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Effect of Lycium barbarum Polysaccharides on the expression of endothelin-1 and its receptors in an ocular hypertension model of rat glaucoma 被引量:14
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作者 Xue-Song Mi Kin Chiu +5 位作者 Geoffrey Van Justin Wai Chung Leung Amy Cheuk Yin Lo SookjaKim Chung Raymond Chuen-Chung Chang Kwok-Fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第9期645-651,共7页
Lycium barbarum, a traditional Chinese anti-aging herb, has been shown to protect retinal ganglion cells (RGCs) in a rat chronic ocular hypertension (COH) model. Here, we investigated the expression of endothelin... Lycium barbarum, a traditional Chinese anti-aging herb, has been shown to protect retinal ganglion cells (RGCs) in a rat chronic ocular hypertension (COH) model. Here, we investigated the expression of endothelin-1 (ET-1), a strong vasoconstrictor, and its receptors, ETA and ETB, in the COH model and assessed the effects of Lycium barbarum on the ET-1 axis. Elevated intraocular pressure (IOP) was induced in the right eye of SD rats using argon laser photocoagulation. (1) The expression of ET-1, ETA and ETB in normal and COH retinas was studied. (2) Some COH rats were fed daily with Lycium barbarum Polysaccharides (LBP) using 1 mg/kg or phosphate-buffered saline (PBS) for 3 weeks (started 1 week before photocoagulation). The effects of LBP on the expression of ET-1 and its receptors, ETA and ETB, in COH retina were evaluated. A semi-quantitative analysis of staining intensity was used to evaluate the expression levels of ET-1, ETA and ETB in retinal vasculature. We found that (1) Under COH condition, the immunoreactivity of ET-1 was increased in retina associated with an increase of ETB receptor immunoreactivity and a decrease of ETA receptor immunoreactivity. (2) After feeding COH rats with LBP, the expression of ET-1 was decreased with an increase of ETA expression and a decrease of ETB expression in the retina, especially in RGCs. (3) By comparing the staining intensity in the vasculature of COH retina in LBP-fed group with PBS-fed group, there was a decrease in the expression of ET-1 and ETA and an increase in ETB. In summary, ET-1 expression was up-regulated in the retina in COH model. LBP could decrease the expression of ET-1 and modulate the expression of its receptors, ETA and ETB, under the condition of COH. The neuroprotective effect of LBP on RGCs might be related to its ability to regulate the ET-1-mediated biological effects on RGCs and retinal vasculature. 展开更多
关键词 retinal ganglion cell Lycium barbarum Polysaccharides GLAUCOMA ENDOTHELIN-1
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Lycium barbarum polysaccharides promotes in vivo proliferation of adult rat retinal progenitor cells 被引量:7
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作者 Hua Wang Benson Wui-Man Lau +4 位作者 Ning-li Wang Si-ying Wang Qing-jun Lu Raymond Chuen-Chung Chang Kwok-fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第12期1976-1981,共6页
Lycium barbarum is a widely used Chinese herbal medicine prescription for protection of optic nerve.However,it remains unclear regarding the effects of Lycium barbarum polysaccharides,the main component of Lycium barb... Lycium barbarum is a widely used Chinese herbal medicine prescription for protection of optic nerve.However,it remains unclear regarding the effects of Lycium barbarum polysaccharides,the main component of Lycium barbarum,on in vivo proliferation of adult ciliary body cells.In this study,adult rats were intragastrically administered low-and high-dose Lycium barbarum polysaccharides(1 and 10 mg/kg)for 35 days and those intragastrically administered phosphate buffered saline served as controls.The number of Ki-67-positive cells in rat ciliary body in the Lycium barbarum polysaccharides groups,in particular low-dose Lycium barbarum polysaccharides group,was significantly greater than that in the phosphate buffered saline group.Ki-67-positive rat ciliary body cells expressed nestin but they did not express glial fibrillary acidic protein.These findings suggest that Lycium barbarum polysaccharides can promote the proliferation of adult rat retinal progenitor cells and the proliferated cells present with neuronal phenotype. 展开更多
关键词 nerve regeneration traditional Chinese medicine Lycium barbarum polysaccharides Lycium barbarum (wolJberry) retinal disease NEUROGENESIS ADULT neural regeneration
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Low dose of corticosterone treatment with exercise increases hippocampal cell proliferation, and improves cognition
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作者 Suk-Yu Yau Jada Chia-Di Lee +4 位作者 Benson Wui-Man Lau Tatia M.C. Lee Yick-Pang Ching Siu-Wa Tang Kwok-Fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第34期2645-2655,共11页
