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Upregulated inflammatory associated factors and blood-retinal barrier changes in the retina of type 2diabetes mellitus model 被引量:4
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作者 Rui-Jin Ran Xiao-Ying Zheng +3 位作者 Li-Ping Du Xue-Dong Zhang Xiao-Li Chen Shen-Yin Zhu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2016年第11期1591-1597,共7页
AIM: To examine the expression of high mobility group box-1(HMGB-1) and intercellular adhesion molecule-1(ICAM-1) in the retina and the hippocampal tissues; and further to evaluate the association of these two mo... AIM: To examine the expression of high mobility group box-1(HMGB-1) and intercellular adhesion molecule-1(ICAM-1) in the retina and the hippocampal tissues; and further to evaluate the association of these two molecules with the alterations of blood-retinal barrier(BRB) and blood-brain barrier(BBB) in a rat model of type 2 diabetes.METHODS: The type-2 diabetes mellitus(DM) model was established with a high-fat and high-glucose diet combined with streptozotocin(STZ). Sixteen weeks after DM induction, morphological changes of retina and hippocampus were observed with hematoxylin-eosin staining, and alternations of BRB and BBB permeability were measured using Evans blue method. Levels of HMGB-1 and ICAM-1 in retina and hippocampus were detected by Western blot. Serum HMGB-1 levels were determined by enzyme-linked immunosorbent assay(ELISA).RESULTS: A significantly higher serum fasting blood glucose level in DM rats was observed 2wk after STZ injection(P 〈0.01). The serum levels of fasting insulin,Insulin resistance homeostatic model assessment(IRHOMA),total cholesterol(TC), total triglycerides(TG) and low density lipoprotein cholesterol(LDL-C) in the DM rats significantly higher than those in the controls(all P 〈0.01).HMGB-1(0.96±0.03, P 〈0.01) and ICAM-1(0.76±0.12, P 〈0.05) levels in the retina in the DM rats were significantly higher than those in the controls. HMGB-1(0.83±0.13, P 〈0.01) and ICAM-1(1.15 ±0.08, P 〈0.01) levels in the hippocampal tissues in the DM rats were alsosignificantly higher than those in the controls. Sixteen weeks after induction of DM, the BRB permeability to albumin-bound Evans blue dye in the DM rats was significantly higher than that in the controls(P 〈0.01).However, there was no difference of BBB permeability between the DM rats and controls. When compared to the controls, hematoxylin and eosin staining showed obvious irregularities in the DM rats.CONCLUSION: BRB permeability increases significantly in rats with type-2 DM, which may be associated with the up-regulated retinal expression of HMGB-1 and ICAM-1. 展开更多
关键词 blood-retinal barrier blood-brain barrier diabetes mellitus permeability: high mobility group box-1protein RATS
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The development of blood-retinal barrier during the interaction of astrocytes with vascular wall cells 被引量:6
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作者 Huanling Yao Tianshi Wang +3 位作者 Jiexin Deng Ding Liu Xiaofei Li Jinbo Deng 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第10期1047-1054,共8页
Astrocytes are intimately involved in the formation and development of retinal vessels. Astrocyte dysfunction is a major cause of blood-retinal barrier injury and other retinal vascular diseases. In this study, the de... Astrocytes are intimately involved in the formation and development of retinal vessels. Astrocyte dysfunction is a major cause of blood-retinal barrier injury and other retinal vascular diseases. In this study, the development of the retinal vascular system and the formation of the blood-ret-inal barrier in mice were investigated using immunolfuorescence staining, gelatin-ink perfusion, and transmission electron microscopy. The results showed that the retinal vascular system of mice develops from the optic disc after birth, and radiates out gradually to cover the entire retina, taking the papilla optica as the center. First, the superifcial vasculature is formed on the inner retinal layer;then, the vasculature extends into the inner and outer edges of the retinal inner nuclear