scholarly journals Selective Upregulation of Per1 mRNA Expression by ATP Through Activation of P2X7 Purinergic Receptors Expressed in Microglial Cells

2011 ◽  
Vol 116 (4) ◽  
pp. 350-361 ◽  
Author(s):  
Ryota Nakazato ◽  
Takeshi Takarada ◽  
Tomomi Yamamoto ◽  
Shogo Hotta ◽  
Eiichi Hinoi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Purinergic Receptors ◽  
Microglial Cells

Piper sarmentosum Roxb. Root Extracts Confer Neuroprotection by Attenuating Beta Amyloid-Induced Pro-Inflammatory Cytokines Released from Microglial Cells

2019 ◽  
Vol 16 (3) ◽  
pp. 251-260 ◽  
Author(s):  
Elaine Wan Ling Chan ◽  
Emilia Tze Ying Yeo ◽  
Kelly Wang Ling Wong ◽  
Mun Ling See ◽  
Ka Yan Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Mrna Expression ◽  
Inflammatory Mediators ◽  
Beta Amyloid ◽  
Microglial Cells ◽  
Root Extracts ◽  
Tnf Α ◽  
P38α Mapk ◽  
Anti Inflammatory ◽  
Bv2 Microglial Cells

<P>Background: Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder that eventually leads to severe cognitive impairment. Although the exact etiologies of AD still remain elusive, increasing evidence suggests that neuroinflammation cascades mediated by microglial cells are associated with AD. Piper sarmentosum Roxb. (PS) is a medicinal plant reported to possess various biological properties, including anti-inflammatory, anti-psychotic and anti-oxidant activity. However, little is known about the anti-inflammatory activity of PS roots despite their traditional use to treat inflammatory- mediated ailments. Objective: This study aimed to evaluate the anti-inflammatory and neuroprotective properties of extracts obtained from the roots of PS against beta-amyloid (Aβ)-induced microglial toxicity associated with the production of pro-inflammatory mediators. Method: BV2 microglial cells were treated with hexane (RHXN), dichloromethane (RDCM), ethyl acetate (REA) and methanol (RMEOH) extracts of the roots of PS prior to activation by Aβ. The production and mRNA expression of pro-inflammatory mediators were evaluated by Griess reagent, ELISA kits and RT-qPCR respectively. The phosphorylation status of p38α MAPK was determined via western blot assay. BV2 conditioned medium was used to treat SH-SY5Y neuroblastoma cells and the neuroprotective effect was assessed using MTT assay. Results: PS root extracts, in particular RMEOH significantly attenuated the production and mRNA expression of IL-1β, IL-6 and TNF-α in Aβ-induced BV2 microglial cells. In addition, RHXN, REA and RMEOH extracts significantly reduced nitric oxide (NO) level and the inhibition of NO production was correlated with the total phenolic content of the extracts. Further mechanistic studies suggested that PS root extracts attenuated the production of cytokines by regulating the phosphorylation of p38α MAPK in microglia. Importantly, PS root extracts have protective effects against Aβ-induced indirect neurotoxicity either by inhibiting the production of NO, IL-1β, IL-6, and TNF-α in BV2 cells or by protecting SHSY5Y cells against these inflammatory mediators. Conclusions: These findings provided evidence that PS root extracts confer neuroprotection against Aβ- induced microglial toxicity associated with the production of pro-inflammatory mediators and may be a potential therapeutic agent for inflammation-related neurological conditions including Alzheimer’s disease (AD).</P>

scholarly journals Anti-Inflammatory Property of the Essential Oil from Cinnamomum camphora (Linn.) Presl Leaves and the Evaluation of Its Underlying Mechanism by Using Metabolomics Analysis

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4796
Author(s):  
Jiali Chen ◽  
Cailin Tang ◽  
Yang Zhou ◽  
Rongfei Zhang ◽  
Shaoxia Ye ◽  
...  
Keyword(s):  
Essential Oil ◽  
Mrna Expression ◽  
Underlying Mechanism ◽  
Treated Group ◽  
Microglial Cells ◽  
Cinnamomum Camphora ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Bv2 Microglial Cells

