Berberine attenuates apoptosis in rat retinal Müller cells stimulated with high glucose via enhancing autophagy and the AMPK/mTOR signaling.

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  • Additional Information
    • Source:
      Publisher: Editions Scientifiques Elsevier Country of Publication: France NLM ID: 8213295 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1950-6007 (Electronic) Linking ISSN: 07533322 NLM ISO Abbreviation: Biomed Pharmacother Subsets: MEDLINE
    • Publication Information:
      Publication: Paris : Editions Scientifiques Elsevier
      Original Publication: New York, N.Y. : Masson Pub. USA, Inc., c1982-
    • Subject Terms:
      AMP-Activated Protein Kinases/*metabolism ; Apoptosis/*drug effects ; Autophagy/*drug effects ; Berberine/*pharmacology ; Ependymoglial Cells/*pathology ; Glucose/*toxicity ; Retina/*pathology ; TOR Serine-Threonine Kinases/*metabolism; Animals ; Berberine/chemistry ; Cell Survival/drug effects ; Ependymoglial Cells/drug effects ; Ependymoglial Cells/metabolism ; Rats, Wistar ; Signal Transduction/drug effects
    • Abstract:
      Berberine (BBR) has beneficial effects on diabetes and the multiple complications of diabetes due to its anti-apoptotic activity; however, the effect of BBR on diabetic retinopathy and its mechanism of action have not been clarified. The present study investigated the effect of BBR on Müller cells stimulated with high glucose (HG). Primary retinal Müller cells were incubated with high glucose to induce cell apoptosis; cells were pretreated with the AMPK inhibitor compound C and the AMPK activator AICAR to further explore the role of the AMPK/mTOR signaling pathway in the anti-apoptotic action of BBR. Immunofluorescence was used to measure apoptosis and autophagy. Western blot analysis was employed to determine the levels of p-AMPK and p-mTOR, as well as apoptosis-related proteins and autophagy-related proteins in Müller cells. Our results showed that BBR attenuated apoptosis, up regulated Bcl-2 and down regulated Bax and caspase-3 expression; enhanced the formation of autophagy, elevated the expression of Beclin-1 and LC3II and activated the AMPK/mTOR signaling pathway in Müller cells under high glucose conditions compared with the control group. The effect of BBR was partly blocked by compound C and strengthened by AICAR. BBR may have therapeutic potential to protect Müller cells from high-glucose-inducing apoptosis through enhancing autophagy and activating the AMPK/mTOR signaling pathway.
      (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)
    • Contributed Indexing:
      Keywords: AMPK/mTOR signaling pathway; Apoptosis; Autophagy; Berberine, BBR; Diabetic retinopathy, DR
    • Accession Number:
      0I8Y3P32UF (Berberine)
      EC 2.7.11.1 (TOR Serine-Threonine Kinases)
      EC 2.7.11.31 (AMP-Activated Protein Kinases)
      IY9XDZ35W2 (Glucose)
    • Publication Date:
      Date Created: 20181031 Date Completed: 20190318 Latest Revision: 20211204
    • Publication Date:
      20221213
    • Accession Number:
      10.1016/j.biopha.2018.09.140
    • Accession Number:
      30372821