Sevoflurane suppresses microglial M2 polarization

Pei, Zengyang; Wang, Shenghao; Li, Qi

doi:10.1016/j.neulet.2017.07.001

Cited by 29 publications

(15 citation statements)

References 30 publications

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“…Unsurprisingly, M2 markers reduced significantly in HUC-MSC medium-treated microglia and IL-4 induced primary microglia cells after pretreating with 2% and 4% sevoflurane. Moreover, the suppression of M2 polarization was due to changes in IL-4 signaling, subsequently leading to repressive effects on STAT6 phosphorylation and suppressing cytokine signaling protein 1 (SOC1) expression, and STAT6 could no longer down-regulate levels of SOC3, which finally resulted in the blockage of M2 polarization [31]. Fluoxetine and S-citalopram are selective serotonin reuptake inhibitors (SSRIs) that are used for depression treatment.…”

Section: Role Of Macrophages In Brain Injuries and Neuron Protectionmentioning

confidence: 99%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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Macrophages can polarize into two different states (M1 and M2), which play contrasting roles during pathogenesis or tissue damage. M1 polarized macrophages produce pro-inflammatory cytokines and mediators resulting in inflammation, while M2 macrophages have an anti-inflammatory effect. Secretion of appropriate cytokines and chemokines from macrophages can lead to the modification of the microenvironment for bridging innate and adaptive immune responses. Increasing evidence suggests that polarized macrophages are pivotal for disease progression, and the regulation of macrophage polarization may provide a new approach in therapeutic treatment of inflammation-related diseases, including cancer, obesity and metabolic diseases, fibrosis in organs, brain damage and neuron injuries, and colorectal disease. Polarized macrophages affect the microenvironment by secreting cytokines and chemokines while cytokines or mediators that are produced by resident cells or tissues may also influence macrophages behavior. The interplay of macrophages and other cells can affect disease progression, and therefore, understanding the activation of macrophages and the interaction between polarized macrophages and disease progression is imperative prior to taking therapeutic or preventive actions. Manipulation of macrophages can be an entry point for disease improvement, but the mechanism and potential must be understood. In this review, some advanced studies regarding the role of macrophages in different diseases, potential mechanisms involved, and intervention of drugs or phytochemicals, which are effective on macrophage polarization, will be discussed.

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Section: Role Of Macrophages In Brain Injuries and Neuron Protectionmentioning

confidence: 99%

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Koh

Yang

Lai

et al. 2018

IJMS

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“…In vivo and in vitro studies had found that sevoflurane anesthesia induced microglial M1 activation and prevented microglial M2 polarization which contributed to cognitive decline in mice [8] , [19] , [20] . Consist with sevoflurane, western blotting analysis showed that the M1 markers (iNOS and CD68) of microglial cells were remarkably increased on Day 3 after long-term isoflurane anesthesia in the hippocampus of adult mice (iNOS: 1.00 ± 0.28 vs. 2.65 ± 0.30, P = 0.002; CD68: 1.00 ± 0.19 vs. 2.66 ± 0.42, P = 0.003) ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Previous evidence has shown that M1 microglia cells activation and A1-like astrocyte reactivation played a key role in general anesthetic-induced cognitive decline in aging and neonatal rodents [6] , [7] , [8] , [18] , [19] . In vitro study also found that prolonged sevoflurane exposure enhanced M1 polarization of microglial cell line BV-2 cells and inhibited M2 polarization of primary microglia and BV-2 cells [19] , [20] . Preventing microglia polarization into the M1 phenotype and attenuating A1-like astrocyte reactivation may mitigate anesthetics-induced neuroinflammation and cognitive decline.…”

Section: Introductionmentioning

confidence: 82%

Metformin alleviates prolonged isoflurane inhalation induced cognitive decline via reducing neuroinflammation in adult mice

Peng

Liu

et al. 2022

International Immunopharmacology

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“…Total RNA was prepared by directly lysing the cultured cells in extraction buffer (Trizol/phenol/chloroform) and reverse transcribing the mRNA into cDNA using oligo-dT and SuperScript II reverse transcriptase (Invitrogen, Carlsbad, CA, USA). The cDNA was subjected to polymerase chain reaction (PCR) for the measurement of mRNA levels of CISD2, BCL2, and M2 microglia specific markers based on a previous report [Pei et al, 2017 ; IL-10, Arginase-1 (Arg-1), Chitinase-3-like-3 (Ym1)]; proinflammatory mediators including TNF-α, IL-1β, iNOS, and COX2 (representative of M1 microglia); and the housekeeping gene GAPDH (internal control). The PCR protocol involved 25 cycles of denaturation for 1 min at 94°C, annealing for 1 min at 55°C to 60°C, and extension for 1 min at 72°C.…”

Section: Methodsmentioning

confidence: 99%

CISD2 Attenuates Inflammation and Regulates Microglia Polarization in EOC Microglial Cells—As a Potential Therapeutic Target for Neurodegenerative Dementia

Lin

2020

Front. Aging Neurosci.

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Background: Accumulating evidence has demonstrated a significant association between microglia-driven inflammation in the brain and neurodegenerative dementia. We previously showed a significant decline in CISD2 expression in mice models with advanced age. Moreover, we observed that the knockdown of CISD2 led to remarkable inflammation and mitochondrial dysfunction in neural cells. In the present study, we investigated whether CISD2 attenuation influences anti-inflammatory effects and M1-M2 polarization in microglia. Materials and Methods: The knockdown of CISD2 expression by siRNA (siCISD2) in EOC microglial cells was performed to mimic the age-driven decline of CISD2 expression. The extent of the inflammatory reaction, polarization in the M1/M2 spectrum, and NFκB activation were verified in EOC microglial cells exhibiting CISD2 deficiency. Results: In the cellular model of microglia, loss of CISD2 function mediated by siCISD2 exhibited a significant augmentation of proinflammatory signaling, as well as reduced expression levels of Arg-1, Ym1, IL-10, and BCL2. Attenuation of CISD2 expression led to a decrease in the proportion of the M2 phenotype of microglia (compared to M1). Enhanced DNA-binding activity of the NFκB p65 subunit was confirmed in cells transfected with siCISD2, as demonstrated by enzyme-linked immunosorbent assay (ELISA). Conclusions: To the best of our knowledge, this is the first report examining the following phenomena: (1) anti-inflammatory effects of CISD2 in microglia via NFκB regulation; and (2) microglial CISD2 assistance in the restoration of M2 microglia phenotype. The anti-inflammatory effects of CISD2 in microglia eventually augment anti-apoptotic effects, which provides a rationale for the development of potential therapeutic target for neurodegenerative diseases and neurodegenerative dementia.

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Sevoflurane suppresses microglial M2 polarization

Cited by 29 publications

References 30 publications

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Chemopreventive Effects of Phytochemicals and Medicines on M1/M2 Polarized Macrophage Role in Inflammation-Related Diseases

Metformin alleviates prolonged isoflurane inhalation induced cognitive decline via reducing neuroinflammation in adult mice

CISD2 Attenuates Inflammation and Regulates Microglia Polarization in EOC Microglial Cells—As a Potential Therapeutic Target for Neurodegenerative Dementia

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