M.S. Thesis Presentation by Shannon Gail Malcolm
Monday, November 20, 2000

(Dr. Robert Cargill, advisor)

"The Role of Progesterone in Attenuating Mitochondrial Injury in Neural Cells In an In Vitro Model of Traumatic Brain Injury"

Abstract

Traumatic brain injury (TBI) is a common injury-affecting people throughout the world, and is the leading cause of death in young adults under the age of 35. Currently, there is no effective pharmacological treatment for TBI that promotes functional recovery. Previous research has shown that progesterone may protect cells from injury associated with TBI. It is the hypothesis of this study that progesterone acts to protect mitochondria, reducing the production of free radicals and maintaining the energy production capability of the cell.

An in vitro model of traumatic brain injury is employed in this research which is based on a mechanical device (the planar elastic deformation device: PEDD) that imparts a known deformation to cells. In this model cells are cultured onto a clear elastic substrate made of Sylgard polymer, which can be attached to the PEDD. The PEDD provides a controlled linear motion to the actuator to stretch a form through the membrane, which results in a homogenous, isotropic, equibiaxial strain in the plane of the membrane, to which the cells are attached.

Following injury, cells will be treated with media with progesterone or ethanol vehicle for 24 hours, and stained for cell viability, manganese superoxide dismutase (MnSOD), and cytochrome oxidase (COX) activity. The level of MnSOD can be used as an index of neuronal exposure to reactive oxygen species, and changes in COX activity can be correlated with physiological activity of neurons.