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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

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Platycodin D protects cortical neurons against oxygen-glucose deprivation/reperfusion in neonatal hypoxic-ischemic

Guifang Wang1, Hongxiang Guo2, Xiaofang Wang1

  • 1Department of Pediatrics, Xinxiang Central Hospital, Xinxiang, Henan, China.

Journal of Cellular Biochemistry
|April 5, 2019
PubMed

Insights

Platycodin D (PLD) protects infant brain cells from hypoxic-ischemic injury by reducing oxidative stress and apoptosis. It activates the PI3K/Akt/mTOR pathway, offering a promising therapeutic target for neonatal encephalopathy.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of infant mortality.
  • Oxidative stress and apoptosis are key mechanisms in HIE-related brain injury.
  • Platycodin D (PLD), a natural saponin, possesses antioxidant properties.

Purpose of the Study:

  • To investigate the neuroprotective effects of Platycodin D (PLD) against oxygen-glucose deprivation/reperfusion (OGD/R) injury in primary cortical neurons.
  • To elucidate the underlying molecular mechanisms of PLD's action, focusing on oxidative stress, apoptosis, and key signaling pathways.

Main Methods:

  • Primary cortical neurons were subjected to oxygen-glucose deprivation/reperfusion (OGD/R) to induce injury.
  • Cell viability and cytotoxicity were assessed.
  • Levels of reactive oxygen species (ROS) and antioxidant enzyme activities (catalase, SOD, GPx) were measured.
  • Apoptosis was evaluated using histone-DNA ELISA and Western blotting for apoptosis-related proteins (Bax, Bcl-2).
  • The PI3K/Akt/mTOR pathway activation was assessed, and its role in PLD's effect was investigated using pathway inhibitors.

Main Results:

  • OGD/R significantly reduced neuronal viability and increased cytotoxicity, which were ameliorated by PLD treatment.
  • PLD inhibited OGD/R-induced oxidative stress by decreasing ROS levels and enhancing antioxidant enzyme activities.
  • PLD significantly reduced apoptosis in OGD/R-treated neurons and reversed the altered expression of Bax and Bcl-2.
  • PLD activated the PI3K/Akt/mTOR signaling pathway.
  • Inhibition of the PI3K/Akt/mTOR pathway abolished the protective effects of PLD against OGD/R-induced neuronal injury.

Conclusions:

  • Platycodin D (PLD) demonstrates significant neuroprotective effects against hypoxic-ischemic injury in primary cortical neurons.
  • PLD mitigates injury by inhibiting oxidative stress and apoptosis.
  • The protective mechanism of PLD involves the activation of the PI3K/Akt/mTOR signaling pathway.

Keywords:
PI3K/Akt/mTOR signaling pathwayapoptosisneonatal hypoxic-ischemic encephalopathyoxidative stressplatycodin D

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