The impact of the histone deacetylase inhibitor sodium butyrate on microglial polarization after oxygen and glucose deprivation

Ziabska, Karolina; Gargas, Justyna; Sypecka, Joanna; Ziemka‐Nałęcz, Małgorzata

doi:10.1007/s43440-022-00384-x

Cited by 5 publications

(1 citation statement)

References 38 publications

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“…Microglia adopt two different activation phenotypes, namely, M1 (classical activation) and M2 (selective activation). These two types of microglia are subgroups with different functions, but their dynamic changes are related to neuroimmune diseases [24][25][26]. M1 microglia produce proinflammatory and neurotoxic effects, while M2 microglia exert anti-inflammatory and neuroprotective effects [27].…”

Section: Discussionmentioning

confidence: 99%

TSAb Modulates Microglia M1 Polarization via Activation of the TSHR-Mediated NF-κB Signaling Pathway

Liu¹,

Yang²,

Wu³

et al. 2022

Neuroendocrinology

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Introduction: TSAb is a pathogenic antibody in the serum of patients with Graves' disease. The binding of TSAb to TSHR in non-thyroid tissue may be associated with the occurrence and development of Graves' disease-related complications. However, only few studies have been conducted on the effects of TSAb on the brain, and the pathogenesis of Acute hyperthyroidism myopathy (ATM) is unclear. Therefore, this study aimed to explore the effect of TSAb on the polarization of BV-2 cells in the brain and its possible mechanism and provide a basic experimental basis for ATM. Methods: BV-2 cells were treated with different concentrations of TSAb. The relative survival rate of BV-2 cells was determined using the CCK-8 assay, the migration ability of BV-2 cells was detected using the Transwell migration assay, and the expression levels of M1/M2 polarization markers (CD86, iNOS, CD206, and Arg-1), TSHR, TNF-α, and NF-κB protein in BV-2 cells were measured using WB. Results: Compared with the negative control group, the proliferative activity of BV-2 cells was significantly increased in the 20, 50, and 100 ng/ml TSAb groups, and the migration ability of BV-2 cells was significantly enhanced in the 50 and 100 ng/ml TSAb groups. The expression levels of M1 polarization markers (CD86 and iNOS), TSHR, TNF-α, and NF-κB protein in BV-2 cells treated with 50 and 100 ng/ml TSAb for 24 h were significantly upregulated, whereas those of M2 polarization markers (CD206 and Arg-1) were significantly decreased. Conclusions: TSAb can induce abnormal activation of microglia, polarize to the M1 phenotype, and promote the inflammatory cascade reaction, in which TSHR plays a key role in NF-κB activation and proinflammatory cytokine release.

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