Article Type
Original Article
Section/Category
Oral Medicine
Abstract
Aim and Objectives: This research was aimed to evaluate the efficacy of a combination treatment comprising the natural compound Naringenin (NAR) and the chemotherapeutic agent Cisplatin (CP) regarding the reduction of cell viability and the induction of apoptosis in human TSCC (HNO-97) and normal oral epithelial cell (NOEC) lines. Material and Methods: The cytotoxicity and IC50 of NAR, CP, and their combinations were evaluated using the MTT assay. The expression levels of the apoptotic marker genes p53 and caspase-3 were assessed using RT-PCR. Western blot analysis was carried out to assess the protein expression levels of the apoptotic markers Bax and Bcl-2 in HNO-97 cells treated with the IC50 of the NAR and CP combination. A oneway ANOVA test was employed for group comparison, followed by a paired t-test to assess the differences between the groups (α=.05). Results: NAR has a non-selective cytotoxic effect on HNO-97 cells. The IC50 of NAR/CP combination was lower than that of either drug alone. Caspase-3 but not p53 was upregulated in HNO-97 cells treated with the IC50 of the NAR and CP combination compared to the control. Bax protein levels were decreased in HNO-97 cells treated with the NAR/CP IC50 combination. Conclusion: The viability of the TSCC cell line was reduced by NAR in a dosedependent manner, and the combination of the two drugs demonstrated enhanced cytotoxic efficacy with lower CP doses. NAR/CP combination could induce apoptosis of HNO-97 cells through caspase-3 dependent apoptosis, possibly with Bax inhibition.
Keywords
Naringenin, apoptosis, oral cancer, Cisplatin, cytotoxicity
How to Cite This Article
Atef N , Hussein N , Grawesh M , Anees M .
Effect of Naringenin Cisplatin combination on apoptosis of human tongue squamous cell carcinoma cell line.
Mans J Dent.
2025;
12(3):
Available at:
https://doi.org/10.61793/2812-5479.1157
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.