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Past studies indicated that attenuation of pathogen-associated molecular pattern-induced proinflammatory responses is coincident with inactivation of the NF-B signaling pathway and hyperactivation of extracellular signal-regulated kinase (ERK) 1/2 following administration of N -acetyl-l-cysteine polysulfides or GSSSG in various kinds of established cells, including mouse macrophage-like and human retinal pigment epithelial cells 33,45

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