layer, forming the deep vasculature that is parallel to the superifcial vasculature. The blood-retinal barrier is mainly composed of endothelium, basal lamina and the end-feet of astrocytes, which become mature during mouse development. Initially, the naive endothelial cells were immature with few organelles and many microvilli. The basal lamina was uniform in thickness, and the glial end-feet surrounded the outer basal lamina incompletely. In the end, the blood-retinal barrier matures with smooth endothelia connected through tight junctions, rela-tively thin and even basal lamina, and relatively thin glial cell end-feet. These ifndings indicate that the development of the vasculature in the retina follows the rules of“center to periphery”and“superifcial layer to deep layers”. Its development and maturation are spatially and tempo-rally consistent with the functional performance of retinal neurons and photosensitivity. The blood-retinal barrier gradually becomes mature via the process of interactions between astro-cytes and blood vessel cells. 展开更多
关键词 nerve regeneration RETINA growth development blood vessels blood-retinal barrier ASTROCYTES IMMUNOFLUORESCENCE ULTRASTRUCTURE mouse collagen IV glial fibrillary acidic protein NSFC grant neural regeneration
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Involvement of moesin phosphorylation in ischemia/reperfusion induced inner blood-retinal barrier dysfunction 被引量:3
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作者 Jing Xu Qiong Liu +4 位作者 Ming Ma Lin-Jiang Chen Jian Yu Ke Xiong Jing Wu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2020年第4期545-551,共7页
AIM: To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion(RIR) insult.METHODS: C57 BL/6 mice were subjected to continued ischemia ... AIM: To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion(RIR) insult.METHODS: C57 BL/6 mice were subjected to continued ischemia for 45 min, followed by blood reperfusion. The expression and phosphorylation of moesin in retinal vessels were detected by immunohistochemistry and Western blotting. The inner blood-retinal barrier was evaluated using FITCdextran leakage assay on whole-mount retina. Further studies were conducted to explore the effects of p38 mitogen-activated protein kinase(MAPK) pathway on the involvement of moesin in RIR-evoked retinal vascular hyperpermeability response. RESULTS: It revealed that RIR induced moesin phosphorylation in a time-dependent manner after reperfusion. The phosphorylation of moesin was alleviated by inhibitions of p38 MAPK, while this treatment also ameliorated the dysfunction of inner blood-retinal barrier. CONCLUSION: The results suggest that moesin is involved in RIR-evoked retinal vascular endothelial dysfunction and the phosphorylation of moesin is triggered via p38 MAPK activation. 展开更多
关键词 RETINAL ISCHEMIA-REPERFUSION MOESIN p38 MITOGEN-ACTIVATED protein kinase INNER blood-retinal barrier mice
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Effect of pyridone agent on blood-retinal barrier in diabetic mice 被引量:2
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作者 Si-Qi Xiong Hai-Bo Jiang +1 位作者 Hui-Zhuo Xu Xiao-Bo Xia 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2017年第6期890-895,共6页
AIM: To evaluate the therapeutic effect of fluorofenidone on disrupted blood-retinal barrier in the diabetic mice and uncover its underlying mechanism. METHODS: db/db mice were randomly chosen for treatment with da... AIM: To evaluate the therapeutic effect of fluorofenidone on disrupted blood-retinal barrier in the diabetic mice and uncover its underlying mechanism. METHODS: db/db mice were randomly chosen for treatment with daily doses of fluorofenidone or placebo at 5-week-old, treatment continued until mice reach 24-week- old. Then, expression of transcriptiona factor insulin gene enhancer binding protein-1 (Islet-I) and vascular endothelial growth factor (VEGF) in murine retinas were evaluated. Retinal vascular permeability was assessed by examining the level of albumin in db/db murine retinas. Furthermore, the retinal vessel tight junction was estimated by checking the level of occludin in the murine retinal