Intermediate level of stress is beneficial for brain functions, whereas extreme low level or high level of stress is deleterious. We have previously shown that chronic exposure to high doses of corticosterone (CORT)... Intermediate level of stress is beneficial for brain functions, whereas extreme low level or high level of stress is deleterious. We have previously shown that chronic exposure to high doses of corticosterone (CORT) suppressed hippocampal plasticity and physical exercise in terms of running counteracted the detrimental effects of CORT treatment. We aimed to study whether a mild stress, that mimicked by a treatment with low CORT dose, improved hippocampal plasticity in terms of hippocampal cell proliferation and dendritic remodeling, and to examine whether running with CORT treatment showed an additive effect on improving hippocampal plasticity. The rats were treated with 20 mg/kg CORT for 14 days with or without running, followed by Morris water maze test or forced swim test. The hippocampal proliferating cells was labeled by intraperitoneal injection of 5-bromo-2'-deoxyuridine. The dendritic morphology was analyzed using Golgi staining method. Treatment with 20 mg/kg CORT alone yielded a higher number of hippocampal cell proliferation and significantly increased dendritic branching compared to vehicle-treated non-runners, but had no behavioral effects. In contrast, CORT treatment with running showed an additive increase in hippocampal cell proliferation and dendritic remodeling that was associated with improved spatial learning and decreased depression-like behavior; however, there was no additive improvement in behavior compared to vehicle-treated runners. These findings suggest that mild stress does not always cause detrimental effect on the brain, and combining mild stress with running could promote hippocampal plasticity via inducing cell proliferation and dendritic remodeling. 展开更多
关键词 hippocampal cell proliferation physical exercise spatial learning stress structural plasticity neural plasticity
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Therapeutic approaches to non-alcoholic fatty liver disease: past achievements and future challenges 被引量:14
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作者 Jia Xiao Rui Guo +2 位作者 Man Lung Fung Emily C Liong George L Tipoe 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2013年第2期125-135,共11页
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver injury and mortality in Western countries and China. However, as to date, there is no direct and effective therapy for this dis... BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver injury and mortality in Western countries and China. However, as to date, there is no direct and effective therapy for this disease. The aim of this review is to analyze the key progress and challenges of main current therapeutic approaches in NAFLD. DATA SOURCE: We carried out a PubMed search of English-language articles relevant to NAFLD therapy. RESULTS: There are two major therapeutic strategies for NAFLD treatment: (1) lifestyle interventions (including weight reduction, dietary modification and physical exercise) and (2) pharmaceutical therapies. Lifestyle interventions, particularly chronic and moderate intensity exercise, are the most effective and recognized clinical therapies for NAFLD. For pharmaceutical therapies, although their effects and mechanisms have been extensively investigated in laboratory studies, they still need further tests and investigations in clinical human trials. CONCLUSION: Future advancement of NAFLD therapy should focus on the mechanistic studies on cell based and animal models and human clinical trials of exercise, as well as the combination of lifestyle intervention and pharmaceutical therapy specifically targeting main signaling pathways related to lipid metabolism, oxidative stress and inflammation. 展开更多
关键词 non-alcoholic fatty liver disease THERAPY pharmaceuticals EXERCISE
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Fat cell-secreted adiponectin mediates physical exercise-induced hippocampal neurogenesis: an alternative anti-depressive treatment? 被引量:8
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作者 Suk Yu Yau Ang Li +1 位作者 Aimin Xu Kwok-fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第1期7-9,共3页
Psychological depression is drawing accumulating attention nowadays, due to the skyrocketing incidence worldwide and the enormous burdens it incurs. Physical exercise has been long recog- nized for its therapeutic eff... Psychological depression is drawing accumulating attention nowadays, due to the skyrocketing incidence worldwide and the enormous burdens it incurs. Physical exercise has been long recog- nized for its therapeutic effects on depressive disorders, although knowledge of the underlying mechanisms remains limited. Suppressed hippocampal neurogenesis in adult brains has been regarded, at least partly, contributive to depression, whereas physical exercise that restores neuro- genesis accordingly exerts the anti-depressive action. Several recent publications have suggested the potential role of adiponectin, a protein hormone secreted by peripheral mature adipocytes, in mediating physical exercise-triggered enhancement of hippocampal neurogenesis and alleviation of depression. Here, we briefly review these novel findings and discuss the possibility of counter- acting depression by modulating adiponectin signaling in the hippocampus with interventions including physical exercise and administration of pharmacological agents. 展开更多
关键词 HIPPOCAMPUS adult neurogenesis physical exercise voluntary wheel running depression neural progenitor cell ADIPOCYTE ADIPONECTIN adiponectin receptor AMP-activated protein kinase
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Modulation of morphological changes of microglia and neuroprotection by monocyte chemoattractant protein-1 in experimental glaucoma 被引量:6
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作者 Kin Chiu Sze-Chun Yeung +1 位作者 Kwok-Fai So Raymond Chuen-Chung Chang 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2010年第1期61-68,共8页
