Discipline: Biological Sciences
Subcategory: Cancer Research
Room: Virginia B
Tanisha R. Hinton - Jackson State University
Co-Author(s): Clement G. Yedjou, Jackson State University, Jackson, MS and Paul B. Tchounwou, Jackson State University, Jackson, MS
The treatment of Acute Promyelocytic Leukemia (APL) has been established on the association of all-trans retinoic acid (ATRA) notwithstanding chemotherapy, which is especially fruitful as a first line treatment; nevertheless, 25% to 30% of patients will relapse, with their disease becoming unmanageable to the common treatment. The overall objective of our study was to determine the therapeutic mechanisms by which Vernonia Amygdalina induced cytotoxic effects, oxidative stress, and apoptosis of HL-60 cells. To accomplish this goal, HL-60 cells were treated with various doses of the Vernonia Amygdalina for 24 hours. Cell viability was examined by the MTS assay; Oxidative stress was estimated by Lipid Peroxidation Assay, Catalase, Glutathione, and Superoxide Dismutase. Cell apoptosis was analyzed by the flow cytometry for Annexin V. The MTS assay indicated that VA significantly reduced the viability of HL-60 cells in dose-dependent manner. Data obtained from the lipid peroxidation assay demonstrated a significant (p < 0.05) reduction in the MDA level in treated HL-60 cells compared to the control cells. Superoxide dismuse and Catalase displayed antioxidant enzyme activity and became toxic after 250µg/mL VA treated cells compared to control cells. The results showed that VA acts as antioxidant by decreasing the levels of oxidative stress biomarkers in treated HL-60 cells. The flow cytometry assessment showed an increased in the number of apoptotic cells in treated HL-60 cells compared to the control group. These results suggest that VA can act as a complement to the current treatment for APL patients. This data provided clear evidence that Vernonia Amygdalina inhibited cell viability, reduced oxidative stress, and induced apoptosis. These outcomes also suggest that VA may act as a supplement to the current treatment for APL patients.
Funder Acknowledgement(s): This research work was supported by a grant from the National Institutes of Health (Grant No. NIMHD-G12MD007581) through the RCMI-Center for Environmental Health at Jackson State University.
Faculty Advisor: Clement Yedjou, email@example.com
Role: I completed all parts of this research.