tissues. RESULTS: After occurrence of diabetic retinopthy in db/ db mice, expressions of transcritpional factor Islet-1 was found to be upregulated in db/db murine retinas compared with non-diabetic controls. Similar to expression pattern of Islet-l, VEGF were also demonstrated to be increased in retinas of db/db mice, which was accompanied by increased retinal vascular leakage and decreased tight junction protein level. Systemetic administration of fluorofenidone repaired broken retinal vascular tight junction by restoring occludin expression in db/db retinal tissue. Consequently, retinal vascular premeability were indicated to be reduced by examining the transudative albumin level in diabetic retinal tissues. Both Islet-1 and VEGF expression were inhibited in the retinas of db/db mice after treatment with fluorofenidone. CONCLUSION: Fluorofenidone significantly protectes retinal tight junction and reduces retinal vascular leakage. The phenomenon can be partially attributed to reducing overexpression of Islet-1 and VEGF in diabetic retinal tissues. 展开更多
关键词 pyridone agent diabetic retinopathy blood-retinal barrier
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Dynamic changes of inducible nitric oxide synthase expression in rat's retina and its role on blood-retinal barrier injury after acute high intraocular pressure 被引量:1
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作者 Min Li Ju-Fang Huang +5 位作者 Yi Li Jing Shen Lu-Jia Yang Qian Chen Quan-Peng Zhang Xi-Nan Yi 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2022年第7期1053-1061,共9页
AIM: To clarify the role of inducible nitric oxide synthase(i NOS) in blood-retinal barrier(BRB) injury after acute high intraocular pressure(IOP) in rats.METHODS: Forty-two Sprague-Dawley(SD) rats were randomized int... AIM: To clarify the role of inducible nitric oxide synthase(i NOS) in blood-retinal barrier(BRB) injury after acute high intraocular pressure(IOP) in rats.METHODS: Forty-two Sprague-Dawley(SD) rats were randomized into 7 groups [control(Cont), 3, 6, 12, 24, 48, and 72 h, n=6]. Except Cont group, other groups’ retina tissue was obtained at corresponding time points after a model of acute high IOP have been established in rats. The expression of i NOS and tight junction protein zonula occludens(ZO)-1 was detected by Western blotting. Evans blue(EB;3%) was injected into the great saphenous vein to detect the leakage of EB by spectrophotometer. Nine rats were divided into Cont, 6 h, 12 h groups, the expression of i NOS was localized by immunofluorescence. In order to verify the role of i NOS in the damage to BRB, thirty-six rats were randomly divided into 4 groups [Cont, Cont+inhibitor(Inh), 6 h and 6 h+Inh, n=9]. After treatment with the i NOSspecific inhibitor 1400 W, the expression of i NOS and ZO-1 and the leakage of BRB were detected again.RESULTS: The immunofluorescence results showed that the expression of i NOS was observed in the Cont group and 6 h group, but not in the 12 h group. i NOS was mainly expressed in the retinal nerve fiber layer, ganglion cell layer and inner nuclear layer and that it did not colocalize with the retinal ganglion cell marker Neu N but was co-expressed with the vascular endothelial cell marker CD31. Western blotting showed that in the early period(3 h, 6 h) after acute high IOP, the expression of i NOS was upregulated, then the down-regulation of i NOS were tested in the follow-up timing spots. ZO-1 expression showed a continuous downregulation after 6 h. The quantitative results for EB showed that the amount of EB leakage began to increase at 3 h after acute high IOP. At 6 h, the leakage of EB was lower, but at 12 h, the leakage of EB was highest, after which it gradually recovered but remained higher than that in the Cont group. The expression of i NOS was down-regulated after 1400 W treatment. ZO-1 expression was not significantly changed in the Cont+Inh group and the 6 h group, and significantly down-regulated in the 6 h+Inh group, and the leakage of EB was significantly increased after 1400 W treatment.CONCLUSION: These results suggest that the upregulation of i NOS expression in the early stage after acute high IOP may have a protective effect on BRB injury. 展开更多
