Swimming exercise attenuates LPS-induced spatial memory deficits associated with IL-17/NF-κB pathway and synaptic dysfunction in developing mice
4 affiliations
- 1Physical Education College, Jiangxi Normal University
- 2School of Sports and Health, Jiangxi Science and Technology Normal University
- 3Jiangxi Provincial Key Laboratory of Organic Functional Molecules, Institute of Organic Chemistry, Jiangxi Science and Technology Normal University
- 4Key Laboratory of Infection and Immunity, Health Commission of Jiangxi Province, Nanchang and School of Basic Medicine, Nanchang Medical College
Abstract
Background: Aerobic exercise is known to enhance learning and memory capabilities, whereas inflammation is detrimental to these cognitive functions. This study aimed to investigate the potential of swimming exercise to mitigate spatial memory deficits induced by lipopolysaccharide (LPS) in developing mice.
Results: Swimming mitigated spatial memory deficits in LPS-treated mice. Transcriptomic analysis indicated that hippocampal gene expression profiles were significantly associated with inflammatory responses, particularly implicating the IL-17/NF-κB signaling pathway. Further investigation using western blotting demonstrated that LPS administration increased the expression of hippocampal inflammatory factors (IL-6 and IL-17) and components of NF-κB p65, while decreasing synaptic proteins (GluA1). In contrast, swimming exercise reduced hippocampal inflammatory factors and NF-κB pathway components and increased synaptic proteins. Additionally, LPS decreased both the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in the CA1 region, as well as the amplitude of evoked excitatory postsynaptic currents (evoked EPSCs) and long-term potentiation (LTP) in the Schaffer collateral-CA1 pathway. Conversely, swimming exercise restored the frequency and amplitude of sEPSCs in the CA1 region and enhanced the amplitude of EPSCs. In conclusion, swimming alleviates LPS-induced spatial memory deficits in juvenile mice, an effect associated with modulation of the IL-17/NF-κB pathway and the enhancement of synaptic activity.
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BibTeX
@article{shi2026swimming,
title = {{Swimming exercise attenuates LPS-induced spatial memory deficits associated with IL-17/NF-κB pathway and synaptic dysfunction in developing mice}},
author = {Lulu Shi and Weiting Li and Su Zhan and Xiaocheng Liu and Zhuhong Wu and Zhibin Liu and Chong Chen and Songhua Wang and Jiang-Hua Li},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1954022},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1954022/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Swimming exercise attenuates LPS-induced spatial memory deficits associated with IL-17/NF-κB pathway and synaptic dysfunction in developing mice
AU - Lulu Shi
AU - Weiting Li
AU - Su Zhan
AU - Xiaocheng Liu
AU - Zhuhong Wu
AU - Zhibin Liu
AU - Chong Chen
AU - Songhua Wang
AU - Jiang-Hua Li
PY - 2026
DA - 2026/10/28
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1954022
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1954022/full
AB - Background: Aerobic exercise is known to enhance learning and memory capabilities, whereas inflammation is detrimental to these cognitive functions. This study aimed to investigate the potential of swimming exercise to mitigate spatial memory deficits induced by lipopolysaccharide (LPS) in developing mice. Results: Swimming mitigated spatial memory deficits in LPS-treated mice. Transcriptomic analysis indicated that hippocampal gene expression profiles were significantly associated with inflammatory responses, particularly implicating the IL-17/NF-κB signaling pathway. Further investigation using western blotting demonstrated that LPS administration increased the expression of hippocampal inflammatory factors (IL-6 and IL-17) and components of NF-κB p65, while decreasing synaptic proteins (GluA1). In contrast, swimming exercise reduced hippocampal inflammatory factors and NF-κB pathway components and increased synaptic proteins. Additionally, LPS decreased both the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in the CA1 region, as well as the amplitude of evoked excitatory postsynaptic currents (evoked EPSCs) and long-term potentiation (LTP) in the Schaffer collateral-CA1 pathway. Conversely, swimming exercise restored the frequency and amplitude of sEPSCs in the CA1 region and enhanced the amplitude of EPSCs. In conclusion, swimming alleviates LPS-induced spatial memory deficits in juvenile mice, an effect associated with modulation of the IL-17/NF-κB pathway and the enhancement of synaptic activity.
SN - 1664-3224
ER -