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Assessment at the single-cell level identifies neuronal glutathione depletion as both a cause and effect of ischemia-reperfusion oxidative stress

In contrast, the total H3 acetylation in the liver was significantly enhanced after NaB intervention in vivo, and the total H3 acetylation was also obviously enhanced in vitro in HepG2 cells after NaB treatment, independent of GPR43 or GPR109a

controls in in vivo brain GSH overall