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Targeting antioxidant enzyme expression as a therapeutic strategy for ischemic stroke
Stephanie M Davis1, Keith R Pennypacker1
1Center for Advanced Translational Stroke Science, Depts of Neurology and Anatomy & Neurobiology, University of Kentucky, 741 S. Limestone Ave., BBSRB B457, Lexington, KY 40536-0509, United States.
Neurochemistry International
|January 4, 2017
Summary
Increasing antioxidant enzymes protects brain cells from damage after ischemic stroke. Therapies like stem cells or leukemia inhibitory factor (LIF) boost these enzymes, improving neural cell survival and recovery.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Ischemic stroke causes neuronal and glial damage via reactive oxygen species (ROS) and neuroinflammation.
- Existing antioxidant drugs have not improved stroke recovery.
- Upregulating endogenous antioxidant enzymes shows promise for stroke protection.
Purpose of the Study:
- To explore strategies for enhancing neural cell survival and recovery after ischemic stroke.
- To investigate the role of antioxidant enzymes in mitigating stroke-induced damage.
- To examine the potential of cellular therapies and soluble factors in upregulating antioxidant enzymes.
Main Methods:
- Review of studies on stroke-induced neurodegeneration and antioxidant defenses.
- Analysis of cellular therapies (neural stem cells, cord blood cells) and their mechanisms.
- Investigation of soluble factors, including leukemia inhibitory factor (LIF), and their effects on enzyme expression.
Main Results:
- Cellular therapies and soluble factors activate PI3K/Akt signaling, upregulating antioxidant enzymes.
- Leukemia inhibitory factor (LIF) increases peroxiredoxin IV and metallothionein III in glia, and superoxide dismutase 3 in neurons.
- Upregulation of antioxidant enzymes (glutathione peroxidase, catalase, superoxide dismutase families) degrades ROS, protecting cellular components.
Conclusions:
- Increasing antioxidant enzyme expression is a viable neuroprotective strategy against ischemic stroke.
- Cellular therapies and factors like LIF offer potential for protecting diverse neural cell types from ROS damage.
- Targeting antioxidant enzyme upregulation may improve outcomes during both acute and later phases of stroke injury.
