The Role of Exercise in Reducing Hyperlipidemia‐Induced Neuronal Damage in Apolipoprotein E‐Deficient Mice
Yumeng Bai, Yali Feng, Bo Jiang, Yan Yang, Zuowei Pei, Qin Yang, Yanzeng Cui
Abstract
Hyperlipidemia causes nervous system‐related diseases. Exercise training has developed into an established evidence‐based treatment strategy that is beneficial for neuronal injury. This study investigated the effect of exercise on hyperlipidemia‐induced neuronal injury in apolipoprotein E‐deficient (ApoE -/- ) mice. Male ApoE -/- mice (age: 8 weeks) were randomly divided into four groups as follows: mice fed a normal diet (ND), normal diet+swimming training (ND+S), high‐fat diet (HD), and high‐fat diet+swimming (HD+S). Exercise training consisted of swimming for 40 min/day, 5 days/week for 12 weeks. After 12 weeks, we measured serum levels of total cholesterol (TC), triglyceride (TG), and low‐density lipoprotein cholesterol (LDL‐c). We also evaluated glial fibrillary acidic protein (GFAP) expression levels using immunohistochemistry, real‐time PCR, and immunoblotting. In addition, NLR family pyrin domain‐containing 3 (NLRP3), interleukin‐ (IL‐) 18, caspase‐1, Bax, Bcl‐2, and phosphorylated extracellular signal‐regulated kinase (p‐ERK) expression levels were measured using immunoblotting. Serum levels of TG, TC, and LDL‐c were lower in ApoE -/- HD+S mice than in ApoE -/- HD mice. Immunohistochemistry, real‐time PCR, and immunoblotting showed increased levels of GFAP in the ApoE -/- HD group. Immunoblotting revealed increased levels of NLRP3, IL‐18, caspase‐1, Bax, Bcl‐2, and p‐ERK in the ApoE -/- HD group; however, they were significantly suppressed in the ApoE -/- HD+S group. Therefore, exercise has protective effects against neuronal injury caused by hyperlipidemia.