Raspberry Ketone Protects Kidney Damage in Diabetic Nephropathy by Improving Kidney Mitochondrial Dysfunction

文献类型: 外文期刊

第一作者: Ma, Jiawang

作者: Ma, Jiawang;Wang, Xin;Xu, Meng;Liu, Wensen;Chang, Ying;Xu, Na;Dong, Mingxin;Sun, Chengbiao;Wang, Yan;Zhang, Jianxu;Liu, Wensen

作者机构:

关键词: diabetic nephropathy; raspberry ketone; mitochondrial dysfunction; oxidative stress; kidney damage

期刊名称:NATURAL PRODUCT COMMUNICATIONS ( 影响因子:1.8; 五年影响因子:1.5 )

ISSN: 1934-578X

年卷期: 2023 年 18 卷 1 期

页码:

收录情况: SCI

摘要: Mitochondrial dysfunction and oxidative stress play essential roles in the pathogenesis of diabetic nephropathy (DN). The respiratory oxygen consumption and oxidative stress status of kidney mitochondria are closely associated with the development of DN. In this study, raspberry ketone (RK), the predominant bioactive component extracted from raspberry, was applied to treat the established DN mice model. This study investigated whether RK protects the kidneys of high-fat and high-sugar/streptozotocin (STZ)-induced diabetic rats by inhibiting oxidative stress and ameliorating mitochondrial dysfunction. Besides, the DN mice models were established by injecting high-fat and high-sugar/STZ (130 mg/kg, intraperitoneal injection). The animals were randomly divided into the control group (normal saline, ig), DN group (normal saline, ig), DN + RK group (200 mg/kg RK + normal saline, ig), DN + RK group (400 mg/kg RK + normal saline, ig), and DN + Metformin (Met) (200 mg/kg Met + normal saline, ig). Regular monitoring of fasting blood glucose (FBG) levels was observed in mice. After 10 weeks of drug treatment, the kidneys of mice in each group were analyzed using ultrasound, and the mice were euthanized humanely. Kidney weight (KW)/body weight (BW) and kidney injury, mitochondrial function, and oxidative stress indicators were determined. The histopathological changes in renal tissue were observed after hematoxylin and eosin (H&E) staining. The results recommended that RK has a renoprotective function on DN mice by improving mitochondrial dysfunction and inhibiting oxidative stress.

分类号:

  • 相关文献
作者其他论文 更多>>