关键词 inducible nitric oxide synthase acute high intraocular pressure blood-retinal barrier ZO-1
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RNA interference targeting NOX4 protects visual function in an experimental model of retinal detachment by alleviating blood-retinal barrier damage
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作者 Kai Dong Nan Yang +3 位作者 Jie Ding Yuan-Ye Yan Li Lu Yi-Sai Wang 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2021年第1期50-56,共7页
AIM:To observe the effects of the inhibition of NADPH oxidase 4(NOX4)expression on the retinal vascular barriers and visual function after retinal detachment(RD).METHODS:RD model was established 3 wk after adenoassoci... AIM:To observe the effects of the inhibition of NADPH oxidase 4(NOX4)expression on the retinal vascular barriers and visual function after retinal detachment(RD).METHODS:RD model was established 3 wk after adenoassocianed virus vector injection.The retinal tissue was harvested 3 d after RD,and the death of retinal vascular endothelial cells and photoreceptors was observed using electron microscopy.The NOX4 expression was detected by Western blot.Confocal microscopy was used to observe a retinal patch that had been perfused with Evans blue.A modified water maze test was used to detect the time required to find the platform on the water surface.The visual function of the rats was evaluated and reactive oxygen species(ROS)expression was detected by a fluorescence microplate reader.RESULTS:The retinal patch showed that NOX4 interference significantly reduced the destruction of the tight junctions between the retinal endothelium of RD rats and reduced leakage.Western blotting showed decreased expression of the NOX4 protein and decreased expression of ROS in retinal tissue;the Morris water maze test results showed that NOX4 interference significantly decreased the escape latency of the rats.CONCLUSION:NOX4 interference reduces the production of ROS in retinal vascular endothelial cells after experimental RD,thereby protecting the blood-retinal barrier and protecting visual function. 展开更多
关键词 NOX4 adeno-associated virus retinal detachment blood-retinal barrier reactive oxygen species
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Vascular endothelial growth factor-165b protects the blood-retinal barrier from damage after acute high intraocular pressure in rats
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作者 Jing Shen Yi Li +4 位作者 Min Li Wei-Xian Liu Hong-Liang Sun Quan-Peng Zhang Xi-Nan Yi 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2022年第8期1231-1239,共9页
AIM:To elucidate the role of vascular endothelial growth factor-165b(VEGF-165b)in blood-retinal barrier(BRB)injury in the rat acute glaucoma model.METHODS:In this study,the rat acute high intraocular pressure(HIOP)mod... AIM:To elucidate the role of vascular endothelial growth factor-165b(VEGF-165b)in blood-retinal barrier(BRB)injury in the rat acute glaucoma model.METHODS:In this study,the rat acute high intraocular pressure(HIOP)model was established before and after intravitreous injection of anti-VEGF-165b antibody.The expression of VEGF-165b and zonula occludens-1(ZO-1)in rat retina was detected by double immunofluorescence staining and Western blotting,and the breakdown of BRB was detected by Evans blue(EB)dye.RESULTS:The intact retina of rats expressed VEGF-165b and ZO-1 protein,which were mainly located in the retinal ganglion cell layer and the inner nuclear layer and were both co-expressed with vascular endothelial cell markers CD31.After acute HIOP,the expression of VEGF-165b was up-regulated;the expression of ZO-1 was down-regulated at 12h and then recovered at 3d;EB leakage increased,peaking at 12h.After intravitreous injection of anti-VEGF-165b antibody,the expression of VEGF-165b protein was no significantly changed;and the down-regulation of the expression of ZO-1 was more obvious;EB leakage became more serious,peaking at 3d.EB analysis also showed that EB leakage in the peripheral retina was greater than that in the central retina.CONCLUSION:The endogenous VEGF-165b protein may protect the BRB from acute HIOP by regulating the expression of ZO-1.The differential destruction of BRB after acute HIOP may be related to the selective loss of retinal ganglion cells. 展开更多
