DOI: 10.1177/09731296261492761 ISSN: 0973-1296

Bergenin Triggers Apoptosis in Human Oral Squamous Cell Carcinoma KB Cells by Targeting the PI3K/Akt Pathway: A Biochemical and Molecular Study

Lin Tian, Jiaxin Li, Jiasu Zhang, Lixin Feng

Background

Bergenin’s anticancer potential in oral squamous cell carcinoma (KB cells) remains underexplored, particularly its modulation of the PI3K/Akt/Nrf2/HO-1 signaling axis.

Purpose

This study investigates its multimodal effects on apoptosis induction, oxidative stress regulation, and inflammatory-angiogenic pathway suppression.

Materials and Methods

KB cells were treated with bergenin (100 and 200 µg/mL) and doxorubicin (DOX). Apoptosis was assessed via molecular markers p53, proliferation via Ki-67 staining and oxidative stress via redox assays through ELISA. Pathway components (PI3K/Akt/Nrf2/HO-1) were analyzed using qRT-PCR and Western blot. Statistical significance was evaluated via one-way ANOVA by using GraphPad Prism. PI3K/Akt pathway inhibition was observed alongside Nrf2/HO-1 downregulation ( p < 0.05).

Results

Oxidative stress mitigation was evidenced by reduced lipid peroxidation and elevated antioxidant enzyme activity ( p < .05). Inflammatory-angiogenic suppression included TNF-α, IL-6, VEGF, and NF-κB reduction ( p < 0.05). Ki-67 expression decreased significantly ( p < .05), and pathway interdependencies were confirmed ( p < .05). Bergenin demonstrated superior NF-κB inhibition compared to DOX ( p < .05).

Conclusion

Bergenin suppresses KB cell growth primarily through apoptosis and necrosis, mediated by PI3K/Akt pathway inhibition. Its multimodal action—restoring redox balance, disrupting inflammatory-angiogenic networks, and impairing cellular adhesion—highlights its therapeutic potential. Further structural analysis of active components is warranted to validate these findings.

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