Reformulating Pro-Oxidant Microglia in Neurodegeneration

García-Revilla, Juan; Alonso-Bellido, Isabel María; Burguillos, Miguel Ángel; Herrera, Antonio J.; Espinosa-Oliva, Ana M.; Ruiz, Rocío; Cruz-Hernández, Luis; García-Domínguez, Irene; Roca-Ceballos, María Angustias; Santiago, Marti; Rodríguez‐Gómez, José A.; Soto, Manuel Sarmiento; Pablos, Rocío M. de; Venero, José L.

doi:10.3390/jcm8101719

Cited by 50 publications

(66 citation statements)

References 266 publications

(313 reference statements)

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“…Neuroinflammation and oxidative stress play a critical role in the neurodegenerative diseases (ND) development, where microglia exert an important function in the mechanisms of response to neuronal damage. Recently, it has been discovered a new microglia‐cell subpopulation named disease‐associated microglia (DAM), which redirects the classic vision of microglia, being a key element in the activation of prooxidative processes and inducing M1 microglia to produce proinflammatory cytokines (García‐Revilla et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect from Salvia hispanica peptide fractions on pro‐inflammatory modulation of HMC3 microglial cells

Leo

Campos

2020

J Food Biochem

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Neuroinflammation plays a critical role in the neurodegenerative disease's development, where microglia's act an important role in the mechanisms of response to neuronal damage. In the present research, the neuroprotective effect from Salvia hispanica peptide fractions on the proinflammatory modulation on HMC3 microglial cells was evaluated. From the enzymatic hydrolysis of a protein‐rich fraction from S. hispanica seeds, three peptide fractions (<1, 1–3 and 3–5 kDa) were obtained, from which its neuroprotective and anti‐inflammatory effect was determined on the production of proinflammatory mediators on HMC3 cells. The F1–3 kDa exhibited the greatest protective effect (79.04%), associated with the decrease in ROS cell production (51.3 ± 2.3%). Likewise, F1–3 kDa at 50 µg/ml, presented the highest reduction percentages of NO (33.1 ± 2.30%), TNFα (26.4 ± 1.1%) and IL6 (17.36 ± 1.6%). F1–3 kDa exhibited a neuroprotective effect in HMC3 cells associated with its antioxidant and anti‐inflammatory effect. Practical applications Currently, neurodegenerative diseases represent a global health problem, so the search for bioactive compounds with neuroprotective effect is useful in the prevention and treatment of this group of diseases. Peptide research with an effect on the proinflammatory and prooxidant mediator's reduction presents a potential application in the functional food's development aimed at the treatment of chronic diseases, that have oxidative stress and inflammation as their etiological factor. The present research adds to the scientific evidence of the potential benefits of bioactive peptides obtained from chia seeds. The results correlate with the main health benefits of whole chia seed in humans, such as antioxidant, anti‐inflammatory, hypoglycemic and hypotensive capacity. This relationship is associated with the protein and peptide composition of chia, which increases its added value as food.

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Section: Introductionmentioning

confidence: 99%

Neuroprotective effect from Salvia hispanica peptide fractions on pro‐inflammatory modulation of HMC3 microglial cells

Leo

Campos

2020

J Food Biochem

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“…However, anti-inflammatory microglia are involved in neurodegeneration and tissue repair by suppressing IL-12 secretion and by inducing the release of IL-10, transforming growth factor (TGF)-β, and arginase-1, instead of iNOS [8]. More recently, a new microglia phenotype, called disease associated microglia (DAM), has been related to neurodegenerative conditions [9,10]. In view of the foregoing, suppression of microglia-mediated inflammation can be considered as an important strategy in neurodegenerative disease prevention.…”

Section: Introductionmentioning

confidence: 99%

Hydroxytyrosol Decreases LPS- and α-Synuclein-Induced Microglial Activation In Vitro

et al. 2019

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I.M.A.-B.); rodriguez@us.es (J.A.R.-G.); jlvenero@us.es (J.L.V.); depablos@us.es (R.M.d.P.)Abstract: Neuroinflammation is a common feature shared by neurodegenerative disorders, such as Parkinson's disease (PD), and seems to play a key role in their development and progression. Microglia cells, the principal orchestrators of neuroinflammation, can be polarized in different phenotypes, which means they are able to have anti-inflammatory, pro-inflammatory, or neurodegenerative effects. Increasing evidence supports that the traditional Mediterranean dietary pattern is related to the reduction of cognitive decline in neurodegenerative diseases. A considerable intake of plant foods, fish, and extra virgin olive oil (EVOO), as well as a moderate consumption of red wine, all characteristic of the Mediterranean diet (MD), are behind these effects. These foods are especially rich in polyphenols, being the most relevant in the MD hydroxytyrosol (HT) and their derivatives present in EVOO, which have demonstrated a wide array of biological activities. Here, we demonstrate that HT is able to reduce the inflammation induced by two different stimuli: lipopolysaccharide and α-synuclein. We also study the possible molecular mechanisms involved in the anti-inflammatory effect of HT, including the study of nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and inflammasome. Our data support the use of HT to prevent the inflammation associated with PD and shed light into the relationship between MD and this neurological disorder.

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“…Recent studies suggest DAM as a new population of microglia under different disease conditions, which has challenged the classical view of microglia polarization, proinflammatory M1, and immunosuppressive M2 state [ 12 , 46 , 47 ]. In neurodegenerative diseases such as AD and PD, microglia-mediated neuroinflammation and oxidative stress are involved in detrimental events.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells

Kim

Shin

Han

et al. 2020

IJMS

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Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer’s disease, Parkinson’s disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.

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Reformulating Pro-Oxidant Microglia in Neurodegeneration

Cited by 50 publications

References 266 publications

Neuroprotective effect from Salvia hispanica peptide fractions on pro‐inflammatory modulation of HMC3 microglial cells

Neuroprotective effect from Salvia hispanica peptide fractions on pro‐inflammatory modulation of HMC3 microglial cells

Hydroxytyrosol Decreases LPS- and α-Synuclein-Induced Microglial Activation In Vitro

Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells

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