关键词 vascular endothelial growth factor-165b blood-retinal barrier high intraocular pressure Evans blue zonula occludens-1
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Regulation of pathological blood-brain barrier for intracranial enhanced drug delivery and anti-glioblastoma therapeutics
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作者 KAI WANG FENGTIAN ZHANG +5 位作者 CHANGLONG WEN ZHIHUA HUANG ZHIHAO HU YUWEN ZHANG FUQIANG HU LIJUAN WEN 《Oncology Research》 SCIE 2021年第5期351-363,共13页
The blood-brain barrier(BBB)is an essential component in regulating and maintaining the homeostatic microenvironment of the central nervous system(CNS).During the occurrence and development of glioblastoma(GBM),BBB is... The blood-brain barrier(BBB)is an essential component in regulating and maintaining the homeostatic microenvironment of the central nervous system(CNS).During the occurrence and development of glioblastoma(GBM),BBB is pathologically destroyed with a marked increase in permeability.Due to the obstruction of the BBB,current strategies for GBM therapeutics still obtain a meager success rate and may lead to systemic toxicity.Moreover,chemotherapy could promote pathological BBB functional restoration,which results in significantly reduced intracerebral transport of therapeutic agents during multiple administrations of GBM and the eventual failure of GBM chemotherapy.The effective delivery of intracerebral drugs still faces severe challenges.However,strategies that regulate the pathological BBB to enhance the transport of therapeutic agents across the barrier may provide new opportunities for the effective and safe treatment of GBM.This article reviews the structure and function of BBB in physiological states,the mechanisms underlying BBB pathological fenestration during the development of GBM,and the therapeutic strategies of GBM based on BBB intervention and medicinal drugs transporting across the BBB. 展开更多
关键词 Blood-brain barrier PHYSIOLOGICAL pathologICAL GLIOBLASTOMA INTERVENTION
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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 被引量:14
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作者 Xue-Song Mi Qian Feng +3 位作者 Amy Cheuk Yin Lo Raymond Chuen-Chung Chang Sookja Kim Chung Kwok-Fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2020年第12期2344-2352,共9页
Our previous study verified the protective effects of Lycium barbarum polysaccharides(LBP)on retinal neurons and blood vessels in acute ocular hypertension(AOH)mice.To investigate the effect of LBP on the reactivity o... Our previous study verified the protective effects of Lycium barbarum polysaccharides(LBP)on retinal neurons and blood vessels in acute ocular hypertension(AOH)mice.To 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 minutes.Either 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 post-insult.After 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 end-products.After intervention with LBP,the above changes were significantly reduced.Remarkably,morphological remodeling of blood vessel-associated retinal astrocytes,marked by glial fibrillary acidic protein,was also observed.These 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 insult.This study was approved by the Committee for the Use of Live Animals in Teaching and Research(approval No.CULTRA-#1664-08). 展开更多
关键词 ASTROCYTE blood-retinal barrier glial cell Lycium barbarum MICROGLIA model PLASTICITY remodel RETINA
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Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in Alzheimer's disease 被引量:8
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作者 Qian Yue Maggie Pui Man Hoi 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第9期1890-1902,共13页