Cinnamomum camphora (Linn.) Presl has been widely used in traditional Chinese medicine for a variety of purposes. Our previous study indicated the antibacterial mechanism of the essential oil (EO) from C. camphora leaves; however, its anti-inflammatory activity and the underlying mechanism have not been clearly demonstrated. Thus, the present study investigated its anti-inflammatory property. Our data revealed that EO significantly decreased the release of nitric oxide (NO) and the mRNA expression of inducible NO synthase (iNOS) in lipopolysaccharide (LPS)-induced BV2 microglial cells. EO also attenuated LPS-induced increase in the mRNA expression and secretion of inflammatory cytokines including interleukin-6 (IL-6), IL-18, IL-1β and tumor necrosis factor-α (TNF-α). Furthermore, the metabolic profiles of LPS-induced BV2 microglial cells treated with or without EO were explored. Thirty-nine metabolites were identified with significantly different contents, including 21 upregulated and 18 downregulated ones. Five pathways were enriched by shared differential metabolites. Compared with the control cells, the glucose level was decreased, while the lactate level was increased, in the culture supernatant from LPS-stimulated cells, which were reversed by EO treatment. Moreover, compared to the LPS-treated group, the activities of phosphofructokinase (PFK) and pyruvate kinase (PK) in EO group were decreased. In summary, the current study demonstrated that EO from C. camphora leaves acts as an anti-inflammatory agent, which might be mediated through attenuating the glycolysis capacity of microglial cells.

Purinergic receptors on microglial cells: functional expression in acute brain slices and modulation of microglial activationin vitro

2003 ◽  
Vol 17 (11) ◽  
pp. 2267-2276 ◽  
Author(s):  
Clemens Boucsein ◽  
Robert Zacharias ◽  
Katrin Färber ◽  
Sanja Pavlovic ◽  
Uwe-Karsten Hanisch ◽  
...  
Keyword(s):  
Purinergic Receptors ◽  
Brain Slices ◽  
Functional Expression ◽  
Microglial Cells

scholarly journals The CD200R1 microglial inhibitory receptor as a therapeutic target in the MPTP model of Parkinson’s disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Neus Rabaneda-Lombarte ◽  
Joan Serratosa ◽  
Jordi Bové ◽  
Miquel Vila ◽  
Josep Saura ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mrna Expression ◽  
Therapeutic Target ◽  
Inflammatory Markers ◽  
Microglial Activation ◽  
Microglial Cells ◽  
Substantia Nigra Pars Compacta ◽  
Mrna Levels ◽  
Dopaminergic Neurodegeneration

Abstract Background It is suggested that neuroinflammation, in which activated microglial cells play a relevant role, contributes to the development of Parkinson’s disease (PD). Consequently, the modulation of microglial activation is a potential therapeutic target to be taken into account to act against the dopaminergic neurodegeneration occurring in this neurological disorder. Several soluble and membrane-associated inhibitory mechanisms contribute to maintaining microglial cells in a quiescent/surveillant phenotype in physiological conditions. However, the presence of activated microglial cells in the brain in PD patients suggests that these mechanisms have been somehow overloaded. We focused our interest on one of the membrane-associated mechanisms, the CD200-CD200R1 ligand-receptor pair. Methods The acute MPTP experimental mouse model of PD was used to study the temporal pattern of mRNA expression of CD200 and CD200R1 in the context of MPTP-induced dopaminergic neurodegeneration and neuroinflammation. Dopaminergic damage was assessed by tyrosine hydroxylase (TH) immunoreactivity, and neuroinflammation was evaluated by the mRNA expression of inflammatory markers and IBA1 and GFAP immunohistochemistry. The effect of the modulation of the CD200-CD200R1 system on MPTP-induced damage was determined by using a CD200R1 agonist or CD200 KO mice. Results MPTP administration resulted in a progressive decrease in TH-positive fibres in the striatum and TH-positive neurons in the substantia nigra pars compacta, which were accompanied by transient astrogliosis, microgliosis and expression of pro- and anti-inflammatory markers. CD200 mRNA levels rapidly decreased in the ventral midbrain after MPTP treatment, while a transient decrease of CD200R1 mRNA expression was repeatedly observed in this brain area at earlier and later phases. By contrast, a transient increase in CD200R1 expression was observed in striatum. The administration of a CD200R1 agonist resulted in the inhibition of MPTP-induced dopaminergic neurodegeneration, while microglial cells showed signs of earlier activation in CD200-deficient mice. Conclusions Collectively, these findings provide evidence for a correlation between CD200-CD200R1 alterations, glial activation and neuronal loss. CD200R1 stimulation reduces MPTP-induced loss of dopaminergic neurons, and CD200 deficiency results in earlier microglial activation, suggesting that the potentiation of CD200R1 signalling is a possible approach to controlling neuroinflammation and neuronal death in PD.

