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This result supports that vitamin B6 may function as a source for brain therapeutics against excitotoxicity, since the release of glutamate in excess can result in neuronal damage (78)

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Previous studies have demonstrated that SalB effectively inhibits the binding of CD36 to its ligand, thereby mitigating its detrimental effects in atherosclerosis and inflammation (88, 89)

An overview of the toxicology and toxicokinetics of fusarenon-X, a type B trichothecene mycotoxin