Blood-brain barrier disruption occurs in the early stages of Alzheimer’s disease.Recent studies indicate a link between blood-brain barrier dysfunction and cognitive decline and might accelerate Alzheimer’s disease ... Blood-brain barrier disruption occurs in the early stages of Alzheimer’s disease.Recent studies indicate a link between blood-brain barrier dysfunction and cognitive decline and might accelerate Alzheimer’s disease progression.Astrocytes are the most abundant glial cells in the central nervous system with important roles in the structural and functional maintenance of the blood-brain barrier.For example,astrocytic cove rage around endothelial cells with perivascular endfeet and secretion of homeostatic soluble factors are two major underlying mechanisms of astrocytic physiological functions.Astrocyte activation is often observed in Alzheimer’s disease patients,with astrocytes expressing a high level of glial fibrillary acid protein detected around amyloid-beta plaque with the elevated phagocytic ability for amyloid-beta.Structural alte rations in Alzheimer’s disease astrocytes including swollen endfeet,somata shrinkage and possess loss contribute to disruption in vascular integrity at capillary and arte rioles levels.In addition,Alzheimer’s disease astrocytes are skewed into proinflammatory and oxidative profiles with increased secretions of vasoactive mediators inducing endothelial junction disruption and immune cell infiltration.In this review,we summarize the findings of existing literature on the relevance of astrocyte alte ration in response to amyloid pathology in the context of blood-brain barrier dysfunction.First,we briefly describe the physiological roles of astrocytes in blood-brain barrier maintenance.Then,we review the clinical evidence of astrocyte pathology in Alzheimer’s disease patients and the preclinical evidence in animal and cellular models.We further discuss the structural changes of blood-brain barrier that correlates with Alzheimer’s disease astrocyte.Finally,we evaluate the roles of soluble factors secreted by Alzheimer’s disease astrocytes,providing potential molecular mechanisms underlying blood-brain barrier modulation.We conclude with a perspective on investigating the therapeutic potential of targeting astrocytes for blood-brain barrier protection in Alzheimer’s disease. 展开更多
关键词 Alzheimer’s disease AMYLOID-BETA astrocyte(astroglial)-endothelial interaction astrocyte pathology blood-brain barrier blood-brain barrier disruption brain endothelial cell NEUROINFLAMMATION reactive astrocyte
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Infl iximab relieves blood retinal barrier breakdown through the p38 MAPK pathway in a diabetic rat model 被引量:2
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作者 Mao-Song Xie Yong-Zheng Zheng +1 位作者 Li-Bin Huang Guo-Xing Xu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2017年第12期1824-1829,共6页
AIM: To clarify the mechanism of infliximab treatment in diabetic macular edema (DME) and to provide a new alternative therapy for DME. METHODS: Rats were randomly divided into the control group, the model group ... AIM: To clarify the mechanism of infliximab treatment in diabetic macular edema (DME) and to provide a new alternative therapy for DME. METHODS: Rats were randomly divided into the control group, the model group and the infliximab treatment group. A diabetic rat model was created. The concentration of TNF-α in the vitreous body was detected by ELISA. The expressions of B-Raf, p38, claudin-1 and occludin in the retina were detected by Western blot. The integrity of the blood retinal barrier (BRB) was measured using Evan's blue as a tracer. RESULTS: After three months and six months of the diabetes model, the vitreous TNF-α level in the model group was higher than that of the control group. It was also higher in treated group than that of the control group but was lower than that of the model group. The differences among the three groups were statistically significant (at 3mo, F=857.098, P〈0.001; 6mo, F=1261.897, P〈0.001). The retina B-Raf and p38 levels in the model group were higher than that of the control group. They were also higher in treated group than that of the control group but were lower than that of the model group. The differences among the three groups were statistically significant (B-Raf at 3mo, F=106.596, P〈0.001 and at 6mo, F=200.681, P〈0.001; p38 at 