2022
DOI: 10.1016/j.mcn.2022.103759
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Taurine inhibits KDM3a production and microglia activation in lipopolysaccharide-treated mice and BV-2 cells

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Cited by 8 publications
(3 citation statements)
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“…Finally, in a recent work, taurine was administered to lipopolysaccharide (LPS)-treated mice and microglial (BV-2) cells. Taurine inhibited the LPS-induced increase in lysine demethylase 3a (KDM3a), a promoter of inflammation and microglia activation, improved the sociability of LPS-treated mice, inhibited microglia activation in the hippocampus, and reduced generation of brain inflammatory factors, such as interleukin-6, tumor necrosis factor-α, inducible nitric oxide synthase, and cyclooxygenase-2 [118].…”
Section: Discussionmentioning
confidence: 99%
“…Finally, in a recent work, taurine was administered to lipopolysaccharide (LPS)-treated mice and microglial (BV-2) cells. Taurine inhibited the LPS-induced increase in lysine demethylase 3a (KDM3a), a promoter of inflammation and microglia activation, improved the sociability of LPS-treated mice, inhibited microglia activation in the hippocampus, and reduced generation of brain inflammatory factors, such as interleukin-6, tumor necrosis factor-α, inducible nitric oxide synthase, and cyclooxygenase-2 [118].…”
Section: Discussionmentioning
confidence: 99%
“…Taurine has been thought to be essential for the development and survival of neural cells and to protect them under cell-damaging conditions, indeed in the brain stem taurine regulates vital functions, including cardiovascular control and arterial blood pressure. Its neuroprotective effects involve also reducing neuronal apoptosis and inflammation [46], making it a subject of interest in research on neurodegenerative diseases and brain injuries and offering benefits during stroke recovery [52][53][54][55][56]. Premature infants are vulnerable to taurine deficiency because they lack some of the enzymes needed to synthesize cysteine and taurine.…”
Section: Tissuementioning
confidence: 99%
“…Meanwhile, transforming growth factor-β (TGF-β1), a cell transformation factor, regulated cellular immune function, fibrosis, and cancer progression [ 17 ]. Remarkably, both KDM3A and TGF-β1 had protective roles under hypoxic organ conditions and contributed to responses to neuroinflammation [ 18 , 19 , 20 , 21 ]. Our research findings lead us to propose that circadian rhythm disruption might exacerbate AD development via the methylation of key gene m 6 A, which might be related to KDM3A and TGF-β1.…”
Section: Introductionmentioning
confidence: 99%