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The cognitive impairment of diabetes mellitus type 2(T2DM)is closely related to neurovascular coupling(NVC)changes,but the exact mechanism remains unclear.Functional MRI(fMRI)technology were able to jointly analyze NVC changes of T2DM,providing new ideas for revealing the mechanism of cognitive dysfunction caused by T2DM.The progresses of fMRI for exploring NVC changes in T2DM were reviewed in this article.
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External physicochemical factors and emotional changes often lead to intermittent facial flushing in patients with rosacea, accompanied by burning, stinging, and itching sensations. Many studies have demonstrated that neurovascular dysfunction and neurogenic inflammation induced by neuropeptides released following the activation of ion channels were associated with the occurrence of rosacea. This review summarizes research progress on the role of ion channels in the pathogenesis of rosacea and provides evidence for further research on ion channels as potential therapeutic targets for rosacea.
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Diabetes retinopathy (DR) is a blinding ocular complication of diabetes, and its pathological mechanism is complex. The damage to the retinal neurovascular unit (NVU) and the imbalance of its coupling mechanism are important pathological foundations. Autophagy plays an important role in the progression of DR. Oxidative stress, endoplasmic reticulum stress, hypoxia, and competitive endogenous RNA regulatory networks can affect the occurrence of autophagy, and autophagy induced cell death is crucial in NVU dysfunction. Retinal neurocyte are non-renewable cells, and adaptive autophagy targeting neuronal cells may provide a new direction for early vision rescue in patients with DR. It is necessary that exploring the possible autophagy interrelationships between ganglion cells, glial cells, and vascular constituent cells, searching for targeted specific cell autophagy inhibitors or activators, and exploring the impact of autophagy on the NVU complex more comprehensively at the overall level. Adopting different autophagy intervention methods at different stages of DR may be one promising research directions for future DR.
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Retzius-sparing robot assisted radical prostatectomy (RS-RARP) can significantly improve the immediate urinary continence without increasing the positive rate of surgical margin.However, the learning curve is long, and fewer than 10% of the surgeons can master it.Therefore,we have optimized the procedures of RS-RARP, applying radical prostatectomy with retrograde release of neurovascular bundle to preserve it to the maximum extent.Urethral anastomosis can be performed with only one suture, which eliminates the need for Hem-o-lok and reduces subsequent complications.Our team routinely carries out this operation, and conlcudes that this surgical method can achieve good tumor control, good urinary continence, fast recovery of sexual function, few complications, and strong operability.This article details the key steps and operation experience of this technique.
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Objective To observe the effects of total saponins of Trillium tschonoskii Maxim(TST)on vascular cognitive impairment(VCI),neurovascular units(NVUs),and neural circuit integrity in rats.Methods Forty-eight male Sprague-Dawley(SD)rats were randomly divided into sham-operated group,model group,TST group(intragastric administration,100 mg/kg),and donepezil group(intragastric administration,0.45 mg/kg),and then subjected to ischemic stroke by 2-VO method(bilateral common carotid artery ligation)or sham surgery.After 28 days of intragastric administration,Mirros water maze test was performed to evaluate the spatial learning and memory abilities of rats in each group.HE and Nissl staining were used to observe the pathological changes of brain tissue in rats.The expression of synuclein(SYN)in rat hippocampus was observed by immunohistochemical staining.Changes in dendritic spines in rat's hippocampal neurons were observed by Golgi staining.Western blotting was used to detect the expression levels of IL-1β,IL-10,vascular endothelial growth factor A(VEGFA),postsynaptic density protein 95(PSD95),and growth associated protein 43(GAP43)in rat's hippocampus in each group.Results In Mirros water maze test,rats in model group showed significant prolonged escape latency(P<0.05),and a significant reduction in the number of crossing platforms and the percentage of activity time in the target quadrant(P<0.05)than those in sham-operated group;while rats in TST group and donepezil group showed significant shortened escape latency(P<0.01),and significant increase of the number of times of crossing platforms and the percentage of activity time in the target quadrant(P<0.05)than those in model group.Compared of sham-operated group,model group showed a decrease in the expression of SYN and the number of neurons,Nissl bodies,and dendritic spines in the CA1 region of the hippocampus(P<0.05).Compared with model group,TST group and donepezil group showed an increase in the expression of SYN and the number of neurons,Nissl bodies,and dendritic spines in the CA1 region of the hippocampus(P<0.05).Western blotting showed a significant increase in the expression of IL-1β and VEGF(P<0.05),and a decrease in the expression of IL-10,PSD95,and GAP43(P<0.01)in rat's hippocampus of model group than those in sham-operated group.Compared with model group,TST group and donepezil group showed a significant decrease in the expression of IL-1β(P<0.05),and an increase in the expression of VEGFA,IL-10,and GAP43(P<0.05).Conclusions TST could alleviate cognitive impairment through promoting synaptic plasticity and neurovascular unit remodeling in 2-VO model rats,suggesting its significance as a potential drug for apoplexy.
