摘要
为了探讨游泳运动对2型糖尿病大鼠脑血管内皮氧化损伤的治疗效果,以及游泳运动对PI3K/Akt/eNOS信号通路的调控作用。将SD大鼠按随机分为4组,正常对照组大鼠给予标准饲料喂养,其他组大鼠给予高糖高脂饲料喂养。通过腹腔注射60 mg/kg的链脲佐菌素(STZ)建立2型糖尿病模型,游泳运动组大鼠进行8周的游泳运动(游泳时间为45 min,每周5次),游泳运动+LY294002组大鼠在游泳运动基础上腹腔注射100 mg/kg的PI3K抑制剂LY294002。8周后分别检测各组大鼠空腹血糖、一氧化氮(NO)、TC、TG、LDL-c、HDL-c、丙二醛(MDA)和超氧化物歧化酶(SOD)水平。苏木精-伊红(HE)染色评价脑组织病理改变。Western blotting检测脑组织中PI3K/Akt/eNOS通路的活化情况。与模型组比较,游泳运动组的空腹血糖、TC、TG和LDL-c水平均显著降低,而HDL-c水平显著升高。与模型组比较,游泳运动组的血清NO水平显著升高。与模型组比较,游泳运动组的SOD水平显著升高,而MDA水平显著降低。与模型组比较,游泳运动组的PI3K蛋白表达水平及Akt和e NOS的磷酸化水平显著升高,LY294002处理可显著减弱游泳运动对上述指标的影响。本研究表明游泳运动可改善2型糖尿病大鼠的糖脂代谢、提高抗氧化能力、减弱脑组织氧化损伤。游泳运动对2型糖尿病大鼠的脑保护作用部分归因于其对PI3K/AKT/eNOS信号通路的激活。
To explore the therapeutic effect of swimming exercise on cerebral vascular endothelial oxidative injury in type 2 diabetic rats,and the effect of swimming exercise on PI3 K/Akt/eNOS signaling pathway.SD rats were randomly divided into 4 groups,normal control rats were fed with standard feed,and other groups were fed with high sugar and high fat feed.A model of type 2 diabetes was established by intraperitoneal injection of streptozotocin(STZ)at 60 mg/kg.Rats in the swimming group performed swimming for 8 weeks(swimming time:45 min,5 times per week).Rats in the swimming+LY294002 group were intraperitoneally injected with a PI3K inhibitor LY294002 at 100 mg/kg on the basis of swimming exercise.After 8 weeks,fasting blood glucose,nitric oxide(NO),TC,TG,LDL-c,HDL-c,Malondialdehyde(MDA)and superoxide dismutase(SOD)levels were measured in each group of rats.Hematoxylin-eosin(HE)staining was used to evaluate the pathological changes of brain tissue.Western blotting was used to detect the activation of PI3K/Akt/eNOS pathway in brain tissue.Results showed that compared with the model group,the fasting blood glucose,TC,TG,and LDL-c levels in the swimming group were significantly reduced,while HDL-c levels were significantly increased.Compared with the model group,the serum NO level in the swimming group was significantly increased.Compared with the model group,the SOD level in the swimming group increased significantly,while the MDA level decreased significantly.Compared with the model group,the PI3 K protein expression level and Akt and eNOS phosphorylation levels in the swimming group were significantly increased.LY294002 treatment can significantly reduce the influence of swimming exercise on the above indicators.This study indicates that swimming can improve glucose and lipid metabolism,increase antioxidant capacity,and reduce oxidative damage in brain tissue in type 2 diabetic rats.The brain protective effect of swimming exercise on type 2 diabetic rats is partly due to its activation of the PI3K/AKT/eNOS signaling pathway.
作者
何伟
He Wei(Shaanxi Institute of International Trade&Commerce,Xi'an,712046)
出处
《基因组学与应用生物学》
CAS
CSCD
北大核心
2020年第9期4243-4248,共6页
Genomics and Applied Biology
