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The answer lies in the "first-pass effect." When glutathione is taken orally, it is often broken down by enzymes in the stomach and liver before it can reach the bloodstream in therapeutic concentrations

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In a mouse model of transient MCAO, KD pre-treatment or BHB post-treatment mitigated ischemic brain damage, reduced infarct volume, and suppressed hyperactivation of microglia by inhibiting NF-B activation through the interleukin-1 (IL-1) receptor-associated kinase M (IRAKM)-dependent pathway [71]

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