Mountain-cultivated ginseng protects against cognitive impairments in aged GPx-1 knockout mice via activation of Nrf2/ChAT/ERK signaling pathwayopen access
- Authors
- Nguyen, B.T.; Shin, E.-J.; Jeong, J.H.; Sharma, N.; Tran, N.K.C.; Nguyen, Y.N.D.; Kim, D.-J.; Wie, M.B.; Lee, Y.; Byun, J.K.; Ko, S.K.; Nah, S.-Y.; Kim, H.-C.
- Issue Date
- Jul-2023
- Publisher
- Elsevier B.V.
- Keywords
- aged GPx-1 knockout mice; aging-induced cognitive impairments; hippocampus; mountain cultivated ginseng; Nrf2/ChAT/ERK signaling cascade
- Citation
- Journal of Ginseng Research, v.47, no.4, pp 561 - 571
- Pages
- 11
- Journal Title
- Journal of Ginseng Research
- Volume
- 47
- Number
- 4
- Start Page
- 561
- End Page
- 571
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/70992
- DOI
- 10.1016/j.jgr.2023.01.005
- ISSN
- 1226-8453
2093-4947
- Abstract
- Background: Escalating evidence shows that ginseng possesses an antiaging potential with cognitive enhancing activity. As mountain cultivated ginseng (MCG) is cultivated without agricultural chemicals, MCG has emerged as a popular herb medicine. However, little is known about the MCG-mediated pharmacological mechanism on brain aging. Methods: As we demonstrated that glutathione peroxidase (GPx) is important for enhancing memory function in the animal model of aging, we investigated the role of MCG as a GPx inducer using GPx-1 (a major type of GPx) knockout (KO) mice. We assessed whether MCG modulates redox and cholinergic parameters, and memory function in aged GPx-1 knockout KOmice. Results: Redox burden of aged GPx-1 KO mice was more evident than that of aged wild-type (WT) mice. Alteration of Nrf2 DNA binding activity appeared to be more evident than that of NFκB DNA binding activity in aged GPx-1 KO mice. Alteration in choline acetyltransferase (ChAT) activity was more evident than that in acetylcholine esterase activity. MCG significantly attenuated reductions in Nrf2 system and ChAT level. MCG significantly enhanced the co-localization of Nrf2-immunoreactivity and ChAT-immunoreactivity in the same cell population. Nrf2 inhibitor brusatol significantly counteracted MCG-mediated up-regulation in ChAT level and ChAT inhibition (by k252a) significantly reduced ERK phosphorylation by MCG, suggesting that MCG might require signal cascade of Nrf2/ChAT/ERK to enhance cognition. Conclusion: GPx-1 depletion might be a prerequisite for cognitive impairment in aged animals. MCG-mediated cognition enhancement might be associated with the activations of Nrf2, ChAT, and ERK signaling cascade. © 2023
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