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Diabetic retinopathy(DR)represents the primary cause of blindness among the global working-age population, and the disruption of the blood-retinal barrier is a crucial factor. Research in recent years has elucidated that DR transcends the scope of a mere microvascular disorder into a complex interplay of retinal glial cells and neurodegeneration microvascular pathology. Neuronal damage may precede vascular endothelial changes in the retinal neurovascular unit(RNVU)in the early stage of DR, and glial cell activation further exacerbates vascular barrier dysfunction. Retinal microglia are immune cells that reside in the retina and are involved in chronic inflammatory responses induced by long-term exposure to high glucose levels. Microglia secrete various inflammatory factors in response to high glucose levels, which can lead to the destruction of the blood-retinal barrier structure, increased neuronal apoptosis, and altered gliosis of Muller cells, thus affecting the retina's homeostatic balance. The RNVU has received increasing attention in recent years as a unitary structural study, and the mechanism of microglia in the RNVU and the progress of the study are reviewed.
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Based on the neurovascular unit(NVU), neurovascular coupling functions as a barrier to maintain the homeostasis of the microenvironment by regulating the signaling and metabolic activity of nerve cells and capillaries. Widely dispersed across the retina, the NVU is essential to preserving its normal physiological function. A disturbance in retinal neurovascular homeostasis produced by a range of factors can result in a variety of retinal disorders, such as diabetic retinopathy(DR), glaucoma, retinitis pigmentosa(RP)and age-related macular degeneration(ARMD). The retina also has a widespread distribution of brain-derived neurotrophic factor(BDNF), which functions to promote neuron growth and repair damage by binding to its receptor TrkB. In recent years, BDNF was found to play a protective role against damage in the early stage of retinal neurovascular homeostasis imbalance, often known as the neurodegenerative stage. It also helps to reduce the production of pro-angiogenic substances of neurological origin and offers a fresh approach for the early detection and treatment of associated eye disorders.
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Glaucoma is one of the leading causes of vision loss worldwide. More and more studies have suggested that glaucoma is a complicated retinal neurovascular disease. The homeostasis imbalance of retinal neurovascular unit(RNVU)composed of neurons, glial cells and microvascular cells not only induces changes in microvascular structure and glial cells, but also affects the nerve tissue of the retina, resulting in vision loss, which there is no effective treatment to reverse, currently. Exploring the cellular composition and molecular structure of RNVU and investigating the destruction mechanism of normal cellular environment and intercellular connections in glaucoma are of great significance in exploring the pathogenesis and the treatment of glaucoma. The research progress on structural changes and dysfunction of RNVU in glaucoma are reviewed, hoping to provide new ideas for the treatment of glaucoma.
