scholarly journals Antioxidant support to ameliorate the oxaliplatin-dependent microglial alteration: morphological and molecular study

2021 ◽  
Vol 65 (s1) ◽  
Author(s):  
Jacopo J.V. Branca ◽  
Donatello Carrino ◽  
Ferdinando Paternostro ◽  
Massimo Gulisano ◽  
Matteo Becatti ◽  
...  
Keyword(s):  
Microglial Activation ◽  
Microglial Cell ◽  
Antioxidant Properties ◽  
Molecular Study ◽  
Third Generation ◽  
Cell Type ◽  
Predominant Role ◽  
Limited Efficacy ◽  
Microglial Cell Line ◽  
Colorectal Cancer Treatment

Oxaliplatin is a third-generation chemotherapy drug mainly used for colorectal cancer treatment. However, it is also known to trigger neuropathy whose underlying neurobiological mechanisms are still under investigation and currently available treatments show limited efficacy. It is now established that neurons are not the only cell type involved in chronic pain and that glial cells, mainly astrocytes and microglia, are involved in the initiation and maintenance of neuropathy. Among all the pathogenetic factors involved in neuropathic pain, an oxaliplatin-dependent oxidative stress plays a predominant role. In our study, the antioxidant properties of magnesium (Mg), manganese (Mn) and zinc (Zn) salts were evaluated in order to counteract microglial activation induced by oxaliplatin. The antioxidant efficacy of these metals was evaluated by the means of molecular and morphological assays on the BV-2 microglial cell line. Our data clearly show that Mg, Mn and Zn are able to prevent oxaliplatin-dependent microglial alterations by reducing both oxidative and endoplasmic reticulum stress.

scholarly journals Neuronutraceuticals Modulate Lipopolysaccharide- or Amyloid-β 1-42 Peptide-Induced Transglutaminase 2 Overexpression as a Marker of Neuroinflammation in Mouse Microglial Cells

2021 ◽  
Vol 11 (12) ◽  
pp. 5718
Author(s):  
Nicola Gaetano Gatta ◽  
Andrea Parente ◽  
Francesca Guida ◽  
Sabatino Maione ◽  
Vittorio Gentile
Keyword(s):  
Microglial Cell ◽  
Amyloid Β ◽  
Transglutaminase 2 ◽  
Microglial Cells ◽  
Tissue Type ◽  
Microglial Cell Line ◽  
Bv2 Cells ◽  
Important Marker

Background: Tissue type 2 transglutaminase (TG2, E.C. 2.3.2,13) is reported to be involved in the phagocytosis of apoptotic cells in mouse microglial BV2 cells and peripheral macrophages. In this study, by using lipopolysaccharide (LPS)- or amyloid-β 1-42 (Aβ 1-42) peptide-stimulated microglial cell line BV2 and mouse primary microglial cells, we examined the effects of different neuronutraceutical compounds, such as curcumin (Cu) and N-Palmitoylethanolamine (PEA), known for their anti-inflammatory activity, on TG2 and several inflammatory or neuroprotective biomarker expressions. Methods: Mouse BV2 cells were treated with LPS or Aβ1-42 in the presence of curcumin or PEA, in order to evaluate the expression of TG2 and other inflammatory or neuroprotective markers using Real Time-PCR and Western blot analyses. Results: Curcumin and PEA were capable of reducing TG2 expression in mouse microglial cells during co-treatment with LPS or Aβ 1-42. Conclusions: The results show the role of TG2 as an important marker of neuroinflammation and suggest a possible use of curcumin and PEA in order to reduce LPS- or Aβ1-42-induced TG2 overexpression in mouse microglial cells.

Neuroinflammation as a possible link between cannabinoids and addiction

2013 ◽  
Vol 26 (6) ◽  
pp. 334-346 ◽  
Author(s):  
Livia C.M. Rodrigues ◽  
Pedro H. Gobira ◽  
Antonio Carlos de Oliveira ◽  
Renan Pelição ◽  
Antonio Lucio Teixeira ◽  
...  
Keyword(s):  
Drug Addiction ◽  
Microglial Activation ◽  
Cell Activation ◽  
Microglial Cell ◽  
Substance Dependence ◽  
Present Review ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
The Past

ObjectiveSubstance dependence disorder is a chronically relapsing condition characterised by neurobiological changes leading to loss of control in restricting a substance intake, compulsion and withdrawal syndrome. In the past few years, (endo)cannabinoids have been raised as a possible target in the aetiology of drug addiction. On the other hand, although the exact mechanisms of the genesis of addiction remain poorly understood, it is possible that neuroinflammation might also play a role in the pathophysiology of this condition. Studies demonstrated that (endo)cannabinoids act as immunomodulators by inhibiting cytokines production and microglial cell activation. Thus, in the present review, we explore the possible role of neuroinflammation on the therapeutic effects of cannabinoids on drug addiction.MethodsWe conducted an evidence-based review of the literature in order to assess the role of cannabinoids on the neuroinflammatory hypothesis of addiction (terms: addiction, cannabinoids and inflammation). We searched PubMed and BioMedCentral databases up to April 2014 with no date restrictions.ResultsIn all, 165 eligible articles were included in the present review. Existing evidence suggests that disruption in cannabinoid signalling during the drug addiction process leads to microglial activation and neuroinflammation.ConclusionThe literature showed that inflammation and changes in endocannabinod signalling occur in drug abuse; however, it remains uncertain whether these changes are causally or coincidentally associated with addiction. Additional studies, therefore, are needed to elucidate the contribution of neuroinflammation on the behavioural and neuroprotective effects of cannabinoids on drug addiction.

