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1.
Although the inducible isoform of nitric oxide synthase (iNOS) is a well-established source of nitric oxide (NO*) during inflammation of the central nervous system (CNS), little is known about the involvement of constitutive isoforms of NOS (cNOS) in the inflammatory process. The aim of this study was to compare the responses of the expression and activity of iNOS and the two cNOS isoforms, neuronal and endothelial (nNOS and eNOS, respectively), in the brain to systemic inflammation and their roles in the cascade of events leading to degeneration and apoptosis. A systemic inflammatory response in C57BL/6 mice was induced by intraperitoneal injection of lipopolysaccharide [LPS; 1 mg/kg body weight (b.w.)]. The relative roles of the NOS isoforms were evaluated after injection of NG-nitro-L-arginine (NNLA; 30 mg/kg b.w.), which preferentially inhibits cNOS, or 1400W (5 mg/kg b.w.), an inhibitor of iNOS. Biochemical and morphological alterations were analyzed up to 48 hr after administration of LPS. Systemic LPS administration evoked significant ultrastructural alterations in brain capillary vessels, neuropils, and intracellular organelles of neurons, astrocytes, and microglia. Apoptotic/autophagic processes occurred in many neurons of the substantia nigra (SN), which coincided with exclusive enhancement of iNOS expression and activity in this brain region. Moreover, inhibitors of both iNOS and cNOS prevented LPS-evoked release of apoptosis-inducing factor (AIF) from SN mitochondria. Collectively, the results indicate that synthesis of NO* by both the inducible and constitutive NOS isoforms contribute to the activation of apoptotic pathways in the brain during systemic inflammation.  相似文献
2.
帕金森病的发病机理:氧化应激,环境影响因素与神经炎症   总被引:10,自引:3,他引:7  
目前,帕金森病的发病机理存在各种假说,包括氧化应激与清除自由基能力下降、线粒体功能异常、兴奋性氨基酸的毒性作用、神经营养因子的缺乏、神经炎症机制、基因与环境影响因素、一氧化氮毒性作用和凋亡等。本文就帕金森病的氧化应激、环境影响因素、神经炎症机制作一综述。  相似文献
3.
Spinal cord and brain injuries lead to complex cellular and molecular interactions within the central nervous system in an attempt to repair the initial tissue damage. Many studies have illustrated the importance of the glial cell response to injury, and the influences of inflammation and wound healing processes on the overall morbidity and permanent disability that result. The abortive attempts of neuronal regeneration after spinal cord injury are influenced by inflammatory cell activation, reactive astrogliosis and the production of both growth promoting and inhibitory extracellular molecules. Despite the historical perspective that the glial scar was a mechanical barrier to regeneration, inhibitory molecules in the forming scar and methods to overcome them have suggested molecular modification strategies to allow neuronal growth and functional regeneration. Unlike myelin associated inhibitory molecules, which remain at largely static levels before and after central nervous system trauma, inhibitory extracellular matrix molecules are dramatically upregulated during the inflammatory stages after injury providing a window of opportunity for the delivery of candidate therapeutic interventions. While high dose methylprednisolone steroid therapy alone has not proved to be the solution to this difficult clinical problem, other strategies for modulating inflammation and changing the make up of inhibitory molecules in the extracellular matrix are providing robust evidence that rehabilitation after spinal cord and brain injury has the potential to significantly change the outcome for what was once thought to be permanent disability.  相似文献
4.
BACKGROUND AND PURPOSE: Although patients with transient ischemic attack (TIA) experience cardiovascular events frequently, strong clinical predictors of recurrence are lacking. High-sensitivity C-reactive protein (hs-CRP) has been shown to be a powerful predictor of future first-ever and recurrent coronary and cerebral ischemic events. We aimed to investigate the relationship between hs-CRP and the risk of further ischemic events in TIA patients. METHODS: High-sensitivity C-reactive protein level was determined <24 h after symptom onset among 135 consecutive TIA patients and stroke recurrence or any new vascular event was recorded during 1 year follow-up period. RESULTS: A total of 38 (28.1%) patients experienced an end point event: 28 (20.7%) cerebral ischemic events, six (4.4%) heart ischemic events, four (3%) peripheral arterial disease, and nine (6.7%) vascular deaths. Cox proportional hazards multivariate analyses identified age [hazard ratio (HR) 1.07, 95% confidence interval (CI) 1.01-1.12, P = 0.01], large-artery occlusive disease (HR 2.73, 95% CI 1.16 to 6.41, P = 0.02) and hs-CRP> 4.1 mg/l (HR 2.81, 95% CI 1.12-7.10, P = 0.03) as independent predictors of stroke. Moreover, age (HR 1.05, 95% CI 1.01-1.10, P = 0.02), large-artery occlusive disease (HR 3.12, 95% CI 1.48-6.58, P < 0.01), coronary disease (HR 2.39, 95% CI 1.11-5.16, P = 0.03), and hs-CRP> 4.1 mg/l (HR 2.71, 95% CI 1.16-6.30, P = 0.02) were also independent predictors of any vascular event. CONCLUSIONS: High-sensitivity C-reactive protein serum level predicts further ischemic events following TIA. Routine CRP measurement might be a useful tool for identifying high-risk TIA patients in order to plan aggressive diagnostic protocols and prevention therapies.  相似文献
5.
