# Boric Acid Mitigates Alcohol-Induced Renal Podocyte Injury, Apoptosis, and Oxidative Stress in HBV Transgenic Mice

## TL;DR

Boric acid helps protect the kidneys of HBV-infected mice from alcohol-related damage by reducing stress and cell death.

## Contribution

This study demonstrates boric acid's renoprotective effects in HBV transgenic mice under chronic alcohol exposure.

## Key findings

- Boric acid reduced alcohol-induced tubular injury, apoptosis, and oxidative stress in HBV mice.
- Boric acid improved BUN and creatinine levels and reduced podocyte injury markers.
- Alcohol alone increased oxidative stress and apoptosis, while boric acid mitigated these effects.

## Abstract

Chronic alcohol consumption exacerbates kidney injury, particularly in individuals with hepatitis B virus (HBV) infection. This study investigated the protective effects of boric acid supplementation against alcohol-induced renal damage in HBV transgenic mice. HBV transgenic mice were divided into four groups: control (C), boric acid (B), alcohol (A), and alcohol + boric acid (A + B). Renal injury was evaluated using H&E, PAS, TUNEL, and desmin staining. The expression of caspase-3, cytochrome c, and APAF-1 was analyzed by qRT-PCR. Biochemical analyses included BUN, creatinine, oxidative stress markers (ROS, MDA, TOS, OSI), total antioxidant status, and antioxidant enzyme activities (SOD, CAT, GPx). Histopathological findings showed activated parietal epithelial cells in all groups, indicating renal injury. Alcohol significantly increased tubular damage, podocyte desmin expression, apoptosis, cytochrome c and APAF-1 mRNA levels, and oxidative stress markers, while reducing antioxidant enzyme activities and BUN levels compared with controls. Boric acid supplementation significantly mitigated alcohol-induced tubular injury, apoptosis, oxidative stress, and serum creatinine levels, and improved BUN values. Boric acid treatment alone also alleviated glomerular and tubular injury and reduced tubular apoptosis compared with HBV control mice. Overall, boric acid exerts renoprotective effects in HBV-transgenic mice subjected to chronic alcohol exposure by inhibiting oxidative stress, apoptosis, and podocyte injury.