| Research Objective: Oxidative stress is a biological phenomenon associated with a range of degenerative diseases observed during aging,including Alzheimer's disease and Parkinson's disease,which cause learning and memory impairment.Long-term running exercise can slow down the oxidative stress caused by aging,improve learning and memory ability and repair neuronal damage.Aerobic exercise is considered an effective way to protect brain function from the aging process,most likely as a result of aerobic exercise activating the brain's Keap1-Nrf2/ARE signaling pathway.Keap1-Nrf2/ARE signaling pathway has an important regulatory effect on the body's oxidative stress response.In this experiment,the protective effect of aerobic exercise on the oxidative stress-induced cognitive memory disorder of D-semi-lactose aging rats by modeling D-semi-lactose-induced aging model and moderate-to-low-intensity aerobic exercise by modeling D-semi-lactose-induced aging models and moderate-to-low-intensity aerobic exercise.Attempts to explore the mechanisms of aerobic exercise to delay brain aging in behavioral and molecular studies provide experimental evidence for the theory of oxidative stress(free radical)aging,and provide experimental referencefor the determination of new treatment objectives and the development of medical rehabilitation strategies to meet the needs of the aging population.Experimental Method: Forty SPF male SD rats aged 6 weeks were randomly divided into five groups: 1.Control group(C),2.Exercise group(E),3.D-galactose aging group(D),4.D-galactose exercise group(DE),5.Exercise inhibition aging group(ADE).Modeling of aging: intraperitoneal injection of D-galactose solution 1mL/(kg.d)for 8 weeks;low-intensity aerobic treadmill exercise(15 m/h,slope 0degree,20 min/d,6 days a week)was used in the exercise model during the modeling of D-galactose aging;moderate-intensity aerobic exercise was used in the exercisemodel after the completion of the modeling,while the control group did not.Motion and exercise groups are trained for a week to gradually speed up the treadmill and make it gradually adapt to the training intensity of the experimental design.Running platform gradient is set to 0,running speed finally reaches 1.1 km/h,lasting from 20 minutes to 60 minutes,six days a week training for 8 weeks.After the intervention of aerobic treadmill exercise,rats in each group were trained in Morris water maze.Then rats were dissected and their hippocampus and cortex were stripped.The expressions of Nrf2 protein and Keap1 protein in the hippocampus and cortex of rats in each group were determined by Western Blot analysis.The content of malondialdehyde(MAD)and the activity of total superoxide dismutase(T-SOD)in hippocampus of rats in each group were measured by kit,and the antioxidant defense ability of aerobic exercise intervention was evaluated.Result: 1.Marris water maze behavioral test results: With the increase of training time,the latency of each group of rats has a downward trend,and the incubation period of the exercise group and the incubation period is significantly shorter than that of the control group,and there is a difference between the second and fourth days of training.(P <0.05-0.01);compared with the D-galactose exercise group,the latency period of the D-galactose aging group was significantly reduced from the second day(p <0.05-0.01).2.Western Blot analysis showed that the expression of Nrf2 protein was up-regulated in the D-galactose exercise group and D-galactose aging group in the hippocampus and cortex of SD rats(p <0.05);the exercise group and exercise-inhibited aging group were compared with the control There was no difference between the groups and there was no statistical significance.In SD rat hippocampus,the D-galactose aging group had no difference compared with the D-galactose aging exercise group,but compared with the control group,the expression of Keap1 protein in the D-galactose aging group was lower than that in the control group(p <0.05);Keap1 protein was not found to be different among the five groups in SD rat cortex.3.The experimental results of propylene glycol(MAD)andtotal superoxide dismutase(T-SOD)in the hippocampus of each group of rats show that compared with the D-galactose aging exercise group,the D-galactose aging group has MAD The increase indicates that nerve cells are more severely attacked by free radicals.Compared with the D-galactose exercise group,the MAD content also increased(p <0.05).The MAD content in the exercise group was lower than that in the control group(p <0.05);there was no difference between the D-galactose exercise group and the exercise inhibiting aging group compared with the control group.The activity of T-SOD in hippocampus of D-galactose exercise group was higher than that of D-galactose aging group(p <0.05);there was no significant difference between exercise group and exercise-inhibited aging group compared with the control group.Conclusion: 1.Marris water maze experiment showed that long-term aerobic treadmill exercise could significantly optimize the path of the experimental rats to find the platform and shorten the latency of the experimental rats.Aerobic exercise intervention can improve age-related brain learning and memory and cognitive deficits,and improve spatial cognitive ability and spatial memory ability of experimental rats.2.Aerobic exercise can up-regulate the expression of Nrf2 protein in hippocampus and cortex of rats,thus activate the Keap-Nrf2/ARE signaling pathway and enhance the antioxidant capacity of the brain of aging rats.3.Aerobic exercise can reduce the content of malondialdehyde(MDA)in hippocampus of rats,increase the activity of superoxide dismutase(T-SOD)in hippocampus of aging rats,enhance the scavenging ability of antioxidant enzyme system to oxygen free radicals,reduce the damage of oxidative stress to brain,and improve learning and memory deficits of aging rats. |
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