Combination therapy with semaglutide and rosiglitazone as a synergistic treatment for diabetic retinopathy in rodent animals

Life Sci. 2021 Mar 15:269:119013. doi: 10.1016/j.lfs.2020.119013. Epub 2021 Jan 5.

Abstract

Objective: To investigate the protective efficacies and potent mechanisms of combination therapy with semaglutide and rosiglitazone (RSG) on the high-glucose incubated human ARPE-19 cells and diabetic retinopathy (DR) model rats.

Main methods: The CCK-8 methods were used to evaluate the protective effects of semaglutide and RSG alone or combination on the cell viability of high-glucose treated ARPE-19 cells. After the DR rat model was established, the effects of combined treatment on general indexes, retinal morphological changes, retinal Müller cells as well as PI3K/Akt/MTOR related factors of DR model rats were investigated.

Results: The CCK-8 assay showed obviously enhanced protective efficacies of combination therapy with semaglutide and RSG on the ARPE-19 with oxidative stress induced by high-glucose with combination index all below 1.5 demonstrating obvious synergistic effects. Combined incubation could also effectively decrease the expression of inflammatory factors, including TNF-α, IL-1β, IL-6, and the increase of ROS content in ARPE cell culture supernatant induced by high-glucose. Combined use of the antioxidant, PI3K/Akt and mTOR inhibitors, we further demonstrated that combined incubation of semaglutide and RSG could effectively by reduce high glucose-induced inflammatory injury inhibiting ROS/PI3K/Akt/mTOR signaling. Furthermore, chronic combination treatment effectively improved the histopathological characteristics and down-regulated the GFAP expression in Müller cells as well as PI3K/Akt/MTOR signaling pathway-related factors in retina which was better than any monomer treatment group.

Conclusions: Combined semaglutide with RSG exhibited synergistically protective efficacies on retinal cells by decreasing the GFAP expression, inhibiting oxidative stress and PI3K/Akt/MTOR signaling-transduction in DR model rats.

Keywords: Combination therapy; Diabetic retinopathy; Rodent animals; Rosiglitazone; Semaglutide.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Cell Line
  • Cell Survival / drug effects
  • Diabetic Retinopathy / drug therapy*
  • Disease Models, Animal
  • Drug Therapy, Combination
  • Ependymoglial Cells / drug effects
  • Ependymoglial Cells / metabolism
  • Ependymoglial Cells / pathology
  • Glial Fibrillary Acidic Protein / metabolism
  • Glucagon-Like Peptides / pharmacology
  • Glucagon-Like Peptides / therapeutic use*
  • Humans
  • Inflammation / pathology
  • Male
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protective Agents / pharmacology
  • Protective Agents / therapeutic use
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Rosiglitazone / pharmacology
  • Rosiglitazone / therapeutic use*
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Antioxidants
  • Glial Fibrillary Acidic Protein
  • Protective Agents
  • Rosiglitazone
  • semaglutide
  • Glucagon-Like Peptides
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases