Tetramethylpyrazine attenuates endotoxin-induced retinal inflammation by inhibiting microglial activation via the TLR4/NF-κB signalling pathway

Han, Xiaokun; Chen, Xi; Chen, Shuilian; Luo, Qian; Li, Xuan; He, Anqi; He, Shengyu; Qiu, Jin; Chen, Pei; Wu, Yihui; Liu, Sian; Yang, Meng; Wu, Chuangran; Wu, Nanping; Yang, Ying; Ge, Jian; Yu, Keming

doi:10.1016/j.biopha.2020.110273

Cited by 26 publications

(19 citation statements)

References 35 publications

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“…which is known to transform microglia 33,34 . LPS injection caused a series of expected morphological changes to microglia in E12 saline -injected control mice; cell soma areas were significantly increased, total process length was shortened, and the number of branches was reduced [34][35][36] . The exact same pattern of changes was seen in E12, and E15 Poly(I:C) -injected mice ( Supplementary Fig.…”

Section: Mia Increases Motility Of Fetal Microglialmentioning

confidence: 99%

Maternal immune activation induces sustained changes in fetal microglia motility

Ozaki

Kato

Ikegami

et al. 2020

Sci Rep

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Maternal infection or inflammation causes abnormalities in brain development associated with subsequent cognitive impairment and in an increased susceptibility to schizophrenia and autism spectrum disorders. Maternal immune activation (MIA) and increases in serum cytokine levels mediates this association via effects on the fetal brain, and microglia can respond to maternal immune status, but consensus on how microglia may respond is lacking and no-one has yet examined if microglial process motility is impaired. In this study we investigated how MIA induced at two different gestational ages affected microglial properties at different developmental stages. Immune activation in mid-pregnancy increased IL-6 expression in embryonic microglia, but failed to cause any marked changes in morphology either at E18 or postnatally. In contrast MIA, particularly when induced earlier (at E12), caused sustained alterations in the patterns of microglial process motility and behavioral deficits. Our research has identified an important microglial property that is altered by MIA and which may contribute to the underlying pathophysiological mechanisms linking maternal immune status to subsequent risks for cognitive disease.

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Section: Mia Increases Motility Of Fetal Microglialmentioning

confidence: 99%

Maternal immune activation induces sustained changes in fetal microglia motility

Ozaki

Kato

Ikegami

et al. 2020

Sci Rep

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“…Chuanxiong and its bioactive component,2,3,5,6-tetramethylpyrazine (TMP) may be used in the clinical treatment of neural ocular diseases, such as DR (Zhu et al, 2015). The study of Han et al (2020) found pretreatment with TMP inhibited RMC activation, migration, and regeneration, especially in GCL. They demonstrated that TMP could attenuate retinal inflammation by inhibiting microglial activation via the TLR4/NF-κB signaling pathway.…”

Section: Homocysteinementioning

confidence: 99%

Retinal microglia polarization in diabetic retinopathy

et al. 2021

Vis Neurosci

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Microglia, the main immune cell of the central nervous system (CNS), categorized into M1-like phenotype and M2-like phenotype, play important roles in phagocytosis, cell migration, antigen presentation, and cytokine production. As a part of CNS, retinal microglial cells (RMC) play an important role in retinal diseases. Diabetic retinopathy (DR) is one of the most common complications of diabetes. Recent studies have demonstrated that DR is not only a microvascular disease but also retinal neurodegeneration. RMC was regarded as a central role in neurodegeneration and neuroinflammation. Therefore, in this review, we will discuss RMC polarization and its possible regulatory factors in early DR, which will provide new targets and insights for early intervention of DR.

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“…Microglia are resident immune cells of the retina, and activated microglia release inflammatory factors including tumor necrosis factor (TNF-α) cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), which further aggravate retinal damage and blood–retina barrier (BRB) dysfunction. In turn, overproduction of inflammatory factors further results in microglial reactivation, and reactivated microglia release more inflammatory factors, frequently aggravating the uncontrolled inflammatory cascade in the retina [ 13 , 14 ]. Microglia activation states can be divided into a proinflammatory M1 state and an anti-inflammatory M2 state.…”

Section: Introductionmentioning

confidence: 99%

Icariin alleviates uveitis by targeting peroxiredoxin 3 to modulate retinal microglia M1/M2 phenotypic polarization

Wang

et al. 2022

Redox Biology

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Tetramethylpyrazine attenuates endotoxin-induced retinal inflammation by inhibiting microglial activation via the TLR4/NF-κB signalling pathway

Cited by 26 publications

References 35 publications

Maternal immune activation induces sustained changes in fetal microglia motility

Maternal immune activation induces sustained changes in fetal microglia motility

Retinal microglia polarization in diabetic retinopathy

Icariin alleviates uveitis by targeting peroxiredoxin 3 to modulate retinal microglia M1/M2 phenotypic polarization

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