Liraglutide Up-regulation Thioredoxin Attenuated Müller Cells Apoptosis in High Glucose by Regulating Oxidative Stress and Endoplasmic Reticulum Stress.

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  • Additional Information
    • Source:
      Publisher: Informa Healthcare Country of Publication: England NLM ID: 8104312 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2202 (Electronic) Linking ISSN: 02713683 NLM ISO Abbreviation: Curr Eye Res Subsets: MEDLINE
    • Publication Information:
      Publication: London : Informa Healthcare
      Original Publication: London : IRL Press, [c1981-
    • Subject Terms:
      Apoptosis/*drug effects ; Endoplasmic Reticulum Stress/*drug effects ; Ependymoglial Cells/*pathology ; Hypoglycemic Agents/*therapeutic use ; Liraglutide/*therapeutic use ; Oxidative Stress/*drug effects ; Thioredoxins/*metabolism; Animals ; Blotting, Western ; Cells, Cultured ; Endoplasmic Reticulum Stress/physiology ; Ependymoglial Cells/drug effects ; Ependymoglial Cells/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Flow Cytometry ; Glial Fibrillary Acidic Protein/metabolism ; Gliosis/drug therapy ; Gliosis/metabolism ; Glucose/toxicity ; Mice ; Microscopy, Fluorescence ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Transfection ; Up-Regulation
    • Abstract:
      Purpose : Diabetic retinopathy (DR) has become one of the most important complications of diabetes which is the leading cause of vision impairment and blindness all over the world. Increasing evidence shows that reactive gliosis are basic pathological features of early DR. The study was aimed to explore the protective effect and mechanism of Liraglutide (LIRA) which has similar properties to Glucagon-like peptide-1 (GLP-1) on Müller cell damage induced by diabetes. Materials and methods : In vitro , the Müller cell was cultured in high glucose (HG) to establish the model of diabetic retinopathy. The apoptosis was detected using flow cytometry. Western blot and immunofluorescence were used to detect the expression of related proteins. DCFH-DA probe was used to detect the ROS generation. Results : The data showed that the apoptosis and the expression of GFAP were increased significantly with HG treatment. However, the apoptosis percentage and the expression of GFAP were decreased after LIRA treatment. Moreover, the expression of p-Erk/Nrf2/Trx-signaling pathway proteins was also up-regulated and the generation of ROS was decreased after LIRA treatment which was inhibited after treatment with U0126 (Erk inhibitor). Besides, endoplasmic reticulum stress (ER stress) related proteins were up-regulated after Trx down-regulation by transfection with sh-RNA. Conclusions : LIRA could protect Müller cells from HG-induced damage via activating p-Erk pathway through increasing Trx expression which attenuated oxidative stress and ER stress. Trx could play a key role in the process.
    • Contributed Indexing:
      Keywords: Liraglutide; Müller cells; endoplasmic reticulum stress; oxidative stress; thioredoxin
    • Accession Number:
      0 (Glial Fibrillary Acidic Protein)
      0 (Hypoglycemic Agents)
      0 (NF-E2-Related Factor 2)
      0 (Nfe2l2 protein, mouse)
      0 (Reactive Oxygen Species)
      0 (glial fibrillary astrocytic protein, mouse)
      52500-60-4 (Thioredoxins)
      839I73S42A (Liraglutide)
      EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
      IY9XDZ35W2 (Glucose)
    • Publication Date:
      Date Created: 20200318 Date Completed: 20211015 Latest Revision: 20211015
    • Publication Date:
      20221213
    • Accession Number:
      10.1080/02713683.2020.1737137
    • Accession Number:
      32180468