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Taurine attenuates methamphetamine-induced autophagy and apoptosis in PC12 cells through mTOR signaling pathway

Yan Li1, Zhengtao Hu, Bo Chen

  • 1National Chengdu Center for Safety Evaluation of Drugs, State Key Lab of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.

Toxicology Letters
|October 9, 2012
PubMed

Insights

Taurine protects against methamphetamine (METH) neurotoxicity by reducing oxidative stress, apoptosis, and autophagy in PC12 cells. This neuroprotection is mediated through the activation of the mTOR signaling pathway.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Methamphetamine (METH) abuse causes neurotoxicity via reactive oxygen species (ROS), apoptosis, and autophagy.
  • Taurine (2-aminoethanesulfonic acid) exhibits neuroprotective roles in the brain.

Purpose of the Study:

  • To investigate taurine's protective effects against METH-induced neurotoxicity in PC12 cells.
  • To elucidate the underlying molecular mechanisms, focusing on autophagy and mTOR signaling.

Main Methods:

  • PC12 cells were treated with METH and/or taurine.
  • Cell viability, LC3-II expression, antioxidase activities, and protein levels (p-mTOR, p-Erk) were assessed.
  • The role of mTOR was further investigated using an mTOR inhibitor (RAD001).

Main Results:

  • Taurine significantly enhanced METH-inhibited cell viability.
  • Taurine attenuated METH-induced increases in LC3-II expression and reversed declines in antioxidase activities.
  • METH inhibited p-mTOR, while taurine increased it; taurine's effect on LC3-II was partially blocked by an mTOR inhibitor.

Conclusions:

  • Taurine protects PC12 cells from METH-induced damage by reducing ROS, apoptosis, and autophagy.
  • Taurine exerts its neuroprotective effects, at least partly, by activating the mTOR signaling pathway, not Erk.
  • Taurine inhibits METH-induced autophagy via mTOR activation.

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