Modulation of cognitive functions by Rumex acetosa L. against scopolamine-induced memory impairment
• RA improved cognitive function in scopolamine-induced memory impairment. • RA decreased acetylcholinesterase activity and pro-inflammatory cytokines. • RA upregulated synaptic plasticity marker proteins in the hippocampus. • RA reduced apoptotic protein levels, indicating anti-apoptotic effects. • RA’s effects linked to anti-inflammatory and synaptic regulation pathways. Rumex acetosa L. (RA), also called sorrel, has been used in traditional medicine owing to its many of biological activities. However, molecular mechanisms underlying the ability of RA to modulate cognitive functions against memory impairment induced by scopolamine (SCO) through anti-inflammatory and -apoptotic activities have not been investigated. Memory impairment assessed using the MWM test. RA significantly decreased escape latency on the acquisition and retention trials of the training days and increased the time to enter the platform quadrant during the probe trial. Furthermore, RA significantly decreased AChE activity, pro-inflammatory cytokines concentrations and the apoptotic signaling proteins and elevated the protein concentrations of PSD-95, phosphorylated ERK1/2 and Akt in the hippocampus. Collectively, these results suggest that RA improves cognitive function in rats with SCO-induced memory impairment by regulating AChE activity and through its anti-inflammatory and anti-apoptotic effects, which associated with the upregulation of synaptic plasticity.
Authors
- Yonguk Kim (ORCID: https://orcid.org/0000-0003-3026-0893)
- Donghyuck Bae (ORCID: https://orcid.org/0000-0002-0002-4243)
- Dool-Ri Oh (ORCID: https://orcid.org/0000-0002-4348-6050)
- H. C. Ko
- Bo Yeong Mun
Institutions
- Jeonnam Bioindustry Foundation (KR)
Publication Details
- Journal
- Journal of Functional Foods
- Published
- 2024-11-26
- DOI
- https://doi.org/10.1016/j.jff.2024.106572
- Primary Topic
- Medicinal Plants and Neuroprotection
- Type
- article
- Field-Weighted Citation Impact
- 0.00