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Effects of aerobic and resistance exercise on antioxidant stress index and brain-derived neurotrophic factor expression in the hippocampus of type 2 diabetic rats
Shui Xiaoping, Li Chunying, Li Mingjuan, Li Shunchang, Sun Junzhi, Su Quansheng
2023, 27 (2):
264-269.
doi: 10.12307/2022.1002
BACKGROUND: Diabetes mellitus will cause damage to the hippocampus and induce cognitive dysfunction. Oxidative stress and reduced neurotrophic factor expression are the main mechanism of diabetes-induced hippocampal damage. Long-term regular exercise is a positive intervention for diabetes-induced hippocampal damage; however, the related mechanism still needs further research.
OBJECTIVE: To observe the effects of aerobic and resistance exercise on the expression of heat shock protein 70, nuclear factor erythroid 2 p45-related factor 2, heme oxygenase 1, and brain-derived neurotrophic factor in the hippocampus of type 2 diabetic rats.
METHODS: The rats that had been fed with high-fat and high-sugar diet for 8 weeks were given a single intraperitoneal injection of streptozotocin to prepare a model of type 2 diabetes. Type 2 diabetic rats were randomly divided into diabetic control group, diabetic aerobic exercise group and diabetic resistance exercise group, with seven rats in each group. Another control rats were randomly divided into quiet control group, aerobic exercise group, and resistance exercise group, with seven rats in each group. The control rats continued to be fed with ordinary feed, while the diabetic rats continued to be fed with high-fat and high-sugar diet. The aerobic and resistance exercise lasted for 8 weeks in each exercise group. After 8-week exercises, fasting blood glucose and insulin resistance index were measured. Hematoxylin-eosin staining was used to observe the changes of hippocampal structure. The level of malondialdehyde and the activity of superoxide dismutase in brain were measured. The expression of heat shock protein 70, nuclear factor erythroid 2 p45-related factor 2, heme oxygenase 1, and brain-derived neurotrophic factor in the hippocampus were detected by western blot assay.
RESULTS AND CONCLUSION: After 8 weeks of exercise, compared with the quiet control group, fasting blood glucose and insulin resistance index of all diabetic rats were significantly increased (P < 0.01). The hippocampus of all diabetic rats showed pathological changes such as decreased number of vertebral cell layers, cell cavitation, cell necrosis, and disappearance of nucleoli. Compared with the diabetic control group, fasting blood glucose and insulin resistance index were significantly decreased (P < 0.01, P < 0.05) and the pathological changes of the hippocampus, such as cell cavitation, cell necrosis, and disappearance of nucleoli, were alleviated in the two diabetic exercise groups. Compared with the quiet control group, the malondialdehyde level was significantly increased in all diabetic rats (P < 0.01) and the superoxide dismutase activity was significantly decreased in the quiet diabetic group (P < 0.01). Compared with the diabetic control group, the malondialdehyde level was significantly decreased and the superoxide dismutase activity was significantly increased in the two diabetic exercise groups (P < 0.01, P < 0.05). Compared with the quiet control group, the expression levels of heat shock protein 70, nuclear factor erythroid 2 p45-related factor 2, heme oxygenase 1, and brain-derived neurotrophic factor were significantly decreased in all diabetic rats (P < 0.01). Compared with the diabetic control group, the expression levels of heat shock protein 70, nuclear factor erythroid 2 p45-related factor 2, and brain-derived neurotrophic factor were significantly increased in the two diabetic exercise groups (P < 0.05), and the expression of heme oxygenase 1 was significantly increased in the diabetic aerobic exercise group (P < 0.05). To conclude, aerobic and resistance exercises can both increase the expression of heat shock protein 70, nuclear factor erythroid 2 p45-related factor 2, heme oxygenase 1, and brain-derived neurotrophic factor proteins in the hippocampus of diabetic rats, thereby reducing hippocampal oxidative stress and promoting hippocampal nerve repair.
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