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In human studies, long-term recreational ketamine use has been associated with structural brain changes, including reduced prefrontal gray matter volume and impaired white matter connectivity, which are potentially linked to chronic low-grade inflammation ( 5.2.2 Mitochondrial dysfunction Ketamine disrupts mitochondrial function by reducing the membrane potential, increasing cytochrome c release, and promoting ROS generation, which collectively induce neuronal apoptosis ( Human studies have identified metabolic abnormalities in ketamine abusers, particularly in the prefrontal cortex, which may reflect mitochondrial dysfunction ( 5.2.3 Dose and frequency dependence The neurotoxic effects of ketamine are highly dependent on its dosage and frequency of use

[383] showed that ferulic acid administered orally one hour after the UC induction and during five days at 20, 40, and 60 mg/kg doses ameliorated UC through the inhibition of the LPS-TLR4-NF-B and NF-B-INOS-NO signaling pathways

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