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Inflammasome microglia

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https://www.readbyqxmd.com/read/29219210/bioenergetic-regulation-of-microglia
#1
REVIEW
Soumitra Ghosh, Erika Castillo, Elma S Frias, Raymond A Swanson
Microglia have diverse actions, ranging from synapse pruning in development to cytotoxic effects in disease. Brain energy metabolism and substrate availability vary under normal and disease states, but how these variations influence microglial function is relatively unknown. Microglia, like most other cell types, express the full complement of gene products required for both glycolytic and oxidative metabolism. Evidence suggests that microglia increase aerobic glycolysis and decrease respiration when activated by various stimuli...
December 8, 2017: Glia
https://www.readbyqxmd.com/read/29212744/selective-nlrp3-pyrin-domain-containing-protein-3-inflammasome-inhibitor-reduces-brain-injury-after-intracerebral-hemorrhage
#2
Honglei Ren, Ying Kong, Zhijia Liu, Dongyun Zang, Xiaoxia Yang, Kristofer Wood, Minshu Li, Qiang Liu
BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) is a devastating disease without effective treatment. As a key component of the innate immune system, the NOD-like receptor (NLR) family, NLRP3 (pyrin domain-containing protein 3) inflammasome, when activated after ICH, promotes neuroinflammation and brain edema. MCC950 is a potent, selective, small-molecule NLRP3 inhibitor that blocks NLRP3 activation at nanomolar concentrations. Here, we examined the effect of MCC950 on brain injury and inflammation in 2 models of ICH in mice...
December 6, 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/29196167/cathepsin-b-links-oxidative-stress-to-the-activation-of-nlrp3-inflammasome
#3
Hua Bai, Bo Yang, Wenfeng Yu, Yan Xiao, Dejun Yu, Qifang Zhang
Oxidative stress-mediated activation of NLRP3 inflammasome in microglia is critical in the development of neurodegerative diseases such as Alzheimer's disease (AD), Parkinson disease (PD). However, the mechanism underlying oxidative stress activates NLRP3 inflammasome remains exclusive. Here we demonstrated cathepsin B (CTSB) as a regulator of the activation of NLRP3 inflammasome by H2O2. H2O2 induced IL-1β secretion in NLRP3 inflammasome-dependent manner. H2O2 treatment increased CTSB activity, which in turn activated NLRP3 inflammasome, and subsequently processed pro-caspase-1 cleavage into caspase-1, resulting in IL-1 β secretion...
November 28, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/29191728/the-sp2-iminosugar-glycolipid-1-dodecylsulfonyl-5n-6o-oxomethylidenenojirimycin-dso2-onj-as-selective-anti-inflammatory-agent-by-modulation-of-hemeoxygenase-1-in-bv-2-microglial-cells-and-retinal-explants
#4
Elena Alcalde-Estévez, Ana I Arroba, Elena M Sánchez-Fernández, Carmen Ortiz Mellet, Jose M García Fernández, Laura Masgrau, Ángela M Valverde
Neuroinflammation is an early event during diabetic retinopathy (DR) that impacts the dynamics of microglia polarization. Gliosis is a hallmark of DR and we have reported the beneficial effects of 1R-DSO-ONJ, a member of the sp2-iminosugar glycolipid (sp2-IGL) family, in targeting microglia and reducing gliosis in diabetic db/db mice. Herein, we analyzed the effect of DSO2-ONJ, another family compound incorporating a sulfone group that better mimics the phosphate group of phosphatidylinositol ether lipid analogues (PIAs), in Bv...
November 27, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/29178967/blocking-atp-sensitive-potassium-channel-alleviates-morphine-tolerance-by-inhibiting-hsp70-tlr4-nlrp3-mediated-neuroinflammation
#5
Jie Qu, Xue-You Tao, Peng Teng, Yan Zhang, Ci-Liang Guo, Liang Hu, Yan-Ning Qian, Chun-Yi Jiang, Wen-Tao Liu
BACKGROUND: Long-term use of morphine induces analgesic tolerance, which limits its clinical efficacy. Evidence indicated morphine-evoked neuroinflammation mediated by toll-like receptor 4 (TLR4) - NOD-like receptor protein 3 (NLRP3) inflammasome was important for morphine tolerance. In our study, we investigated whether other existing alternative pathways caused morphine-induced activation of TLR4 in microglia. We focused on heat shock protein 70 (HSP70), a damage-associated molecular pattern (DAMP), which was released from various cells upon stimulations under the control of KATP channel and bound with TLR4-inducing inflammation...