3mo, F=41.662, P〈0.001 and at 6mo, F=67.979, P〈0.001). The retina claudin-1 and occludin levels in the model group were lower than that of the control group. They were also lower in treated group than that of the control group but were higher than that of the model group. The differences among three groups were statistically significant (claudin-1 at3mo, F=-139.088, P〈0.001 and at 6mo, F=128.415, P〈0.001; occludin at 3mo, F=-92.733, P〈0.001 and at 6mo, F--104.478, P〈0.001). The retinal Evans blue leakage in the model group was higher than that of the control group. It was also higher in treated group than that of the control group but was lower than that of the model group. The differences among the three groups were statistically significant (at 3mo, F=-447.946, P〈0.001; at 6mo, F'=-1610.732, P〈0.001). CONCLUSION: In-α diabetic rat model, infliximab may relieve TNF-α induced BRB breakdown via the B-Raf and p38 signaling pathway. 展开更多
关键词 tumor necrosis factor-α blood-retinal barrier diabetic macular edema INFLIXIMAB PATHOGENESIS
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治疗脾胃病的含救必应药对对溃疡性结肠炎的治疗作用
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作者 李瑶 李照悦 +5 位作者 张萌萌 王娟 卫培峰 谢艳华 王四旺 李敏 《广西医学》 CAS 2024年第7期1047-1056,共10页
目的分析治疗脾胃病的含救必应药对对溃疡性结肠炎(UC)的治疗作用。方法(1)在中国知网数据库和万方数据知识服务平台中检索使用救必应治疗脾胃病的临床研究,收集其临床处方。应用数据挖掘技术分析治疗脾胃病的含救必应核心药对。(2)选... 目的分析治疗脾胃病的含救必应药对对溃疡性结肠炎(UC)的治疗作用。方法(1)在中国知网数据库和万方数据知识服务平台中检索使用救必应治疗脾胃病的临床研究,收集其临床处方。应用数据挖掘技术分析治疗脾胃病的含救必应核心药对。(2)选择90只小鼠,将其随机分为正常组、模型组、救必应组及6组救必应药对组,每组10只。除正常组外,给予其余组小鼠饮用3%葡聚糖硫酸钠以建立UC模型,同时给予各给药组小鼠灌胃1.8 g/kg的相应药物,连续灌胃6 d,1次/d。在实验期间记录各组小鼠的一般症状,实验第7天观察其结肠外观、病理改变,检测其结肠组织Occludin蛋白、抗黏蛋白2(MUC2)、ATOH1蛋白的表达水平。结果(1)共获得6组含救必应的核心药对,分别为救必应-白芍、救必应-白术、救必应-茯苓、救必应-蒲公英、救必应-柴胡、救必应-党参。(2)与正常组比较,模型组小鼠的结肠长度缩短,体重下降率、疾病活动指数(DAI)及肺脏系数升高,结肠组织中MUC2、ATOH1和Occludin的蛋白表达水平降低(P<0.05)。与模型组相比,救必应-党参组小鼠体重下降率降低,救必应组、救必应-白芍组及救必应-党参组小鼠的结肠长度增加,救必应组、救必应-茯苓组及救必应-党参组小鼠的DAI降低,救必应组及救必应-白芍组小鼠的肺脏系数降低(P<0.05);救必应组及救必应-白芍组、救必应-柴胡组、救必应-党参组小鼠结肠组织黏膜下层水肿及炎症细胞浸润有所改善,救必应-白术组、救必应-茯苓组、救必应-蒲公英组小鼠结肠的黏液屏障损伤有所改善;救必应组MUC2、ATOH1和Occludin的蛋白表达水平上调,救必应-白术组、救必应-茯苓组、救必应-蒲公英组和救必应-党参组MUC2的蛋白表达水平上调,救必应-白芍能组ATOH1的蛋白表达水平上调,救必应-白术组Occludin的蛋白表达水平上调(P<0.05)。与救必应组相比,救必应-党参组的结肠长度增加,救必应-党参组及救必应-白芍药组对结肠病理改变的改善作用更为明显,救必应-白术组MUC2的蛋白表达水平更高(P<0.05)。结论救必应治疗脾胃病常用配伍药物为白芍、白术、茯苓、蒲公英、柴胡和党参。大多数含救必应药对可不同程度地改善UC小鼠模型的一般症状、病理表现及黏膜屏障蛋白的表达,其中,救必应-党参药对在改善结肠短缩及结肠病理改变方面均优于单用救必应,而救必应-白术药对在上调MUC2蛋白表达方面优于单用救必应。 展开更多
关键词 溃疡性结肠炎 救必应 药对 病理改变 黏膜屏障蛋白 数据挖掘技术 小鼠
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TBI后应激性肠屏障损害的研究进展
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作者 叶敏 杨文菲 +7 位作者 王丹心 周建 谭绍英 谢碧姣 李玉敏 许铃 孙海 王涛 《海南医学院学报》 CAS 北大核心 2024年第14期1111-1120,共10页
创伤性脑损伤后应激性肠屏障损害增加了患者的死亡风险,严重影响疾病预后,目前其发病机制和治疗策略仍不完全清楚。本文旨在总结创伤性脑损伤应激性肠屏障损害的病理机制和保护策略等关键问题的研究进展,发现肠上皮细胞通透性增加、紧... 创伤性脑损伤后应激性肠屏障损害增加了患者的死亡风险,严重影响疾病预后,目前其发病机制和治疗策略仍不完全清楚。本文旨在总结创伤性脑损伤应激性肠屏障损害的病理机制和保护策略等关键问题的研究进展,发现肠上皮细胞通透性增加、紧密连接、内质网应激、细胞自噬、缺血再灌注损伤可能是创伤性脑损伤应激后肠屏障损害的主要机制。此外,本文还综述了迷走神经刺激、益生菌、外源性补充饥饿素、氧疗等对创伤性脑损伤后应激性肠屏障损害的保护作用。本文将为探索精准有效的创伤性脑损伤后应激性肠屏障损害防治提供新视角和干预靶点。 展开更多
关键词 创伤性脑损伤 肠屏障损害 病理机制 保护策略 研究进展
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Blood-retinal barrier as a converging pivot in understanding the initiation and development of retinal diseases 被引量:7
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作者 Xue Yang Xiao-Wei Yu +1 位作者 Dan-Dan Zhang Zhi-Gang 《Chinese Medical Journal》 SCIE CAS CSCD 2020年第21期2586-2594,共9页
Clinical ophthalmologists consider each retinal disease as a completely unique entity.However,various retinal diseases,such as uveitis,age-related macular degeneration,diabetic retinopathy,and primary open-angle glauc... Clinical ophthalmologists consider each retinal disease as a completely unique entity.However,various retinal diseases,such as uveitis,age-related macular degeneration,diabetic retinopathy,and primary open-angle glaucoma,share a number of common pathogenetic pathways.Whether a retinal disease initiates from direct injury to the blood-retinal barrier(BRB)or a defect/injury to retinal neurons or glia that impairs the BRB secondarily,the BRB is a pivotal point in determining the prognosis as self-limiting and recovering,or developing and progressing to a clinical phenotype.The present review summarizes our current knowledge on the physiology and cellular and molecular pathology of the BRB,which underlies its pivotal role in the initiation and development of common retinal diseases. 展开更多
