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Cold stress-induced brain injury regulates TRPV1 channels and the PI3K/AKT signaling pathway

Ying Liu1, Yunen Liu1, Hongxu Jin1

  • 1Emergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, Shenyang 110016, China.

Brain Research
|July 4, 2017
PubMed

Insights

Cold stress causes brain injury and behavioral deficits in mice. Inhibiting Transient Receptor Potential Vanilloid 1 (TRPV1) and PI3K/Akt pathways reduces inflammation and brain damage, suggesting a therapeutic target.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Physiology

Background:

  • Transient receptor potential vanilloid 1 (TRPV1) channels are implicated in neuroprotection.
  • TRPV1 interacts with intracellular proteins like PI3K/Akt signaling pathway.
  • Cold stress is a potential environmental factor affecting brain health.

Purpose of the Study:

  • To investigate the effects of cold stress on the mouse brain.
  • To elucidate the role of TRPV1 in cold stress-induced brain injury.
  • To examine the involvement of the PI3K/Akt signaling pathway.

Main Methods:

  • Adult male C57BL/6 mice were exposed to cold stress (4°C for 8 hours daily for 2 weeks).
  • Behavioral deficits were assessed using the Morris water maze.
  • Brain injury markers, inflammation, TRPV1, and PI3K/Akt expression were analyzed via Western blot, immunofluorescence, and RT-PCR.

Main Results:

  • Cold stress induced behavioral deficits, inflammation, and altered brain injury markers.
  • TRPV1 and PI3K/Akt expression levels were upregulated following cold stress.
  • TRPV1 inhibition significantly reduced brain injury markers and inflammation.

Conclusions:

  • Cold stress can lead to brain injury, potentially mediated by TRPV1 activation and the PI3K/Akt pathway.
  • Inhibiting TRPV1 and PI3K/Akt signaling may offer a protective strategy against cold stress-induced brain damage.
  • Targeting TRPV1 presents a potential therapeutic avenue for mitigating cold stress-related neuroinflammation.
Keywords:
Brain injuryCold stressPI3K/AktTRPV1

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