In the hippocampus, DRD2, cleaved caspase-3, and γ-H2AX expression levels were significantly increased in the METH group but decreased in the krill oil–treated group. The KEGG pathway and GO enrichment analyses showed that the MAPK signaling pathway, cAMP signaling pathway, and dopaminergic synapse pathway were involved in the neuroprotective effects of krill oil. 20 hub genes such as DRD2, MAPK3, CREB, BDNF, and caspase-3 were filtered out as the underlying mechanisms of krill oil on improving memory deficits induced by METH. 210 predicted targets constituted the drug–compound–target network by network pharmacology analysis. With krill oil treatment, memory impairment induced by METH was significantly improved. The predicted hub genes and pathways were validated by the Western blot technique. The drug–component–target network was constructed in combination with network pharmacology. Learning and memory functions were evaluated by the Morris water maze. METH-exposed mice were treated with or without krill oil. The aim of the present study was to investigate the protective effect of krill oil on METH-induced memory deficits and to explore the molecular mechanisms by using an integrated strategy of bioinformatics analysis and experimental verification. Krill oil is rich in polyunsaturated fatty acids, while its effect on METH-induced cognitive impairment and mental disorders, and the underlying mechanism remain unknown. Methamphetamine (METH) abuse exerts severe harmful effects in multiple organs, especially the brain, and can induce cognitive dysfunction and memory deficits in humans. 2Department of Health and Physical Education, Jianghan University, Wuhan, China.1Wuhan Institutes of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan, China.Qin Ru 1, Xiang Tian 1, Qi Xiong 1, Congyue Xu 1, Lin Chen 2* and Yuxiang Wu 2*
0 kommentar(er)