November 25, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29173188/innate-immune-surveillance-in-the-central-nervous-system-in-legionella-pneumophila-infection
#6
Pasqualina Lagana, Luca Soraci, Maria Elsa Gambuzza, Santi Delia
Innate immune response represents a common event in many neuroinflammatory diseases. The resident immune cells of the central nervous system (CNS) are capable of sensing and reacting to both infections and sterile trauma. Peripheral immune cell migration into CNS is regulated by the blood-brain barrier (BBB), although peripheral immune cells can invade CNS through meninges, choroid plexus, perivascular spaces, and cerebrospinal fluid. Consequently, in the brain immune reactions can be mediated by both resident and peripheral immune cells...
November 23, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/29163015/resveratrol-attenuates-early-brain-injury-after-experimental-subarachnoid-hemorrhage-via-inhibition-of-nlrp3-inflammasome-activation
#7
Xiangsheng Zhang, Qi Wu, Qingrong Zhang, Yue Lu, Jingpeng Liu, Wei Li, Shengyin Lv, Mengliang Zhou, Xin Zhang, Chunhua Hang
Previous studies have demonstrated resveratrol (RSV) has beneficial effects in early brain injury (EBI) after subarachnoid hemorrhage (SAH). However, the beneficial effects of RSV and the underlying mechanisms have not been clearly identified. The nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation plays a crucial role in the EBI pathogenesis. The aim of this study was to investigate the role of RSV on the NLRP3 inflammasome signaling pathway and EBI in rats after SAH...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29111328/3-naphthalen-2-yl-propoxy-methyl-azetidine-hydrochloride-attenuates-nlrp3-inflammasome-mediated-signaling-pathway-in-lipopolysaccharide-stimulated-bv2-microglial-cells
#8
Ji Woong Yang, Seung-Ju Yang, Jung-Min Na, Hoh-Gyu Hahn, Sung-Woo Cho
The nucleotide-binding and oligomerization domain-like receptor containing a pyrin domain 3 (NLRP3) inflammasome is a multiprotein complex with a role in innate immune responses. NLRP3 inflammasome dysfunction is a common feature of chronic inflammatory diseases. Microglia activation is also associated with neuroinflammatory pathologies. We previously reported that 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride (KHG26792) reduced hypoxia-induced toxicity by modulating inflammation. However, no studies have elucidated the precise mechanisms for the anti-inflammatory action of KHG26792, in particular via inflammasome mediation...
October 27, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29070054/targeting-the-nlrp3-inflammasome-to-attenuate-spinal-cord-injury-in-mice
#9
Wu Jiang, Maoqiang Li, Fan He, Shaobo Zhou, Liulong Zhu
BACKGROUND: Spinal cord injury (SCI) is a devastating disease, which results in tissue loss and neurologic dysfunction. NLRP3 inflammasome plays an important role in the mechanism of diverse diseases. However, no studies have demonstrated the role of NLRP3 inflammasome and the effects of NLRP3 inflammasome inhibitors in a mouse model of SCI. We investigated whether inhibition of NLRP3 inflammasome activation by the pharmacologic inhibitor BAY 11-7082 or A438079 could exert neuroprotective effects in a mouse model of SCI...
October 25, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29067455/hyperbaric-oxygen-alleviates-the-activation-of-nlrp%C3%A2-3%C3%A2-inflammasomes-in-traumatic-brain-injury
#10
Huihui Qian, Qinghe Li, Woda Shi
Growing evidence has demonstrated that the nucleotide‑binding oligomerization domain‑like receptor family pyrin domain containing 3 (NLRP‑3) inflammasome‑mediated inflammatory pathways have been involved in the secondary injury of traumatic brain injury (TBI). In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP‑3 inflammasome pathway following TBI. Following the evaluation of motor deficits and brain edema, the therapeutic effects of HBO on interleukin (IL)‑1β and IL‑18 expression were assessed, as well as NLRP‑3 inflammasome activation following TBI...
