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Thus, collectively, excessive L-Glu levels can contribute to neuronal damage and degradation through different aetiology processes, including oxidative stress, excitotoxicity, mitochondrial dysfunction, inflammation, and protein aggregation, and thereby contribute to the progression of NDDs [37,38,39,40]
Under hepatitis B virus (HBV) infection in vitro and in vivo, sulforaphane promotes macrophages to the pro-inflammatory M1 phenotype [374], while, under inflammatory conditions both in vitro and in vivo, it induces macrophages to change to the anti-inflammatory M2 phenotype [375], as explained in the various sections of this article
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