Cornin protects SH‑SY5Y cells against oxygen and glucose deprivation‑induced autophagy through the PI3K/Akt/mTOR pathway

Mol Med Rep. 2018 Jan;17(1):87-92. doi: 10.3892/mmr.2017.7864. Epub 2017 Oct 25.

Abstract

It has been reported that cornin may reduce neuronal death during cerebral ischemia; however, little is known about the molecular mechanism of the role of corninin autophagy in SH‑SY5Y neuronal cells. In the present study, oxygen‑glucose deprivation (OGD)‑treated cells were used as a cerebral ischemia model in vitro. The results demonstrated that cornin was able to reduce neuronal cell loss, increase the apoptosis regulator Bcl‑2/apoptosis regulator BAX ratio, and decrease the protein levels of caspase‑3. In addition, cornin decreased the microtubule‑associated proteins 1A/1B light chain 3B (LC3)‑II/LC3‑I ratio and beclin‑1 protein expression, and resulted in an upregulation in phosphorylated (p)‑RAC‑α serine/threonine‑protein kinase (Akt), p‑protein kinase mTOR (mTOR) in OGD‑treated SH‑SY5Y cells. Additionally, it was observed that following inhibition of PI3K/Akt by LY294002, the levels of p‑Akt and p‑mTOR were markedly decreased, and the LC3‑II/LC3‑I ratio and beclin‑1 were increased. Similarly, following inhibition of mTOR by rapamycin, LC3‑II/LC3‑I and Beclin‑1 were significantly increased in SH‑SY5Y cells. These results indicated that cornin protected SH‑SY5Y cells against OGD‑induced autophagy through the PI3K/Akt/mTOR pathway.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism
  • Autophagy / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Complex Mixtures / pharmacology*
  • Glucose / metabolism*
  • Humans
  • Oxygen / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Apoptosis Regulatory Proteins
  • Complex Mixtures
  • cornin peptide
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • Glucose
  • Oxygen