。(3)15 mmol/L葡萄糖组与25 mmol/L葡萄糖组细胞核形态正常,均未见明显凋亡。结论:ESC传代12 h后将培养基中传统的高糖(25 mmol/L)降低为15 mmol/L,不影响mESC细胞活力及多能分化潜能和未分化状态。

关键词：胚胎干细胞葡萄糖浓度

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SYNERGISTIC EFFECT OF OSMOTIC AND OXIDATIVE STRESS IN SLOW-DEVELOPING CATARACT

SYNERGISTIC EFFECT OF OSMOTIC AND OXIDATIVE STRESS IN SLOW-D...

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第十八届国际眼科研究大会

作者： Stephen chung Alfred Chan sookja chung University of Hong Kong

＜正＞Diabetes is the major contributing factor in cataract *** animal models where cataracts develop within days or weeks of diabetes it is well established that osmotic stress from the accumulation of sorbitol leads to cataract *** mechanism might explain the rare cases of acute cataract sometimes found in patients with

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