Investigation of Neuroprotection using a Novel Antioxidant Therapy to Reduce Cellular Stress in Rat Cortical Astrocytes
Presenter Hometown
Greenup County, Kentucky
Major
Biology
Department
Biological Sciences
Degree
Undergraduate
Mentor
Tanea T. Reed
Mentor Department
Chemistry
Recommended Citation
Aeh, David J., "Investigation of Neuroprotection using a Novel Antioxidant Therapy to Reduce Cellular Stress in Rat Cortical Astrocytes" (2016). University Presentation Showcase Event. 18.
https://encompass.eku.edu/swps/2016/undergraduate/18
Abstract
Recent evidence shows that biochemical mechanisms that occur in response to traumatic brain injury collectively increase the production of reactive oxygen species (ROS), forming an imbalance between free radicals and antioxidants. This imbalance is known as oxidative stress, which lowers the body’s defense against ROS, eventually leading to neuronal dysfunction and death. Astrocytes are highly abundant in the central nervous system and maintain high intracellular concentrations of antioxidants, thereby playing a critical role in homeostasis. Gamma-glutamylcysteine ethyl ester (GCEE) is an antioxidant that has shown to protect the brain against oxidative stress. Additionally, bromoenol lactone (BEL), an irreversible inhibitor of calcium-independent phospholipase beta, decreases arachidonic acid production, a marker for neurological dysfunction in times of severe cellular stress. Therefore it can be hypothesized that upon administration of GCEE and BEL to oxidative stress-induced primary rat cortical astrocytes, a decrease in oxidative stress will be observed. GCEE and BEL will be used to treat the cells, while 2’7’-dichlorofluorescein (DCF) will be measured to determine cellular ROS levels. Multiple oxidants (tert-butyl hydroperoxide, octanol, and hydrogen peroxide) will be used to induce oxidative stress. ROS levels will be analyzed measuring DCF fluorescence. Astrocytes treated with GCEE and BEL post oxidative incident should demonstrate a decrease in fluorescence, and thus a decrease of ROS. Decreased production of ROS correlates with elevated antioxidant intervention, and thus reducing overall oxidative stress making this a plausible treatment for traumatic brain injury.
Presentation format
Poster
Poster Number
035
Investigation of Neuroprotection using a Novel Antioxidant Therapy to Reduce Cellular Stress in Rat Cortical Astrocytes
Recent evidence shows that biochemical mechanisms that occur in response to traumatic brain injury collectively increase the production of reactive oxygen species (ROS), forming an imbalance between free radicals and antioxidants. This imbalance is known as oxidative stress, which lowers the body’s defense against ROS, eventually leading to neuronal dysfunction and death. Astrocytes are highly abundant in the central nervous system and maintain high intracellular concentrations of antioxidants, thereby playing a critical role in homeostasis. Gamma-glutamylcysteine ethyl ester (GCEE) is an antioxidant that has shown to protect the brain against oxidative stress. Additionally, bromoenol lactone (BEL), an irreversible inhibitor of calcium-independent phospholipase beta, decreases arachidonic acid production, a marker for neurological dysfunction in times of severe cellular stress. Therefore it can be hypothesized that upon administration of GCEE and BEL to oxidative stress-induced primary rat cortical astrocytes, a decrease in oxidative stress will be observed. GCEE and BEL will be used to treat the cells, while 2’7’-dichlorofluorescein (DCF) will be measured to determine cellular ROS levels. Multiple oxidants (tert-butyl hydroperoxide, octanol, and hydrogen peroxide) will be used to induce oxidative stress. ROS levels will be analyzed measuring DCF fluorescence. Astrocytes treated with GCEE and BEL post oxidative incident should demonstrate a decrease in fluorescence, and thus a decrease of ROS. Decreased production of ROS correlates with elevated antioxidant intervention, and thus reducing overall oxidative stress making this a plausible treatment for traumatic brain injury.
