Background: Capsaicin exhibits free radical scavenging activity. In the present study, we evaluated the impact of capsaicin on the expression level of apoptosis-related genes (CASP3, BCL2, BAX, TP53), the transcription factor NRF2 (which regulates the antioxidant response), and the level and activity of antioxidant enzymes (SOD, CAT, GPx) in the human cell line of neuroblastoma BE(2)-C. Methods: BE(2)-C neuroblastoma cells were administered with capsaicin at the amounts of 25, 50, and 75 μM, or with 50 μM ascorbic acid, for 24 hours. Subsequently, the cells were exposed to oxidative stress by treatment with hydrogen peroxide for two hours. A gene expression study was performed by real-time PCR, and antioxidant enzyme activity was evaluated by colorimetric methods. Results: Gene expression analysis indicated that capsaicin significantly decreased the level of pro-apoptotic genes CASP3 and BAX, while TP53 expression remained unchanged. Capsaicin also upregulated NRF2 and PPAR gene expression (P<0.05). Notably, vitamin C reduced Caspase-3 and Bax levels but did not significantly affect Bcl-2 or p53. SOD gene expression was reduced in the capsaicin-treated groups, whereas antioxidant enzyme activity, including SOD, CAT, and GPx, significantly increased in all treatment groups. Malondialdehyde (MDA) levels, a marker of oxidative stress, were significantly lower in capsaicin-treated groups than in the H2O2 group (P<0.05). Conclusion: Capsaicin modulated the expression of apoptosis-related genes and enhanced antioxidant defense mechanisms. While it inhibited key apoptotic markers, it had no significant effect on TP53 expression but increased PPAR expression, indicating a shift toward a regulated antioxidant and antiapoptotic cellular state.
Hormozi et al. (2026) studied this question.