Non-steroidal anti-inflammatory drugs in Parkinson's disease   总被引:7,自引:0,他引:7  
Parkinson's disease (PD) is known to be a chronic and progressive neurodegenerative disease caused by a selective degeneration of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNc). A large body of experimental evidence indicates that the factors involved in the pathogenesis of this disease are several, occurring inside and outside the DAergic neuron. Recently, the role of the neuron-glia interaction and the inflammatory process, in particular, has been the object of intense study by the research community. It seems to represent a new therapeutic approach opportunity for this neurological disorder. Indeed, it has been demonstrated that the cyclooxygenase type 2 (COX-2) is up-regulated in SNc DAergic neurons in both PD patients and animal models of PD and, furthermore, non-steroidal anti-inflammatory drugs (NSAIDs) pre-treatment protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6 hydroxydopamine (6-OHDA)-induced nigro-striatal dopamine degeneration. Moreover, recent epidemiological studies have revealed that the risk of developing PD is reduced in humans who make therapeutical use of NSAIDs. Consequently, it is hypothesized that they might delay or prevent the onset of PD. However, whether or not these common drugs may also be of benefit to those individuals who already have Parkinson's disease has not as yet been shown. In this paper, evidence relating to the protective effects of aspirin or other NSAIDs on DAergic neurons in animal models of Parkinson's disease will be discussed. In addition, the pharmacological mechanisms by which these molecules can exert their neuroprotective effects will be reviewed. Finally, epidemiological data exploring the effectiveness of NSAIDs in the prevention of PD and their possible use as adjuvants in the therapy of this neurodegenerative disease will also be examined.  相似文献
6.
Sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is of unknown cause and lacks successful treatment. Here we summarize diagnostic criteria and discuss our current understanding of the steps in the pathogenic cascade. While it is agreed that both degeneration and mononuclear-cell inflammation are components of the s-IBM pathology, how each relates to the pathogenesis remains unsettled. We suggest that the intra-muscle-fiber degenerative component plays the primary role, leading to muscle-fiber destruction and clinical weakness, since anti-inflammatory treatments are not of sustained benefit. We discuss possible treatment strategies aimed toward ameliorating a degenerative component, for example, lithium and resveratrol. Also discussed are the intriguing phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer and Parkinson’s diseases, the most common neurodegenerative diseases associated with aging. Similarities include, in the respective tissues, cellular aging, mitochondrial abnormalities, oxidative and endoplasmic-reticulum stresses, proteasome inhibition and multiprotein aggregates.  相似文献
7.
8.
C反应蛋白与动脉粥样硬化性疾病的关系研究及进展   总被引:6,自引:0,他引:6  
心脑血管疾病已经越来越成为现代社会危害人类健康的主要疾病,大多数心脑血管疾病都与动脉粥样硬化存在直接关系。近几年来,炎症在动脉粥样硬化及其并发症中起关键性作用的观点受到学者们相当的关注。炎症细胞侵润确见于动脉粥样硬化的各个阶段,从脂纹到晚期,到斑块破裂和血栓形成。  相似文献
9.
超敏C-反应蛋白与脑梗死关系的研究   总被引:5,自引:2,他引:3  
目的 研究血清中超敏C-反应蛋白(hs-CRP)与脑梗死发生的关系.方法 采用免疫比浊法测定血清中hs-CRP浓度.结果 与健康对照组比较,脑梗死组血清中hs-CRP浓度差异有统计学意义(P<0.01).首发和复发脑梗死组急性期患者血清中hs-CRP浓度比较无显著性差异(P>0.05).重度神经功能缺损患者和中度以及轻度神经功能缺损患者血清hs-CRP 浓度比较有显著性差异(P<0.05);脑梗死患者血清hs-CRP 浓度与神经功能缺损程度呈正相关( r = 0.48, P<0.05).结论 hs-CRP可能是导致脑梗死的独立危险因素之一,血清hs-CRP检测对于脑梗死的临床诊断和病情评估具有重要意义.  相似文献
10.
Cerebral inflammation and apoptotic cell death are two processes implicated in the progressive tissue damage that occurs following traumatic brain injury (TBI), and strategies to inhibit one or both of these pathways are being investigated as potential therapies for TBI patients. The tetracycline derivative minocycline was therapeutically effective in various models of central nervous system injury and disease, via mechanisms involving suppression of inflammation and apoptosis. We therefore investigated the effect of minocycline in TBI using a closed head injury model. Following TBI, mice were treated with minocycline or vehicle, and the effect on neurological outcome, lesion volume, inflammation and apoptosis was evaluated for up to 7 days. Our results show that while minocycline decreases lesion volume and improves neurological outcome at 1 day post-trauma, this response is not maintained at 4 days. The early beneficial effect is likely not due to anti-apoptotic mechanisms, as the density of apoptotic cells is not affected at either time-point. However, protection by minocycline is associated with a selective anti-inflammatory response, in that microglial activation and interleukin-1beta expression are reduced, while neutrophil infiltration and expression of multiple cytokines are not affected. These findings demonstrate that further studies on minocycline in TBI are necessary in order to consider it as a novel therapy for brain-injured patients.  相似文献
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