Key Points
• Conclusion/Relevance: “In conclusion, the results of the present study showed that exercise treatment had a protective effect on hyperlipidemia-induced neuronal injury in ApoE-/- mice [apolipoprotein E-deficient]. Exercise reduced the increases in serum LDL-c and TC and protected against neuronal damage by inhibiting GFAP [glial fibrillary acidic protein] expression, inflammation, apoptosis, and activation of the p-ERK signaling pathway. The findings of this study could be beneficial in developing novel strategies for the prevention and treatment of neuronal injury.”
• Results of the current study showed that exercise protected against injury by impacting proinflammatory cytokine levels, apoptosis, GFAP expression, and the p-ERK pathway.
• The researchers observed no significant variation in body weights in the four groups of mice: normal diet (ND), normal diet+swimming training (ND+S), high-fat diet (HD), and high-fat diet+swimming (HD+S). Compared with ApoE-/- ND group mice, however, the investigators observed increased LDL-c and TC levels in ApoE-/- HD group mice.
• “In the current study, we found that p-ERK expression was significantly increased in the HD group. This showed that hyperlipidemia caused neuronal injury by activating the p-ERK signaling pathway, and exercise can inhibit this effect,” the authors wrote.