Aerobic exercise suppresses atherosclerosis through adiponectin- nuclear transcription factor-κB pathway pathway in apolipoprotein E-deficient mice

• Published in: The American journal of the medical sciences 2016
• Main Authors: Wu, Weidong, MD, Jiao, Guangfa, PhD, Wang, Haiying, MD, Yue, Jingjing, MD, Wang, Guowei, MD
• Format: Article
• Language: English
• Subjects: Internal Medicine
• ISSN: 0002-9629
• DOI: 10.1016/j.amjms.2016.11.002

Abstract Background We aimed to investigate the therapeutic effect of aerobic exercise on atherosclerosis (AS) in apolipoprotein E-deficient mice and the adiponectin (ApN)-nuclear transcription factor-κB (NF-κB) pathway involved in the related anti-inflammation. Materials and Methods ApoE-deficient mice with AS (AS+C), and ApoE-deficient mice with AS and aerobic exercise (AS+E) were investigated for body weight and visceral fat. Pathomorphology of aortic vascular wall was qualitatively and quantitatively evaluated with hematoxylin-eosin staining. The ApN mRNA level in adipose tissue and ApN level in plasma were determined. The aortic adiponectin receptor 1 (AdipoR1) and NF-κB levels were determined with western blot. Results There was no significant difference in body weight between the AS+C and AS+E groups, but visceral fat in the AS+E group was significantly smaller than that in the AS+C group. Aortic vascular wall fiber board in the AS+C group broke, but this aortic disease in the AS+E group was obviously alleviated. The AS+E group showed a smaller neointimal hyperplasia and plaque area compared to AS+C group. After a high-fat diet, the ApN levels in both adipose tissue and plasma were decreased in the AS+C group and returned to a relative high level in the AS+E group. The expression of AdipoR1 protein in the AS+C group was significantly lower than those in the AS+E group. As for NF-κB protein, its enhanced expression in the AS+C group was reversed to a relatively low level in the AS+E group. Conclusion Aerobic exercise suppressed AS through the ApN-NF-κB pathway in apolipoprotein E -deficient mice.