Discipline: Chemistry and Chemical Sciences
Subcategory: Cell and Molecular Biology
Victoria Ubanyionwu - Texas Southern University
Co-Author(s): Vignesh Krishnamoorthy, University of Texas at Dallas, Dallas, TX Raghu Krishnamoorthy and Dorota Stankowska, University of North Texas Health Science Center, Forth Worth, TX Dorota Stankowska, University of North Texas Health Science Center, Forth Worth, TX
Alzheimer’s disease is a progressive neurodegeneration disease. It is a common form of dementia, general term for memory loss and other intellectual abilities serious enough to interfere with daily life. Endothelin-1 (ET-1) is a vasoactive peptide whose level is elevated in the circulation in a number of cardiovascular pathologies. Recent studies also suggest that levels of ET-1 are also increased in the brain tissue of Alzheimer’s patients. It is possible that ET-1 may be a contributor to the pathology of Alzheimer’s disease. Curcumin found in the spice turmeric, has been shown to have anti-inflammatory, anti-cancer and neuroprotective effects. However the mechanisms underlying some of these beneficial effects are not completely be understood. We hypothesized that curcumin prevents activation of the immediate early gene, c-Jun, that contributes to neuronal death caused by ET-1 treatment in primary hippocampal neurons. Primary hippocampal neurons from rat pups were isolated using a published protocol. The purity of the culture was checked by immunocytochemistry using a β-tubulin III antibody. Immunoblot analysis was performed to investigate the status of c-Jun expression in hippocampal neurons treated with ET-1 alone or a combination of ET-1 and curcumin. The purity of primary hippocampal neuronal cells in culture was found to be greater than 95%. Treatment of hippocampal neurons with ET-1 produced a 2-fold increase in the levels of c-Jun as determined by an immunoblot analysis. Curcumin treatment alone did not appreciably alter c-Jun levels. Co-treatment of curcumin with ET-1 significant attenuated the ET-1 mediated increase in c-Jun. This data suggests that one mechanism by which curcumin protects against ET-1 mediated cell death is through blocking c-Jun activation in hippocampal neurons.
Funder Acknowledgement(s): Funded by the Department of Health and Human Services, National Institute of Health, National Heart, Lung and Blood Institute, SMART grant 2R25HL007786-21 to Dr. Thomas Yorio.
Faculty Advisor: Bobby Wilson, firstname.lastname@example.org
Role: I did the hypothesis analysis, ran the experiment and collected the data in the 10 weeks program watched over by my mentor.