Abstract 208: Action of Multifaceted Microglia on Blood Pressure Control

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
You Li ◽  
Liang Li ◽  
Zhiying Shan ◽  
Kenneth E Bernstein ◽  
Xiao Shen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Neuronal Plasticity ◽  
Microglial Activation ◽  
Myeloid Cell ◽  
Mannose Receptor ◽  
Pressure Control ◽  
Ang Ii ◽  
Differentiation Markers ◽  
Microglial Cell Line ◽  
Blood Pressure Responses

Microglia are the resident surveillance cells in the CNS, and are involved in shaping neuronal plasticity. Previous studies show that hypertension is associated with neuroinflammation. Interference of neuroinflammation by targeting microglia can inhibit or attenuate hypertension. To investigate the phenotypic changes of microglia during hypertension, we compared the profiles of microglia dissociated from normotensive and Ang II-induced hypertensive mice by flow cytometry. We found significant increases in the expression of CD89 (76%), CCR7 (52%), IFNγR (150%), MHC II (85%), CCR2 (51%), IL-4R (164%), mannose receptor (61%) and CD36 (60%) in Ang II microglia compared to the controls. To understand whether the microglial activation has a direct effect on blood pressure, we utilized microglia adoptive transfer strategy via intracerebroventricular (ICV) injection and then examined the blood pressure responses. Mouse microglial cell line, N9, was stimulated in groups as follows: 1) medium control, 2) 10 ng/ml LPS, 3)10 ng/ml LPS + 100 μM minocycline. After 6 hr treatment, half a million N9 cells were transferred into mice via ICV injection. Twenty-four hr later, the recipient mice were anesthetized, cannulated and positioned on the stereotaxic frame. The baseline blood pressure and heart rates were similar among groups (82±2 mmHg, 328±12.8 bpm). However, when we injected Ang II (50 ng in 1μl, ICV), there was a significant prolonged response in the recipient mice transferred with LPS-primed microglia compared to the ones receiving naïve controls (LPS 817±170 sec vs. control 475±70 sec; P<0.05 by unpaired T-test). This increase was fully abolished by co-incubation with minocycline, an inhibitor for microglial activation (LPS+minocycline 507±33 sec). There were no differences observed in pressure magnitude to ICV Ang II across the groups (11±2 mmHg). These data suggest that activated microglia alter neuronal plasticity and potentiate the neuronal responses to Ang II challenge. Taken together, microglial cells are activated, manifested by up-regulation of myeloid cell differentiation markers during hypertension, and then participate in the modulation of blood pressure.

scholarly journals Lipopolysaccharide induces mouse translocator protein (18 kDa) expression via the AP-1 complex in the microglial cell line, BV-2

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222861 ◽  
Author(s):  
Shuji Shimoyama ◽  
Tomonori Furukawa ◽  
Yoshiki Ogata ◽  
Yoshikazu Nikaido ◽  
Kohei Koga ◽  
...  
Keyword(s):  
Cell Line ◽  
Microglial Cell ◽  
Translocator Protein ◽  
Microglial Cell Line ◽  
Translocator Protein 18 Kda

scholarly journals Analgesic and Antidepressant Effects of Oltipraz on Neuropathic Pain in Mice by Modulating Microglial Activation

2019 ◽  
Vol 8 (6) ◽  
pp. 890 ◽  
Author(s):  
Andrés Felipe Díaz ◽  
Sara Polo ◽  
Núria Gallardo ◽  
Sergi Leánez ◽  
Olga Pol
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Prefrontal Cortex ◽  
Emotional Disorders ◽  
Microglial Activation ◽  
Antioxidant Properties ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Antidepressant Effects

Nerve injury provokes microglial activation, contributing to the sensory and emotional disorders associated with neuropathic pain that do not completely resolve with treatment. In C57BL/6J mice with neuropathic pain induced by chronic constriction of the sciatic nerve (CCI), we evaluated the effects of oltipraz, an antioxidant and anticancer compound, on (1) allodynia and hyperalgesia, (2) microglial activation and pain signaling pathways, (3) oxidative stress, and (4) depressive-like behaviors. Twenty-eight days after surgery, we assessed the effects of oltipraz on the expression of CD11b/c (a microglial marker), phosphoinositide 3-kinase (PI3K)/ phosphorylated protein kinase B (p-Akt), nuclear factor-κB (NF-κB) transcription factor, and mitogen activated protein kinases (MAPK) in the spinal cord, hippocampus, and prefrontal cortex. Our results show that oltipraz alleviates neuropathic pain by inhibiting microglial activation and PI3K/p-Akt, phosphorylated inhibitor of κBα (p-IκBα), and MAPK overexpression, and by normalizing and/or enhancing the expression of antioxidant proteins, nuclear factor erythroid derived-2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) in the spinal cord. The inhibition of microglial activation and induction of the Nrf2/HO-1/NQO1 signaling pathway in the hippocampus and/or prefrontal cortex may explain the antidepressant effects of oltipraz during neuropathic pain. These data demonstrate the analgesic and antidepressant effects of oltipraz and reveal its protective and antioxidant properties during chronic pain.

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