Monocyte chemoattractant protein-1(MCP-1)/CCL2 is a C–C chemokine involved in the activation and recruitment of monocytic cells to injury sites.MCP-1/CCL2 can induce either neuroprotection or neurodestruction in vitr... Monocyte chemoattractant protein-1(MCP-1)/CCL2 is a C–C chemokine involved in the activation and recruitment of monocytic cells to injury sites.MCP-1/CCL2 can induce either neuroprotection or neurodestruction in vitro,depending on the experimental model.We aim to use MCP-1/CCL2 as an experimental tool to investigate the morphological changes of microglia when loss of healthy retinal ganglion cells(RGCs)is exacerbated or attenuated in an experimental glaucoma model.While a high concentration(1000 ng)of MCP-1/CCL2 and lipopolysaccharide(LPS)-exacerbated RGC loss,100 ng MCP-1/CCL2 provided neuroprotection towards RGC.Neuroprotective MCP-1/CCL2(100 ng)also upregulated insulin-like growth factor-1(IGF-1)immunoreactivity in the RGCs.The neuroprotective effect of MCP-1/CCL2 was not due to the massiveinfiltration of microglia/macrophages.Taken together,this is the first report showing that an appropriate amount of MCP-1/CCL2 can protect RGCs in experimental glaucoma. 展开更多
关键词 GLAUCOMA IGF-1 MCP-1/CCL2 MICROGLIA NEUROPROTECTION
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Modulation of Neuroimmune Responses on Glia in the Central Nervous System: Implication in Therapeutic Intervention against Neuroinflammation 被引量:5
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作者 Raymond Chuen-Chung Chang Kin Chiu +1 位作者 Yuen-Shan Ho Kwok-Fai So 《Cellular & Molecular Immunology》 SCIE CAS CSCD 2009年第5期317-326,共10页
It has long been known that the brain is an immunologically privileged site in normal conditions. Although the cascade of immune responses can occur as long as there is a neuronal injury or a potent immune stimulation... It has long been known that the brain is an immunologically privileged site in normal conditions. Although the cascade of immune responses can occur as long as there is a neuronal injury or a potent immune stimulation, how the brain keeps glial cells in a quiescent state is still unclear. Increasing efforts have been made by several laboratories to elucidate how repression oi~ immune responses is achieved in the neuronal environment. The suppression factors include neurotransmitters, neurohormones, neurotrophic factors, anti-inflammatory factors, and cell-cell contact via adhesion molecules or CD200 receptor. This review discusses how these factors affect the cascade of cerebral immune responses because no single factor listed above can fully account for the immune suppression. While several factors contribute to the suppression of immune responses, activation of glial cells and their production of pro-inflammatory factors do occur as long as there is a neuronal injury, suggesting that some neuronal components facilitate immune responses. This review also discusses which signals initiate or augment cerebral immune responses so that stimulatory signals override the suppressive signals. Increasing lines of evidence have demonstrated that immune responses in the brain are not always detrimental to neurons. Attempt to simply clear off inflammatory factors in the CNS may not be appropriate for neurons in neurological disorders. Appropriate control of immune cells in the CNS may be beneficial to neurons or even neuroregeneration. Therefore, understanding the mechanisms underlying immune suppression may help us to reshape pharmacological interventions against inflammation in many neurological disorders. 展开更多
关键词 neural cell adhesion molecule NEUROTROPHINS potassium ions MICROGLIA NEUROINFLAMMATION
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Surface Modification of Intraocular Lenses 被引量:4
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作者 Qi Huang George Pak-Man Cheng +1 位作者 Kin Chiu Gui-Qin Wang 《Chinese Medical Journal》 SCIE CAS CSCD 2016年第2期206-214,共9页
Objective: This paper aimed to review the current literature on the surface modification ofintraocular lenses (IOLs). Data Sources: All articles about surface modification of IOLs published up to 2015 were identif... Objective: This paper aimed to review the current literature on the surface modification ofintraocular lenses (IOLs). Data Sources: All articles about surface modification of IOLs published up to 2015 were identified through a literature search on both PubMed and ScienceDirect. Study Selection: The articles on the surface modification of 1OLs were included, but those on design modification and surface coating were excluded. Results: Technology of surface modification included plasma, ion beam, layer-by-layer self-assembly, ultraviolet radiation, and ozone. The main molecules introduced into IOLs surface were poly (ethylene glycol), polyhedral oligomeric silsesquioxane, 2-methacryloyloxyethyl phosphorylcholine, TiO2, heparin, F-heparin, titanium, titanium nitride, vinyl pyrrolidone, and inhibitors of cytokines. The surface modification either resulted in a more hydrophobic lens, a more hydrophilic lens, or a lens with a hydrophilic anterior and hydrophobic posterior surface. Advances in research regarding surface modification of |OLs had led to a better biocompatibility in both in vitro and animal experiments. Conclusion: The surface modification is an efficient, convenient, economic and promising method to improve the biocompatibility of IOLs. 展开更多
关键词 BIOCOMPATIBILITY Capsule Biocompatibility CATARACT Intraocular Lenses Surface Modification Uveal Biocompatibility
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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 被引量:13
