This study aimed to investigate the protective effect of boric acid supplementation against liver damage in chronic alcohol-dependent HBV transgenic mice. The HBV transgenic mice were divided into four groups: control(C), boric acid(B), alcohol(A), and alcohol + boric acid(A + B). Blood alcohol concentration (BAC), alanine aminotransferase (ALT), aspartate aminotransferase(AST), reactive oxygen species(ROS), malondialdehyde(MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAS), total oxidant capacity (TOS) levels, and oxidative stress index (OSI) were examined biochemically. H&E, PAS, Masson trichrome, and TUNEL staining were performed. Caspase 3, cytochrome c, and APAF-1 expression levels were determined by qRT-PCR. The alcohol group exhibited significantly higher levels of ROS, MDA, TOS, OSI, and mRNA expressions of Cytochrome c, caspase 3, and APAF-1, while TAS level and CAT activity were significantly lower compared to the boric acid group. Compared to the control group, the alcohol group exhibited significantly increased TOS, OSI, AST levels, APAF-1 mRNA expression, and the number of TUNEL-positive cells, along with a reduction in GPx activity (p < 0.05). However, in the alcohol + boric acid group, TOS and AST levels were significantly higher compared to the control group (p < 0.05), and TOS was higher compared to the boric acid group (p < 0.01). Among the boron-treated groups, only the TOS level was lower in the boric acid group compared to the alcohol + boric acid group (p < 0.01). Histopathological examination revealed reduced sinusoidal dilatation and connective tissue distribution in the boric acid-supplemented groups. These findings suggest that boric acid supplementation may mitigate oxidative damage and histopathological alterations associated with chronic alcohol consumption in HBV-transgenic mice.
Keywords: Alcoholic hepatitis; Apoptosis; Boric acids; Liver; Oxidative stress.
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