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Introducción: Los síndromes de compresión de la salida torácica, en ocasiones poco definidos, se caracterizan por cervicobraquialgia como principal síntoma. Se deben a una compresión del tronco inferior del plexo braquial o de los vasos subclavios, estructuras que atraviesan la salida torácica. No ha sido establecida ninguna técnica diagnóstica y su tratamiento incluye la fisioterapia, medicamentos como los analgésicos y, en algunos casos, la cirugía. Objetivo: Presentar los resultados obtenidos con el tratamiento quirúrgico a pacientes que fueron diagnosticados, según su etiología, con diferentes síndromes de la salida torácica. Métodos: Se realizó un estudio a 131 pacientes diagnosticados como síndromes de la salida torácica, atendidos con síntomas referentes a estos en un periodo de 12 años, y que fueron intervenidos quirúrgicamente. El diagnóstico causal se basó en la clínica, estudios radiológicos, ultrasonográficos y electromiográficos y valoración de los factores de riesgo. Resultados: La edad más frecuente fue la tercera década de la vida y el sexo femenino fue más afectado. Como agente causal, las costillas cervicales supernumerarias y las apófisis costiformes se presentaron en mayor porcentaje, contituyendo la escalenotomia anterior y media el proceder quirúrgico más efectuado. Conclusiones: Los síntomas neurológicos evidenciaron una compresión nerviosa en la mayoría de los casos, y los resultados evaluados como buenos los más frecuentes, demostrando que el tratamiento quirúrgico de esta patología forma parte esencial de las mismas(AU)
Introduction: Thoracic outlet compression syndromes, sometimes poorly defined, are characterized by cervicobrachialgia as the main symptom. They are due to compression of the lower trunk of the brachial plexus or the subclavian vessels, structures that cross the thoracic outlet. No diagnostic technique has been established and its treatment includes physiotherapy, medications such as analgesics and, in some cases, surgery. Objective: To present the results obtained with the surgical treatment of patients who were diagnosed, according to their etiology, with different thoracic outlet syndromes. Methods: A study was carried out on 131 patients diagnosed as thoracic outlet syndromes, treated with symptoms related to these in a period of 12 years, and who underwent surgery. The causal diagnosis was based on the symptoms, radiological, ultrasonographic and electromyographic studies and assessment of risk factors. Results: The most frequent age was the third decade of life and the female sex was more affected. As a causal agent, the supernumerary cervical ribs and the costiform processes were present in a higher percentage, constituting the anterior and median scalenotomy the most performed surgical procedure. Conclusions: The neurological symptoms evidenced nerve compression in most cases, and the results evaluated as good in the most frequent, demonstrating that the surgical treatment of this pathology is an essential part of them(AU)
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HumainsRésumé
Objective:To investigate the correlation between adverse events and antiplatelet drug resistance after neurovascular intervention for cerebrovascular stenosis.Methods:A total of 148 patients with cerebrovascular stenosis who underwent neurovascular intervention at Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine from January 2020 to December 2020 were included in this study. The platelet function of patients before and 24 hours after antiplatelet drug treatment was recorded. Platelet drug resistance was analyzed. At 3, 6 months, and 1 year after neurovascular intervention, adverse events were recorded through follow-up. The patients were divided into the occurrence group and the non-occurrence group according to whether adverse events occurred or not using the case-control study method. The Spearman correlation coefficient was used to analyze the correlation between adverse events and antiplatelet drug resistance after neurovascular intervention for cerebrovascular stenosis.Results:After 1 year of follow-up, among the 148 patients, 29 patients lost their follow-up, and 119 were included in the final analysis. Of the 119 patients, 41 patients had adverse events and 78 patients had no adverse events. In the occurrence group, the expression levels of platelet membrane glycoprotein P-selectin and platelet activating complex were (20.22 ± 6.33)% and (68.80 ± 11.52)%, respectively, before drug treatment, and they were (15.77 ± 4.12)% and (43.19 ± 5.90%)%, respectively, after drug treatment, all of which were significantly higher than those in the non-occurrence group [before drug treatment: (16.85 ± 3.24)%, (62.34 ± 10.77)%, after drug treatment: (8.31 ± 2.97)%, (35.85 ± 5.14)%] (before drug treatment: t = 3.20, 2.97, both P < 0.05; after drug treatment: t = 10.28, 6.74, both P < 0.05). The incidences of aspirin resistance and clopidogrel resistance in the occurrence group were 51.2% (21/41) and 43.9% (20/41), respectively, which were significantly higher than 26.9% (8/78) and 19.2% (9/78) in the non-occurrence group ( χ2 = 24.47, 20.23, both P < 0.001). Spearman correlation analysis showed that both aspirin resistance and clopidogrel resistance were moderately positively correlated with adverse events after neurovascular intervention ( r = 0.45, 0.41, both P < 0.05). Conclusion:Adverse events after neurovascular intervention are moderately positively correlated with resistance to the antiplatelet drugs aspirin and clopidogrel.
