Comparative Effects of Metformin, Boric Acid, and Lithium Chloride on Oxidative Stress-Mediated Cytotoxicity in HepG2 Hepatocarcinoma Cells.

Authors

Burcu Biltekin, Sevgin Değirmencioğlu, Naile Misirlioglu, Hafize Uzun

Published in

Biological trace element research. Sep 17, 2026. Epub Sep 17, 2026.

Abstract

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, highlighting the need for novel therapeutic strategies targeting tumor growth, migration, and oxidative stress. Metformin, boric acid (BA), and lithium chloride (LiCl) have been reported to exert anticancer properties through diverse molecular mechanisms; however, their combined effects on HCC cells remain insufficiently characterized. In this study, we investigated the effects of metformin, BA, and LiCl, alone and in combination, on cell viability, migration, oxidative stress, inflammation, and apoptosis in HepG2 hepatocarcinoma cells. Cell viability was assessed using the CCK-8 assay, while cell migration was evaluated by wound healing analysis. Oxidative stress status was examined through catalase (CAT) activity (Aebi method) and superoxide dismutase (SOD) levels measured by ELISA. Inflammatory responses were assessed by determining IL-17 and NF-κB p105 levels. Apoptotic activity was evaluated via immunocytochemical analysis of caspase-3 and caspase-9 expression. Our results demonstrated that metformin, BA, and LiCl significantly reduced HepG2 cell viability and migration in a time- and concentration-dependent manner. These effects were accompanied by marked alterations in antioxidant enzyme activity, suppression of IL-17 and NF-κB signaling, and robust activation of intrinsic apoptotic pathways, as evidenced by increased caspase-3 and caspase-9 immunoreactivity. Notably, combinatorial treatments, particularly metformin with LiCl, exerted more pronounced antiproliferative and pro-apoptotic effects than monotherapies. Collectively, these findings suggest that metformin, BA, and LiCl modulate oxidative stress, inflammatory signaling, and apoptosis in HepG2 cells, supporting their potential utility as complementary agents in HCC treatment strategies.

PMID:
42753068
Bibliographic data and abstract were imported from PubMed on 18 Sep 2026.

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