October 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29057315/mitochondrial-impairment-in-microglia-amplifies-nlrp3-inflammasome-proinflammatory-signaling-in-cell-culture-and-animal-models-of-parkinson-s-disease
#11
Souvarish Sarkar, Emir Malovic, Dilshan S Harishchandra, Shivani Ghaisas, Nikhil Panicker, Adhithiya Charli, Bharathi N Palanisamy, Dharmin Rokad, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G Kanthasamy
The NLRP3 inflammasome signaling pathway is a major contributor to the neuroinflammatory process in the central nervous system. Oxidative stress and mitochondrial dysfunction are key pathophysiological processes of many chronic neurodegenerative diseases, including Parkinson's disease (PD). However, the inter-relationship between mitochondrial defects and neuroinflammation is not well understood. In the present study, we show that impaired mitochondrial function can augment the NLRP3 inflammasome-driven proinflammatory cascade in microglia...
2017: NPJ Parkinson's Disease
https://www.readbyqxmd.com/read/29038005/prednisone-alleviates-demyelination-through-regulation-of-the-nlrp3-inflammasome-in-a-c57bl-6-mouse-model-of-cuprizone-induced-demyelination
#12
Hao Yu, Mingfeng Wu, Geng Lu, Tingting Cao, Nan Chen, Yijia Zhang, Higuo Jiang, Hongbin Fan, Ruiqin Yao
Myelin abnormalities, oligodendrocyte damage, and concomitant glia activation are common in demyelinating diseases of the central nervous system (CNS). Increasing evidence has demonstrated that the inflammatory response triggers demyelination and gliosis in demyelinating disorders. Numerous clinical interventions, including those used to treat multiple sclerosis (MS), have confirmed prednisone (PDN) as a powerful anti-inflammatory drug that reduces the inflammatory response and promotes tissue repair in multiple inflammation sites...
October 13, 2017: Brain Research
https://www.readbyqxmd.com/read/28985759/role-of-microglial-amylin-receptors-in-mediating-beta-amyloid-a%C3%AE-induced-inflammation
#13
Wen Fu, Vlatka Vukojevic, Aarti Patel, Rania Soudy, David MacTavish, David Westaway, Kamaljit Kaur, Valeri Goncharuk, Jack Jhamandas
BACKGROUND: Neuroinflammation in the brain consequent to activation of microglia is viewed as an important component of Alzheimer's disease (AD) pathology. Amyloid beta (Aβ) protein is known to activate microglia and unleash an inflammatory cascade that eventually results in neuronal dysfunction and death. In this study, we sought to identify the presence of amylin receptors on human fetal and murine microglia and determine whether Aβ activation of the inflammasome complex and subsequent release of cytokines is mediated through these receptors...
October 6, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28977782/edaravone-attenuates-the-proinflammatory-response-in-amyloid-%C3%AE-treated-microglia-by-inhibiting-nlrp3-inflammasome-mediated-il-1%C3%AE-secretion
#14
Hong-Mei Wang, Ting Zhang, Jian-Kang Huang, Jing-Yan Xiang, Jing-Jiong Chen, Jian-Liang Fu, Yu-Wu Zhao
BACKGROUND/AIMS: Microglial activation is an important pathological feature in the brains of patients with Alzheimer's disease (AD), and amyloid-β (Aβ) peptides play a crucial role in microglial activation. In addition, edaravone (EDA) was recently shown to suppress oxidative stress and proinflammatory cytokine production in APPswePS1dE9 (APP/PS1) mice. However, the mechanism by which EDA inhibits the Aβ-induced proinflammatory response in microglia is poorly understood. METHODS: The mitochondrial membrane potential (∆ψm) was evaluated using JC-1 staining...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28941191/activating-%C3%AE-7-nicotinic-acetylcholine-receptor-inhibits-nlrp3-inflammasome-through-regulation-of-%C3%AE-arrestin-1
#15
Ping Ke, Bo-Zong Shao, Zhe-Qi Xu, Xiong-Wen Chen, Wei Wei, Chong Liu
AIMS: To evaluate whether activating α7 nicotinic acetylcholine receptor (α7nAChR) could inhibit the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of β-arrestin-1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation. METHODS: The protein levels of NLRP3, caspase-1 (Casp-1) p20 and proCasp-1, interleukin-1β (IL-1β) p17 and proIL-1β, IL-18 and proIL-18 were measured using Western blotting...
