NONSTEROIDAL ANTI-INFLAMMATORY DRUG INDUCED APOPTOSIS VIA A NOVEL COX-I/COX-2 INDEPENDENT PATHWAY

Authors

Gregory C. Chipman, Brigham Young University
Dr. Daniel L. Simmons, Brigham Young University

Keywords

nonsteroidal anti-inflammatory drug, apoptosis, cyclooxygenase COX- I, COX-2

College

Physical and Mathematical Sciences

Department

Chemistry and Biochemistry

Abstract

My efforts were concentrated in assisting Phillip M. Robertson, a graduate student in the Department of Chemistry and Biochemistry, in researching the cellular action of a family of drugs, nonsteroidal anti-inflammatory drugs. Nonsteroidal anti-inflammatory drugs (NSAIDS) include aspirin, ibuprofen, diclofenac, and other pharmacologically important agents. They have many applications, including reduction of inflammation and pain. These drugs have also been shown to induce apoptosis, or programmed cell death, in tumor cells. It has been generally accepted that NSAIDs function by inhibiting prostaglandin synthesis by enzymes called cyclooxygenases (COX). However, studies have questioned whether all NSAID actions are exerted through the two described forms of cyclooxygenase COX- I and COX-2. For instance, mice in which the COX-2 gene was disrupted showed unaltered inflammation response.1

Recommended Citation

Chipman, Gregory C. and Simmons, Dr. Daniel L. (2013) "NONSTEROIDAL ANTI-INFLAMMATORY DRUG INDUCED APOPTOSIS VIA A NOVEL COX-I/COX-2 INDEPENDENT PATHWAY," Journal of Undergraduate Research: Vol. 2013: Iss. 1, Article 2562.
Available at: https://scholarsarchive.byu.edu/jur/vol2013/iss1/2562