Curcumin Efficacy in a Serum/Glucose Deprivation-Induced Neuronal PC12 Injury Model

Tahereh Farkhondeh, Milad Ashrafizadeh, Mohsen Azimi-Nezhad, Fariborz Samini, Michael Aschner, Saeed Samarghandian

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

Background: Glucose/serum deprivation (GSD), has been used for understanding molecular mechanisms of neuronal damage during ischemia. It has been suggested that curcumin may improve neurodegenerative diseases. Aim: In this study, the protective effects of curcumin and its underlying mechanisms were investi-gated in PC12 cells upon GSD-induced stress. Methods: PC12 cells were cultured in DMEM overnight and then incubated in GSD condition for either 6 or 12h. GSD-treated cells were pretreated with various concentrations of curcumin (10, 20, and 40 μM) for 5h. The cell viability, apoptosis, reactive oxygen species (ROS) level, oxidative stress, expression of apoptosis-related genes, and IL-6 were determined. Results: Curcumin increased cell viability and caused an anti-apoptotic effect in PC12 cells exposed for 12h to GSD . Curcumin also increased antioxidant enzyme expression, suppressed lipid peroxidation, and decreased interleukin-6 secretion in PC12 cells subjected to GSD. In addition, pretreatment with curcumin down-regulated pro-apoptotic (Bax), and up-regulated antiapoptotic (Bcl2) mediators. Conclusion: Curcumin mitigates many of the adverse effects of ischemia, and therefore, should be considered as an adjunct therapy in ischemic patients.

Original languageEnglish (US)
Pages (from-to)1146-1155
Number of pages10
JournalCurrent Molecular Pharmacology
Volume14
Issue number6
DOIs
StatePublished - Dec 2021

Keywords

  • Apoptosis
  • Curcumin
  • Cytotoxicity
  • Inflammation
  • Oxidative stress
  • PC12 cell
  • Serum/glucose deprivation

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery

Fingerprint

Dive into the research topics of 'Curcumin Efficacy in a Serum/Glucose Deprivation-Induced Neuronal PC12 Injury Model'. Together they form a unique fingerprint.

Cite this