November 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28940479/activation-of-the-nlrp3-inflammasome-in-microglia-the-role-of-ceramide
#16
Hannah Scheiblich, Anna Schlütter, Douglas T Golenbock, Eicke Latz, Pilar Martinez-Martinez, Michael T Heneka
Inflammation within the CNS is a major component of many neurodegenerative diseases. A characteristic feature is the generation of microglia-derived factors that play an essential role in the immune response. IL-1β is a pro-inflammatory cytokine released by activated microglia, able to exacerbate injury at elevated levels. In the presence of caspase-1, pro-IL-1β is cleaved to the mature cytokine following NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation. Growing evidence suggests that ceramide plays a critical role in NLRP3 inflammasome assembly, however, the relationship between ceramide and inflammasome activation in microglia remains unknown...
September 23, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28903766/fluoxetine-enhanced-autophagy-ameliorates-early-brain-injury-via-inhibition-of-nlrp3-inflammasome-activation-following-subrachnoid-hemorrhage-in-rats
#17
Jian-Ru Li, Hang-Zhe Xu, Sheng Nie, Yu-Cong Peng, Lin-Feng Fan, Zhi-Jiang Wang, Cheng Wu, Feng Yan, Jing-Yin Chen, Chi Gu, Chun Wang, Jing-Sen Chen, Lin Wang, Gao Chen
BACKGROUND: The NLRP3 inflammasome is a multiprotein complex that regulates the innate immune inflammatory response by activating caspase-1 and subsequent IL-1β and IL-18. Fluoxetine has been shown to have the anti-inflammatory properties in many disease models. However, the effects and mechanisms of these effects of fluoxetine in early brain injury after subarachnoid hemorrhage (SAH) have not been defined. METHODS: The SAH model was induced by an endovascular perforation in adult male Sprague-Dawley (SD) rats weighing 300-320 g...
September 13, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28866823/neuroprotective-effects-of-baicalein-on-acrolein-induced-neurotoxicity-in-the-nigrostriatal-dopaminergic-system-of-rat-brain
#18
Wei-Zhong Zhao, Hsiang-Tsui Wang, Hui-Ju Huang, Yu-Li Lo, Anya Maan-Yuh Lin
Elevated levels of acrolein, an α,β-unsaturated aldehyde are detected in the brain of patients with Parkinson's disease (PD). In the present study, the neuroprotective effect of baicalein (a phenolic flavonoid in the dried root of Scutellaria baicalensis Georgi) on acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using local infusion of acrolein in the substantia nigra (SN) of rat brain. Systemic administration of baicalein (30 mg/kg, i.p.) significantly attenuated acrolein-induced elevations in 4-hydroxy-2-noneal (a product of lipid peroxidation), N-(3-formyl-3,4-dehydropiperidino)lysine (a biomarker of acrolein-conjugated proteins), and heme-oxygenase-1 levels (a redox-regulated protein) in the infused SN, indicating that baicalein inhibited acrolein-induced oxidative stress and protein conjugation...
September 2, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28843178/esculentoside-a-exerts-anti-inflammatory-activity-in-microglial-cells
#19
Hui Yang, Yijian Chen, Linjie Yu, Yun Xu
Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. This study was designed to evaluate the pharmacological effects of EsA on lipopolysaccharide (LPS)-stimulated BV2 microglia and primary microglia cells. Our results indicated that EsA pretreatment significantly decreased LPS-induced production of Nitric Oxide (NO) and Prostaglandin E2 (PGE2) and impeded LPS-mediated upregulation of pro-inflammatory mediators' expression such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-12 (IL-12) and tumor necrosis factor-a (TNF-α) in both BV2 microglia and primary microglia cells...
August 23, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/28836226/the-ketone-body-%C3%AE-hydroxybutyrate-does-not-inhibit-synuclein-mediated-inflammasome-activation-in-microglia
#20
Vandana Deora, Eduardo A Albornoz, Kevin Zhu, Trent M Woodruff, Richard Gordon
Parkinson's disease (PD) is recognized as the most common neurodegenerative movement disorder and results in debilitating motor deficits. The accumulation and spread of neurotoxic synuclein aggregates in the form of Lewy bodies is a key pathological feature of PD. Chronic activation of the NLRP3 inflammasome by protein aggregates is emerging as a major pathogenic mechanism in progressive neurodegenerative disorders and is considered an important therapeutic target. Recently the ketone body, β-hydroxy butyrate (BHB), was shown to efficiently inhibit the NLRP3 inflammasome in macrophages, and in vivo models of inflammatory disease...
December 2017: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
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