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In recent years,increasing attention has been paid to the study on the pathogenesis of cerebral ischemia in terms of the overall structure and function of neurovascular unit(NVU),which has become one of the hot spots in the field of brain sciences and major brain diseases.This paper is intended to outline the roles of the four main NVU cells(neurons,astrocytes,microglia and cerebral microvascular endothelial cells)in brain function and pathogenesis of cerebral ischemia,which are closely related in structure,work together to maintain cerebral homeostasis in function,and play an important role in brain function and cerebral ischemic injuries.NVU injury leads to microvascular and blood brain barrier integrity impairment,neuronal cell death,glial reaction and immune cell infiltration,and even tissue injury and brain edema.This paper also aims to elucidate the roles of NVU structure and function in the pathogenesis of cerebral ischemia,and offer new ideas and strategies for the research related to drugs for prevention and treatment of cerebral ischemia based on NVU structure and function.
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@#Objective To investigate the relationship between neurovascular coupling and cognitive impairment in patients with type 2 diabetes mellitus (T2DM). Methods We consecutively enrolled 192 patients with T2DM admitted to the Department of Endocrinology in The Second Affiliated Hospital of Hainan Medical University as well as 30 healthy controls matched for sex, age, and years of education from February 1, 2022 to February 28, 2023. General clinical data were collected. All the participants were tested with the Montreal Cognitive Assessment (MoCA). Neurovascular coupling function was assessed through the dynamic changes in cerebral blood flow velocity (CBFV) induced by active elbow flexion monitored using functional transcranial Doppler sonography (fTCD). Patients with T2DM were divided into normal cognition (T2DM-NC) group and impaired cognition (T2DM-IC) group according to the MoCA score. The fTCD parameters were compared between the HC group, T2DM-NC group, and T2DM-IC group. The correlation between fTCD parameters and MoCA score was analyzed. Results A total of 81 patients with T2DM (52 with T2DM-NC and 29 with T2DM-IC) and 21 healthy volunteers were enrolled in this study. The glycated hemoglobin level was significantly higher in the T2DM-IC group than in the T2DM-NC and HC groups. Compared with the HC group, the T2DM group showed a significantly smaller percentage change from baseline in mean CBFV (Vm) during motor (ΔVm), a significantly smaller normalized area under the curve of Vm during motor (nAUC), and a significantly lower Vm slope (all P < 0.05). After normalization, the nAUC was significantly lower in the T2DM-IC group than in the T2DM-NC and HC groups, and the upward slope of Vm was significantly higher in the HC group than in the T2DM-NC and T2DM-IC groups (all P < 0.01). The ΔVm (r = 0.343, P = 0.001) and nAUC (r = 0.356, P = 0.001) were positively correlated with MoCA score. Baseline pulsatility index (PI, r = -0.496, P < 0.001), baseline resistance index (RI, r = -0.475, P < 0.001), PI during motor (r = -0.542, P < 0.001), and RI during motor (r = -0.523, P < 0.001) were negatively correlated with MoCA score. Conclusion Neurovascular uncoupling is a possible cause of cognitive impairment in patients with T2DM.
