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In ozonolysis, ozone is used to cleave a carbon–carbon double bond to form aldehydes and ketones, or carboxylic acids, depending on the work-up.
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Ozone therapy mitigates parthanatos after ischemic stroke.

Jiahui Li1, Xiaolei Liu1, Zengze Wang1

  • 1The Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.

Biological Research
|October 4, 2024
PubMed
Summary

Ozone therapy reduces parthanatos, a cell death pathway, in cerebral ischemia-reperfusion injury by targeting oxidative stress and calcium overload. This neuroprotective effect involves activating Nrf2 and PPARg pathways, offering a potential treatment for stroke.

Keywords:
Ca2+Cerebral ischemia–reperfusionOzoneParthanatosROS

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Stroke is a leading global cause of death, with oxidative stress and calcium overload key in its pathology.
  • Ozone therapy, known for antioxidant properties, is used clinically, but its effect on parthanatos in cerebral ischemia-reperfusion injury (CIRI) is not well understood.

Purpose of the Study:

  • To investigate ozone therapy's impact on reducing parthanatos during CIRI.
  • To elucidate the underlying molecular mechanisms of ozone's action.

Main Methods:

  • Used hydrogen peroxide (H2O2) to induce reactive oxygen species (ROS) in vitro and established an in vivo ischemic stroke model.
  • Administered ozone saline and assessed apoptosis, oxidative stress, and parthanatos protein expression.
  • Investigated mechanisms via peroxisome proliferator-activated receptor gamma (PPARg) and nuclear factor erythroid 2-related factor 2 (Nrf2) inhibition.

Main Results:

  • Ozone mitigated H2O2-induced parthanatos by upregulating Nrf2 or activating PPARg.
  • ROS directly induced parthanatos and calcium elevation, forming a feedback loop.
  • Ozone therapy inhibited ROS production and parthanatos in vitro and in vivo, showing neuroprotective effects.

Conclusions:

  • Ozone therapy shows potential for reducing parthanatos in CIRI.
  • The therapy impacts key molecular pathways of oxidative stress and calcium regulation.