Silibinin ameliorates diabetic nephropathy via improving diabetic condition in the mice

Eur J Pharmacol. 2019 Feb 15:845:24-31. doi: 10.1016/j.ejphar.2018.12.031. Epub 2018 Dec 28.

Abstract

Diabetic nephropathy (DN) is a major cause of end-stage renal disease and one of the most severe diabetic complications. However, there is lack of effective treatments for DN and the underlying mechanisms of the renal injury remain unclear. In current study, we evaluated the effects of silibinin on DN and further explored the underlying mechanisms. We administrated silibinin to db/db mice for 10 weeks. Then we monitored the diabetic metabolic parameters, kidney function, oxidative stress and AKT signaling pathway in db/db mice. Administration of silibinin to db/db mice improved diabetic condition, as evidenced by the decrease of body weight, HbAc1level and serum insulin level in db/db mice. Silibinin prevented kidney injury and attenuated oxidative stress in db/db mice. Silibinin activated AKT signaling pathway and decreased the levels of p-GSK-3β, Bax and cleaved caspase-3. Silibinin ameliorates diabetic nephropathy by activating the AKT signaling pathway.

Keywords: AKT signaling pathway; Diabetic nephropathy; Injury; Oxidative stress; Silibinin.

MeSH terms

  • Animals
  • Caspase 3 / metabolism
  • Diabetic Nephropathies / drug therapy*
  • Glycated Hemoglobin / metabolism
  • Glycogen Synthase Kinase 3 beta / metabolism
  • Insulin / metabolism
  • Mice
  • Oxidative Stress / drug effects
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • Silybin / administration & dosage
  • Silybin / pharmacology
  • Silybin / therapeutic use*
  • bcl-2-Associated X Protein / metabolism

Substances

  • Bax protein, mouse
  • Glycated Hemoglobin A
  • Insulin
  • bcl-2-Associated X Protein
  • Silybin
  • Glycogen Synthase Kinase 3 beta
  • Proto-Oncogene Proteins c-akt
  • Casp3 protein, mouse
  • Caspase 3