30 April 2019 : Animal Research
Effect of Aerobic Exercise on Serum Metabolites in Mice with Hepatocellular Carcinoma After Surgery
Tong Zhao1ABCDEF, Fanfu Fang1ABCD, Haiming Wang1BCD, Can Lv1BCD, Mengfei Han1BCD, Zhan Zhang1CD, Fuzhe Wang1CD, Bai Li1AEFG*, Changquan Ling2AEFGDOI: 10.12659/MSM.913377
Med Sci Monit 2019; 25:3181-3189
Abstract
BACKGROUND: Modern medicine has suggested exercise therapy is one of the main treatments for postoperative rehabilitation of tumors. It can influence the recovery of cancer patients by changing the body’s material metabolism and energy metabolism. However, studies on metabolic changes of exercise therapy on hepatocellular carcinoma (HCC) patients after surgery are limited. The aim of this study was to explore the effect of aerobic exercise on mice after orthotopic HCC surgery by serum metabolomics test and explore the related mechanism.
MATERIAL AND METHODS: A total of 60 C57Bl/6 mice were used to establish an orthotopic xenograft model of H22 mouse hepatoma cells. Mice were randomly divided into 6 groups and it was found that the metabolic products of the early postoperative exercise group and sedentary group mainly included L-tryptophan, citric acid, and other energy-related metabolites.
RESULTS: Energy metabolites, such as succinic acid of the high-intensity exercise group were increased after surgery, whereas phospholipid metabolites, including phosphatidylethanolamine (18: 0/0: 0), were decreased. In the moderate-intensity exercise group, the change tendency was consistent, and the level of various metabolites decreased.
CONCLUSIONS: Thus, it is likely that aerobic exercise reduced the degree of postoperative stress responses and improved energy metabolism in mice. The underlying mechanism involves improving the tricarboxylic acid cycle, intervening in energy metabolism, reorganization caused by the tumor, reducing the abnormal increase of phospholipase activity caused by the stress of liver cancer, reducing the level of hemolytic phospholipids, thereby inhibiting mitochondrial pathway-initiated apoptosis.
Keywords: Carcinoma, Hepatocellular, Exercise, Metabolomics, Rehabilitation, Alanine Transaminase, Aspartate Aminotransferases, Energy Metabolism, Globins, Liver Neoplasms, Mice, Inbred C57BL, Physical Conditioning, Animal, Random Allocation, Serum Albumin
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