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The purpose of this paper is to analyze the pathogenesis of depression from the correlation between Nao Xuanfu and neurovascular unit(NVU).Previous studies have shown that NVU instability is a common pathophysiological link in the pathophysiological mechanism of depression,which involves neurotransmitters,immunity,inflammation,oxidation,heredity and their interaction,multi-targets,multi-pathways,and more complex.Under the principles of TCM holistic view and syndrome differentiation and treatment,it is considered that there is a great similarity between NVU and Naozhixuanfu.Therefore,this paper verifies the correlation between Nao Xuanfu and NVU from four aspects:morphological structure,energy supply,waste excretion and information exchange,and holds that there is a common connotation between NVU instability and Xuanfu depression,and then discusses the etiology and pathogenesis of depression from the perspective of Nao Xuanfu theory.It is considered that depression is located in the brain,the lesion is in Xuanfu,and the blockage of brain Xuanfu is the core pathogenesis,"communication"should be the most important in the treatment.Through the analogy between Nao Xuanfu and NVU,we look for the same pathogenic link in the seemingly independent pathogenesis,so as to provide new ideas for the clinical research of integrated traditional Chinese and western medicine.On the other hand,applying the pathogenesis of Xuanfu depression to clinical diagnosis and treatment will also provide new ideas for the clinical treatment of depression.
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Neurodegenerative diseases are a collective term for a large group of diseases caused by degenerative changes in nerve cells. Aging is the main risk factor for neurodegenerative diseases. The neurovascular unit(NVU) is the smallest functional unit of the brain, which regulates brain blood flow and maintains brain homeostasis. Accelerated aging of NVU cells directly impairs NVU function and leads to the occurrence of various neurodegenerative diseases. The intrinsic mechanisms of NVU cell aging are complex and involve oxidative stress damage, loss of protein homeostasis, DNA damage, mitochondrial dysfunction, immune inflammatory response, and impaired cellular autophagy. In recent years, studies have found that traditional Chinese medicine(TCM) can inhibit NVU aging through multiple pathways and targets, exerting a brain-protective effect. Therefore, this article aimed to provide a theoretical basis for further research on TCM inhibition of NVU cell aging and references for new drug development and clinical applications by reviewing its mechanisms of anti-aging, such as regulating relevant proteins, improving mitochondrial dysfunction, reducing DNA damage, lowering inflammatory response, antioxidant stress, and modulating cellular autophagy.
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Humains , Médecine traditionnelle chinoise , Maladies neurodégénératives/traitement médicamenteux , Encéphale , Vieillissement , Neurones , Barrière hémato-encéphaliqueRésumé
The concept of neurovascular unit(NVU), formalized in 2001 at a stroke conference, emphasizes the intimate relationship between the brain and its vessels, i.e., symbiotic relationship between brain cells and cerebral blood vessels in the developmental, structural and functional interdependence. The retina is a piece of brain. Several researchers have introduced the concept of NVU to the retina since 2007. The NVU in the retina includes neurons, glial cells, microvascular endothelial cells and pericytes. Dysfunctional NVU plays a critical role in diabetic retinopathy(DR). The current limited treatments for DR focus on the late-stage complications, i.e., diabetic macular edema and proliferative DR. While the further study on retinal NVU will develop efficacious therapeutic options for the early and all stages of DR.
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Neurovascular coupling is the function of regulating blood flow of the central nervous system at the level of neurovascular units. The central nervous system diseases related to neurovascular coupling mainly include cerebrovascular diseases such as chronic cerebral ischemia and neurodegenerative diseases such as Alzheimer's disease,Parkinson's disease and Lewy body dementia. The main mechanism of neurovascular coupling dysfunction leading to the above diseases is cerebrovascular dysfunction or loss,which leads to serious damage to neuronal ischemia and affects its function. Therefore,this paper reviews the research status of neurovascular coupling and its related central nervous system diseases,in order to guide the follow-up research. The purpose of this paper is to provide a basis for the prevention,relief and treatment of central nervous system diseases related to neurovascular coupling through the mechanism of neurovascular coupling.