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作者 LIU Jin YEUNG Patrick Ka Kit +3 位作者 CHENG Lu LO Amy Cheuk Yin CHUNG Stephen Sum Man CHUNG Sookja Kim 《Science China(Life Sciences)》 SCIE CAS CSCD 2015年第6期521-530,共10页
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 endoth... 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. 展开更多
关键词 Epac RETINA ischemia RETINOPATHY
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Monoamine oxidase-B (MAO-B) inhibitors: implications for disease-modification in Parkinson’s disease 被引量:6
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作者 Kay Cheong Teo Shu-Leong Ho 《Translational Neurodegeneration》 SCIE CAS 2013年第1期124-133,共10页
There is a substantial amount of evidence from experimental parkinsonian models to show the neuroprotective effects of monoamine oxidase-B(MAOB)inhibitors.They have been studied for their potential disease-modifying e... There is a substantial amount of evidence from experimental parkinsonian models to show the neuroprotective effects of monoamine oxidase-B(MAOB)inhibitors.They have been studied for their potential disease-modifying effects in Parkinson’s disease(PD)for over 20 years in various clinical trials.This review provides a summary of the clinical trials and discusses the implications of their results in the context of disease-modification in PD.Earlier clinical trials on selegiline were confounded by symptomatic effects of this drug.Later clinical trials on rasagiline using delayed-start design provide newer insights in disease-modification in PD but success in achieving the aims of this strategy remain elusive due to obstacles,some of which may be insurmountable. 展开更多
关键词 Parkinson's disease Monoamine oxidase-B inhibitors Disease-modification Neuroprotection SELEGILINE RASAGILINE
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Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in Parkinson’s disease Philip 被引量:3
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作者 WL Ho Jessica WM Ho +5 位作者 Hui-Fang Liu Danny HF So Zero HM Tse Koon-Ho Chan David B Ramsden Shu-Leong Ho 《Translational Neurodegeneration》 SCIE CAS 2012年第1期11-19,共9页
This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson’s disease(PD).Mitochondria provide cellular energy in the... This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson’s disease(PD).Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation,but as an integral part of this process,superoxides and other reactive oxygen species are also produced.Excessive free radical production contributes to oxidative stress.Cells have evolved to handle such stress via various endogenous anti-oxidant proteins.One such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner membrane.There are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural cells.In a series of previous publications,we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium(MPP+;toxic metabolite of MPTP)and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential,and reducing oxidative stress.We also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in UCP4.Furthermore,we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin(hormone produced by adipocytes)acting via UCP2 against MPP+-induced toxicity.There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD.Their expression,which can be induced,may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease. 展开更多
关键词 uncoupling proteins MITOCHONDRIA Parkinson??s disease ATP oxidative stress NEUROPROTECTION
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Neurogenic hypothesis and psychiatric disorders
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作者 LAU Benson WuiMan LEE Jada ChiaDi SO KwokFai 《Chinese Science Bulletin》 SCIE EI CAS 2013年第26期3188-3198,共11页
Psychiatric illness, such as affective disorders, anxiety disorders and schizophrenia, exerts exceptional personal burden on affected individuals. Although not physically noticeable, these disorders cost enormously on... Psychiatric illness, such as affective disorders, anxiety disorders and schizophrenia, exerts exceptional personal burden on affected individuals. Although not physically noticeable, these disorders cost enormously on ones' family and society. Currently pharma-ceutical and psychological treatments are generally accepted as effective for psychiatric disorders, while the exact mechanisms underlying the treatment efficacy, etiology and neurobiology of the disorders remain elusive. In the past decade, "neurogenic hy-pothesis" emerged as an attempt to explain the nature of psychiatric illness. The origination of the hypothesis is based on several pre-clinical and clinical observations. First, stress, which is a common risk factor of the disorders, was found to suppress neurogenesis; second, treatment for the illnesses like antidepressants and antipsychotics were shown to improve neurogenesis and behavioral deficits simultaneously; and third, the therapeutic effect of antidepressants was abolished in animal models when neuro-genesis was blocked. Increasing efforts were invested to determine whether neurogenesis is a key to the understanding and treatment of psychiatric disorders, although contrasting results are also found and thus the importance of neurogenesis remains a matter of debate. The present chapter will discuss the recent findings about the involvement of neurogenesis in major depression, anxiety disorders and schizophrenia, and whether neurogenesis would be a potential target for development of the treatment in the future. 展开更多
关键词 精神疾病 神经发生 假说 精神分裂症 心理治疗 临床观察 抗抑郁药 治疗效果
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