关键词 blood-retinal barrier Retinal inflammatory diseases Age-related macular degeneration Diabetic retinopathy Primary open-angle glaucoma NEUROINFLAMMATION
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SPF级大鼠自发性乳腺肿瘤的流行病学与病理学特点 被引量:10
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作者 赵磊 谷长勤 +4 位作者 张万坡 张金明 杨文祥 张道宏 唐利军 《中国实验动物学报》 CAS CSCD 2007年第2期116-119,F0003,共5页
目的自发性肿瘤的研究是实验动物学的研究内容之一,对其流行病学和病理学的研究可为动物模型的开发、肿瘤发病机制的探讨提供有价值的线索。方法对SPF级大鼠生产群进行流行病学调查和临床病理学观察。收集大鼠自发乳腺肿瘤病例,通过巨... 目的自发性肿瘤的研究是实验动物学的研究内容之一,对其流行病学和病理学的研究可为动物模型的开发、肿瘤发病机制的探讨提供有价值的线索。方法对SPF级大鼠生产群进行流行病学调查和临床病理学观察。收集大鼠自发乳腺肿瘤病例,通过巨检与镜下观察对肿瘤进行定性并分类。结果SD大鼠自发乳腺肿瘤发生率为10.5%,其中良性肿瘤为8.5%,恶性肿瘤为2.0%;Wistar大鼠乳腺自发肿瘤发生率为2.0%,其中良性肿瘤为1.5%,恶性肿瘤为0.5%。SD大鼠、Wistar大鼠乳腺良性肿瘤自发率均高于恶性肿瘤,并以纤维腺瘤和乳腺腺瘤最为多见。结论丰富了封闭群SPF级大鼠生物学背景资料,并为人类相应疾病动物模型的建立提供了一种途径。 展开更多
关键词 屏障系统 大鼠 乳腺肿瘤 流行病学 病理学
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血脑屏障与脑小血管病 被引量:48
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作者 李伟 李桂林 王拥军 《中国卒中杂志》 2010年第2期164-167,共4页
脑小血管病是指主要累及直径400μm以下的脑微小动脉血管病,临床表现为无症状性脑梗死,各种腔隙综合征和血管性认知功能障碍,影像学表现为腔隙性脑梗死灶,脑白质缺血性损害,微出血及血管间隙扩大的多种病因性疾病。血脑屏障渗透性的改... 脑小血管病是指主要累及直径400μm以下的脑微小动脉血管病,临床表现为无症状性脑梗死,各种腔隙综合征和血管性认知功能障碍,影像学表现为腔隙性脑梗死灶,脑白质缺血性损害,微出血及血管间隙扩大的多种病因性疾病。血脑屏障渗透性的改变与脑小血管病之间有着重要的关系,即血管内皮及相关结构功能障碍导致血脑屏障渗透性增加,造成血液成分漏出到血管周围组织和脑实质内,继发相应的病理生理改变,导致脑小血管病相关的影像学和病理变化。 展开更多
关键词 脑动脉疾病 血脑屏障 渗透 病理过程
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谷氨酰胺不同时点给药对内毒素致大鼠急性肺损伤的影响 被引量:3
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作者 白涛 孙艳红 王俊科 《中国医科大学学报》 CAS CSCD 北大核心 2007年第4期418-420,共3页
目的:观察不同时点给予谷氨酰胺对内毒素致大鼠急性肺损伤的影响。方法:静脉注射脂多糖(LPS)5mg/kg复制大鼠急性肺损伤模型。雄性SD大鼠80只,随机分为5组:对照组(C组);LPS组(L组);G1,G2,G3组为谷氨酰胺+LPS组,分别于LPS注入前1h、LPS注... 目的:观察不同时点给予谷氨酰胺对内毒素致大鼠急性肺损伤的影响。方法:静脉注射脂多糖(LPS)5mg/kg复制大鼠急性肺损伤模型。雄性SD大鼠80只,随机分为5组:对照组(C组);LPS组(L组);G1,G2,G3组为谷氨酰胺+LPS组,分别于LPS注入前1h、LPS注入即刻、LPS注入后1h静脉注射谷氨酰胺0.75g/kg。所有动物于注射LPS4h后颈动脉放血处死,取肺组织测定肺湿/干重比、肺组织TNF-α蛋白水平、伊文斯蓝含量。光镜下观察肺组织形态学变化,透射电镜下观察肺组织超微结构变化。结果:G1组和G2组肺湿/干重比、伊文斯蓝含量、肺组织TNF-α蛋白水平较L组明显下降,光镜下肺组织结构及透射电镜下肺组织超微结构明显改善;G3组上述指标变化与L组相似。结论:谷氨酰胺早期给药可降低内毒素所致急性肺损伤肺泡毛细血管膜的通透性,使肺组织病理损伤减轻。 展开更多
关键词 谷氨酰胺 成人型呼吸窘迫综合症 血气屏障 病理学
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双酚A的毒性作用机制 被引量:8
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作者 纪红蕊 陈家驹 +3 位作者 张茜 邹凤娟 李芬 刘波 《沈阳工业大学学报》 EI CAS 北大核心 2015年第6期710-715,共6页
针对环境污染日益严重的现状,探讨了双酚A(BPA)对小鼠的肝脏毒性和生殖毒性的作用机制.对血浆和肝脏中的关键酶与精子畸形率进行了检测,并利用紫外可见分光光度计观察了肝脏和睾丸的病理改变.结果表明,BPA可以显著升高谷丙转氨酶(GPT)... 针对环境污染日益严重的现状,探讨了双酚A(BPA)对小鼠的肝脏毒性和生殖毒性的作用机制.对血浆和肝脏中的关键酶与精子畸形率进行了检测,并利用紫外可见分光光度计观察了肝脏和睾丸的病理改变.结果表明,BPA可以显著升高谷丙转氨酶(GPT)、谷草转氨酶(GOT)、碱性磷酸酶(AKP)和谷胱甘肽S转移酶(GST)的活力、丙二醛(MDA)和一氧化氮(NO)的含量以及精子畸形率.BPA可以显著降低超氧化物歧化酶(SOD)的活力,并改变了肝脏和睾丸组织的正常形态.BPA不仅可以对肝脏造成损伤,还可以透过血睾屏障损害睾丸的支持细胞和间质细胞,从而干扰精子的生长、发育和能量代谢过程,进而对生殖系统造成损伤. 展开更多
关键词 双酚A 肝脏毒性 生殖毒性 脂质过氧化损伤 血睾屏障 精子活力 精子畸形率 病理改变
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克服肿瘤生理病理屏障的纳米药物递送系统的研究进展 被引量:7
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作者 苏志桂 莫然 张灿 《中国药科大学学报》 CAS CSCD 北大核心 2015年第1期28-39,共12页
纳米药物递送系统在肿瘤的靶向治疗中发挥着越来越重要的作用。由于机体的生理特征以及肿瘤的异质性,递送系统从给药到靶点发挥作用需要克服多重生理及病理屏障,包括血液、肿瘤组织、细胞和胞内转运等屏障。本文综述了近年来为克服药物... 纳米药物递送系统在肿瘤的靶向治疗中发挥着越来越重要的作用。由于机体的生理特征以及肿瘤的异质性,递送系统从给药到靶点发挥作用需要克服多重生理及病理屏障,包括血液、肿瘤组织、细胞和胞内转运等屏障。本文综述了近年来为克服药物递送屏障提出的新思路与新方法,为设计克服肿瘤生理病理屏障的递送系统、实现对药物的有效递送和肿瘤的高效安全治疗提供理论参考。 展开更多
关键词 纳米药物递送系统 生理病理屏障 肿瘤微环境 在体响应 靶向治疗
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邻苯二甲酸二丁酯的毒性作用及机制 被引量:15
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作者 纪红蕊 杜霞 +1 位作者 宋永彬 刘欣 《沈阳工业大学学报》 EI CAS 北大核心 2017年第2期230-235,共6页
针对环境污染日益严重的现状,探讨了邻苯二甲酸二丁酯(DBP)的肝脏与生殖毒性作用.检测了血浆和肝脏中的关键酶、精子活动力与畸形率,观察了肝脏和睾丸的病理改变.结果表明,DBP可以显著升高谷丙转氨酶(GPT)、谷草转氨酶(GOT)、碱性磷酸酶... 针对环境污染日益严重的现状,探讨了邻苯二甲酸二丁酯(DBP)的肝脏与生殖毒性作用.检测了血浆和肝脏中的关键酶、精子活动力与畸形率,观察了肝脏和睾丸的病理改变.结果表明,DBP可以显著升高谷丙转氨酶(GPT)、谷草转氨酶(GOT)、碱性磷酸酶(AKP)和丙二醛(MDA),显著降低超氧化物歧化酶(SOD)和过氧化氢酶(CAT),表明DBP会诱发小鼠肝脏发生脂质过氧化过程,引起早期的肝脏损伤.DBP能够穿透血-睾屏障,干扰精子的生长和发育过程.因此,DBP是一种对雄性生殖细胞具有潜在诱变危害的遗传毒性化合物. 展开更多
关键词 邻苯二甲酸二丁酯 肝脏毒性 生殖毒性 脂质过氧化损伤 血-睾屏障 精子活力 精子畸形率 病理改变
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