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Metformin inhibits Aβ25-35 -induced apoptotic cell death in SH-SY5Y cells

Li-Xia Li1, Meng-Yu Liu1, Xue Jiang1

  • 1Department of Zoology and Developmental Biology, College of Life Sciences, Nankai University, Tianjin, China.

Basic & Clinical Pharmacology & Toxicology
|June 21, 2019
PubMed

Insights

Metformin may protect against Alzheimer's disease (AD) by reducing cell death and improving cellular processes. This study investigated its neuroprotective effects and mechanisms in an AD cell model.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • Type-2 diabetes drug Metformin shows potential in preventing Alzheimer's disease (AD).
  • The precise mechanisms behind Metformin's neuroprotective effects in AD remain largely unknown.
  • Alzheimer's disease is characterized by neuronal damage and dysfunction.

Purpose of the Study:

  • To investigate the neuroprotective effects of Metformin in an Alzheimer's disease (AD) cell model.
  • To elucidate the underlying molecular mechanisms of Metformin's action in AD.

Main Methods:

  • Utilized SH-SY5Y cells treated with amyloid-beta (Aβ) 25-35 as an in vitro model for AD.
  • Assessed cell apoptosis, cell death, protein expression (Bcl-2, Bax, NR2A, NR2B, LC3), and levels of glutamate (Glu), calcium (Ca2+), and reactive oxygen species (ROS).

Main Results:

  • Metformin significantly decreased apoptosis and cell death in Aβ-treated cells.
  • Metformin altered the expression of key proteins involved in apoptosis and autophagy (Bcl-2/Bax ratio, LC3).
  • Metformin reduced intracellular/extracellular glutamate, intracellular Ca2+, and ROS levels, mitigating excitotoxicity and oxidative stress.

Conclusions:

  • Metformin demonstrates neuroprotective effects against Aβ-induced neurotoxicity in SH-SY5Y cells.
  • Mechanisms include inhibition of apoptosis, reduction of intracellular Ca2+ and ROS via decreased excitotoxicity, and potential regulation of autophagy.
  • Metformin's multifaceted action suggests a promising therapeutic avenue for Alzheimer's disease.
Keywords:
Aβ25-35apoptosismetforminneuroprotectiontoxicity of excitatory amino acids

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