AI Article Synopsis

  • This study explored how ginsenoside Re (Re) impacts sociability and memory issues caused by phencyclidine (PCP) in mice, focusing on the GPx-1 gene's role in mitochondrial dysfunction.
  • It was found that PCP caused more severe sociability and memory deficits in mice lacking the GPx-1 gene compared to normal mice.
  • Treatment with Re significantly improved neurotoxic effects from PCP, showing similar efficacy as a PHOX inhibitor, suggesting that Re's protective effects rely on the interaction between GPx-1 activity and PHOX.

Article Abstract

We investigated whether ginsenoside Re (Re) modulates phencyclidine (PCP)-induced sociability deficits and recognition memory impairments to extend our recent finding. We examined the role of GPx-1 gene in the pharmacological activity of Re against mitochondrial dysfunction induced by PCP in the dorsolateral cortex of mice. Since mitochondrial oxidative stress activates NADPH oxidase (PHOX), we applied PHOX inhibitor apocynin for evaluating interactive modulation between GPx-1 and PHOX against PCP neurotoxicity. Sociability deficits and recognition memory impairments induced by PCP were more pronounced in GPx-1 knockout (KO) than in wild type (WT) mice. PCP-induced mitochondrial oxidative stress, mitochondrial dysfunction, and membrane translocation of p47phox were more evident in GPx-1 KO than in WT. Re treatment significantly attenuated PCP-induced neurotoxic changes. Re also significantly attenuated PCP-induced sociability deficits and recognition memory impairments. The attenuation by Re was comparable to that by apocynin. The attenuation was more obvious in GPx-1 KO than in WT. Importantly, apocynin did not show any additional positive effects on the neuroprotective activity of Re, indicating that PHOX is a molecular target for therapeutic activity of Re. Our results suggest that Re requires interactive modulation between GPx activity and PHOX (p47phox) to exhibit neuroprotective potentials against PCP insult.

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Source
http://dx.doi.org/10.1016/j.fct.2017.10.019DOI Listing

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