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We began analyzing https://link.springer.com/article/10.1007/s00726-011-0885-3, but it redirected us to https://link.springer.com/article/10.1007/s00726-011-0885-3. The analysis below is for the second page.

Title[redir]:
Anti-inflammatory mechanism of taurine against ischemic stroke is related to down-regulation of PARP and NF-κB | Amino Acids
Description:
Taurine is reported to reduce tissue damage induced by inflammation and to protect the brain against experimental stroke. The objective of this study was to investigate whether taurine reduced ischemic brain damage through suppressing inflammation related to poly (ADP-ribose) polymerase (PARP) and nuclear factor-kappaB (NF-κB) in a rat model of stroke. Rats received 2 h ischemia by intraluminal filament and were then reperfused. Taurine (50 mg/kg) was administered intravenously 1 h after ischemia. Treatment with taurine markedly reduced neurological deficits, lessened brain swelling, attenuated cell death, and decreased the infarct volume 72 h after ischemia. Our data showed the up-regulation of PARP and NF-κB p65 in cytosolic fractions in the core and nuclear fractions in the penumbra and core, and the increases in the nuclear poly (ADP-ribose) levels and the decreases in the intracellular NAD+ levels in the penumbra and core at 22 h of reperfusion; these changes were reversed by taurine. Moreover, taurine significantly reduced the levels of tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and intracellular adhesion molecule-1, lessened the activities of myeloperoxidase and attenuated the infiltration of neutrophils in the penumbra and core at 22 h of reperfusion. These data demonstrate that suppressing the inflammatory reaction related to PARP and NF-κB-driven expression of inflammatory mediators may be one mechanism of taurine against ischemic stroke.

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Keywords {🔍}

article, google, scholar, pubmed, cas, taurine, stroke, cerebral, ischemia, kim, brain, poly, cell, ischemic, adpribose, focal, amino, polymerase, parp, nfκb, inflammatory, acids, damage, myeloperoxidase, acid, related, experimental, nuclear, rat, death, nitric, oxide, activation, effect, content, mechanism, sun, inflammation, model, core, injury, nfkappab, role, chloramine, neurochem, med, privacy, cookies, data, zhao,

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month download article/chapter regulating parp-nf-κb signaling nf-κb-driven expression stress-induced transcription factors tumor necrosis factor-α ras-erk-nf-kappab defective nf-κb activation yi gu & chao xu granulocyte-colony stimulating factor human iκ b-α post-ischemic brain damage neuronal death/survival signaling decreased nf-kappab activation taurine chloramine-induced inhibition nf-κb p65 reactive oxygen species cerebral ischemia–reperfusion injury tnf-alpha gene expression full article pdf nf-kappab signaling nf-κb activation ischemia-induced apoptosis myeloperoxidase-quantified neutrophil accumulation nicotinamide adenine dinucleotide promotes cell death focal cerebral ischemia–reperfusion intracellular adhesion molecule-1 cell damage induced privacy choices/manage cookies cell death induced ischemic brain injury anti-inflammatory mechanism related subjects hypochlorous acid generation nuclear factor-kappab nuclear factor kappab ikappab kinase activity anti-inflammatory effects article sun ischemic cell death inflammatory gene expression taurine significantly reduced neuromodulator amino acids nf-κb myeloperoxidase activity assay free radicals damage schuller-levis neural cell damage cultured murine leukocytes programmed cell death

Questions {❓}

Yap YW, Whiteman M, Cheung NS (2007) Chlorinative stress: an under appreciated mediator of neurodegeneration?

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