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Beyond BDNF modulation, Semax has been shown in animal ischemia models to modulate gene expression in neurotransmitter and inflammatory signaling pathways, and earlier pharmacological studies have described antioxidant and anti-neuroinflammatory properties (Dolotov et al., 2006

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Notably, schisandrin maintained intracellular glutathione (GSH) levels and prevented the depletion of caspase-acting factors that glutamate toxicity would normally cause (58)

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