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中国临床药理学与治疗学 ›› 2022, Vol. 27 ›› Issue (6): 632-638.doi: 10.12092/j.issn.1009-2501.2022.06.005

• 基础研究 • 上一篇    下一篇

游泳运动通过促进自噬改善糖尿病小鼠肾功能的研究

王珍1,2,全海燕1,洪陈亮2,袁李佳龙3,秦旭平2   

  1. 1湖南环境生物职业技术学院药学教研室,衡阳 421001,湖南;2南华大学药学院药物药理研究所,衡阳 421001,湖南;3怀化市第一人民医院临床药学研究室,怀化 418000,湖南

  • 收稿日期:2021-08-18 修回日期:2022-01-25 出版日期:2022-06-26 发布日期:2022-07-08
  • 通讯作者: 秦旭平,男,博士,教授,硕士研究生导师,研究方向:心血管药理。 E-mail: qinxp333@hotmail.com
  • 作者简介:王珍,女,硕士,主管药师,研究方向:心血管药理。 E-mail: wangzhenuse1@163.com
  • 基金资助:
    湖南省分子靶标新药研究协同创新项目[湘教通(2014)405号];南华大学归国人员基金资助项目(2010XQD44);南华大学研究生创新项目(0223-0002-00031);衡阳市指导性科技计划项目(2022jh042693);湖南环境生物职业技术学院青年基金项目(ZK2021-05)

Swimming improves renal function of diabetic mice by promoting autophagy

WANG Zhen1,2, QUAN Haiyan1, HONG Chenliang2, YUAN Lijialong3, QIN Xuping2   

  1. 1Department of Pharmacology, Hunan Environmental Biology College; 2Institute of Pharmacy and Pharmacology, School of Pharmacy, University of South China, Hengyang 421001, Hunan, China; 3Department of Pharmacy, the First People's Hospital of Huaihua, Huaihua 418000, Hunan, China
  • Received:2021-08-18 Revised:2022-01-25 Online:2022-06-26 Published:2022-07-08

摘要: 目的:研究游泳运动对糖尿病小鼠肾脏的保护作用及机制。方法:正常小鼠随机分成正常对照组、正常游泳组、2型糖尿病(T2DM)小鼠模型组、糖尿病游泳组和二甲双胍组。用链脲佐菌素(STZ)法建立T2DM小鼠模型。正常游泳组和糖尿病游泳组小鼠给予游泳运动(每天1 h),二甲双胍组小鼠给予二甲双胍(200 mg/kg)每天一次灌胃,持续7周。测定小鼠空腹血糖、血清胰岛素值,计算胰岛素抵抗指数值。测定血清尿酸、尿素及肌酐的含量。计算肾质量/体质量比值,观察肾组织病理结构变化,Western blot法检测肾组织自噬相关蛋白LC3和p62的相对表达。结果:与正常对照组比,模型组胰岛素抵抗指数、肾质量/体质量比值显著升高;血清尿酸、尿素及肌酐含量升高,肾小球病理变化明显;LC3II/LC3I比值显著降低;p62的表达显著增加。与模型组比,糖尿病游泳组胰岛素抵抗指数、肾质量/体质量比值显著降低;血清尿酸、尿素及肌酐含量降低,肾小球病理改变也减轻;LC3II/LC3I比值显著升高;p62的表达显著下降(均P<0.05)。 结论:游泳运动保护T2DM小鼠的肾脏损伤,其机制可能与促进肾组织细胞自噬过程有关。

关键词: 游泳运动, 糖尿病小鼠, 肾损伤, 自噬, 二甲双胍

Abstract: AIM: To study the protective effect and mechanism of swimming on kidney of diabetic mice.  METHODS: The mice were randomly divided into normal control group, normal swimming group, type 2 diabetes mellitus (T2DM) mice model group, diabetic swimming group and metformin group. T2DM model was established by streptozotocin (STZ) method. The mice in normal swimming group and diabetic swimming group were given swimming exercise (1 h a day), and the metformin group were given metformin (200 mg/kg) by gavage once a day for 7 weeks. Fasting blood glucose and serum insulin were measured and insulin resistance index was calculated. The contents of uric acid, urea and creatinine in serum were determined. The ratio of renal mass to body mass was calculated, and the pathological changes of renal tissues were observed. The relative expressions of autophagy related proteins LC3 and P62 in renal tissues were detected by Western blot. RESULTS: Compared with normal control group, insulin resistance index and renal mass/body mass ratio in model group were significantly increased. Serum uric acid, urea and creatinine levels increased, and glomerular pathological changes were obvious. LC3II/LC3I ratio decreased significantly. The expression of P62 was significantly increased. Compared with model group, insulin resistance index and renal mass/body mass ratio in diabetic swimming group were significantly decreased. The contents of serum uric acid, urea and creatinine decreased, and the pathological changes of glomerular were alleviated. LC3II/LC3I ratio increased significantly. The expression of P62 decreased significantly (P even <0.05). CONCLUSION: Swimming protects the kidney injury of T2DM mice, and its mechanism may be related to promoting the autophagy process of renal tissue.

Key words: swimming, diabetic mice, kidney injury, autophagy, metformin

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