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Diabetic retinopathy(DR)is a neurovascular disease caused by the neurovascular unit(NVU)impairment. Immune imbalance and inflammation are key factors that affect the normal function of NVU and lead to the progression of DR. Nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome is indicated as an important component of the inflammatory response, and it can identify endogenous danger signals, leading to the activation of caspase-1 and then activating a series of inflammatory cytokines and pyroptosis. Early activation of inflammasome maintains and promotes innate immunity against bacterial and viral infections, while excessive inflammasome activation results in excessive expression and ongoing action of inflammatory proteins, which in turn triggers off immune disorders and an inflammatory cascade that seriously harms the body. This review summarizes the recent research progress on the mechanism of NLRP3 inflammasome in NVU impairment of DR, including the related drugs targeting NLRP3 pathways.
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OBJECTIVE@#To evaluate the effectiveness of neurovascular staghorn flap for repairing defects in fingertips.@*METHODS@#Between August 2019 and October 2021, a total of 15 fingertips defects were repaired with neurovascular staghorn flap. There were 8 males and 7 females with an average age of 44 years (range, 28-65 years). The causes of injury included 8 cases of machine crush injury, 4 cases of heavy object crush injury, and 3 cases of cutting injury. There were 1 case of thumb, 5 cases of index finger, 6 cases of middle finger, 2 cases of ring finger, and 1 case of little finger. There were 12 cases in emergency, and 3 cases with finger tip necrosis after trauma suture. Bone and tendon exposed in all cases. The range of fingertip defect was 1.2 cm×0.8 cm to 1.8 cm×1.5 cm, and the range of skin flap was 2.0 cm×1.5 cm to 2.5 cm×2.0 cm. The donor site was sutured directly.@*RESULTS@#All flaps survived without infection or necrosis, and the incisions healed by first intention. All patients were followed up 6-12 months, with an average of 10 months. At last follow-up, the appearance of the flap was satisfactory, the wear resistance was good, the color was similar to the skin of the finger pulp, and there was no swelling; the two-point discrimination of the flap was 3-5 mm. One patient had linear scar contracture on the palmar side with slight limitation of flexion and extension, which had little effect on the function; the other patients had no obvious scar contracture, good flexion and extension of the fingers, and no dysfunction. The finger function was evaluated according to the total range of motion (TAM) system of the Hand Surgery Society of Chinese Medical Association, and excellent results were obtained in 13 cases and good results in 2 cases.@*CONCLUSION@#The neurovascular staghorn flap is a simple and reliable method to repair fingertip defect. The flap has a good fit with the wound without wasting skin. The appearance and function of the finger are satisfactory after operation.
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Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Sujet âgé , Cicatrice/chirurgie , Contracture/chirurgie , Lésions d'écrasement/chirurgie , Traumatismes du doigt/chirurgie , , Transplantation de peau/méthodes , Traumatismes des tissus mous/chirurgie , Résultat thérapeutiqueRésumé
A complex pathophysiological mechanism is involved in the brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of endothelial cells , neurons, glia, smooth muscle cells, and pericytes. The dyshomeostasis of NVU directly participates in the inflammatory immune regulation process. The components of NVU promote inflammatory overreaction and also synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunosuppression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage and worsening the condition. This article reviews the mechanism of SIID and the roles of NVU components in SIID, to provide a perspective for recanalization, prognosis and immune regulation therapy of cerebral infarction.
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A complex pathophysiological mechanism is involved in brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of neurons, endothelial cells, pericyte, astrocyte, microglia and extracellular matrix, etc. The dyshomeostasis of NVU directly participates in the regulation of inflammatory immune process. The components of NVU promote inflammatory overreaction and synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunodepression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage. This article reviews the mechanism of SIID and the roles of NVU in SIID, to provide a perspective for reperfusion, prognosis and immunomodulatory therapy of cerebral infarction.