scholarly journals Cross talk between P2 purinergic receptors modulates extracellular ATP-mediated interleukin-10 production in rat microglial cells

2008 ◽  
Vol 40 (1) ◽  
pp. 19 ◽  
Author(s):  
Dong Reoyl Seo ◽  
Soo Yoon Kim ◽  
Kyung You Kim ◽  
Hwan Goo Lee ◽  
Ju Hyun Moon ◽  
...  
Keyword(s):  
Cross Talk ◽  
Purinergic Receptors ◽  
Interleukin 10 ◽  
Extracellular Atp ◽  
Microglial Cells ◽  
P2 Purinergic Receptors

Cannabinoids inhibit LPS-inducible cytokine mRNA expression in rat microglial cells

Glia ◽  
2000 ◽  
Vol 29 (1) ◽  
pp. 58-69 ◽  
Author(s):  
Robyn A. Puffenbarger ◽  
A. Catherine Boothe ◽  
Guy A. Cabral
Keyword(s):  
Mrna Expression ◽  
Microglial Cells ◽  
Cytokine Mrna ◽  
Cytokine Mrna Expression

scholarly journals Anti-inflammatory Property of the Essential Oil From Cinnamomum Camphora (Linn.) Presl Leaves and the Evaluation of Its Underlying Mechanism by Using Metabolomics Analysis

2020 ◽  
Author(s):  
Jiali Chen ◽  
Cailin Tang ◽  
Yang Zhou ◽  
Rongfei Zhang ◽  
Shaoxia Ye ◽  
...  
Keyword(s):  
Essential Oil ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Underlying Mechanism ◽  
Inflammatory Activity ◽  
Microglial Cells ◽  
Cinnamomum Camphora ◽  
Anti Inflammatory ◽  
Bv2 Microglial Cells ◽  
Metabolomics Analysis

Abstract Background: Cinnamomum camphora (Linn.) Presl has been widely used in traditional Chinese medicine for a variety of purposes. Our previous study indicated the antibacterial mechanism of the essential oil (EO) from C. camphora; however, the anti-inflammatory activity of EO and its underlying mechanism have not been clearly demonstrated. The present study aims to evaluate the anti-inflammatory principle and mechanism of EO.Methods: The anti-inflammatory activity of EO was evaluated in lipopolysaccharide (LPS)-induced BV2 microglial cells. Nitric oxide (NO) production was measured by NO assay kit. The mRNA expression levels of inducible NO synthase (iNOS), interleukin-6 (IL-6), IL-18 and IL-1β were examined by real time-PCR (RT-PCR). The secretion of pro-inflammatory cytokines in cell supernatants, including IL-6, IL-18 and IL-1β, were assessed by ELISA kits. Furthermore, the metabolic profile of BV2 microglial cells treated with or without EO was explored by GC-MS-based metabolomics analysis. Phosphofructokinase (PFK) and pyruvate kinase (PK) activities were detected by commercial kits.Results: EO significantly decreased the release of NO and the mRNA expression of iNOS in LPS-induced BV2 microglial cells. EO also attenuated LPS-induced increase in the mRNA expression and secretion of inflammatory cytokines including IL-6, IL-18 and IL-1β. 39 metabolites were identified with significantly different contents, including 21 upregulated and 18 downregulated ones, in the metabolomics analysis. Five pathways were enriched by shared differential metabolites. Additionally, compared with the control group, the glucose level was decreased, while the lactate level was increased, in the culture supernatant of LPS-induced BV2 microglia cells, which were reversed by EO treatment. Besides, compared to the LPS-treated group, the activities for PK and PFK in EO group were decreased by 17.59% and 18.23%, respectively.Conclusions: The EO from C. camphora acts as an anti-inflammatory agent, which might be mediated through attenuating the glycolysis capacity of microglial cells.

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