# The Protective Effect of Geraniol Against Hepatic Ischemia–Reperfusion Injury by Attenuating Oxidative Stress, Inflammatory Response, and Apoptosis in Rat Model

## TL;DR

Geraniol protects against liver injury caused by ischemia and reperfusion by reducing oxidative stress, inflammation, and cell death in rats.

## Contribution

This study demonstrates geraniol's novel protective effects against hepatic ischemia–reperfusion injury through multiple biological mechanisms.

## Key findings

- Geraniol reduced liver enzyme levels and pathological changes in a rat model of HIRI.
- Geraniol mitigated oxidative stress and inflammatory responses in liver tissue.
- Geraniol decreased apoptotic factors such as Bax and caspase-3 expression.

## Abstract

Hepatic ischemia–reperfusion injury (HIRI) is one of the main causes of hepatic fibrosis that occurs during liver surgery. This study aimed to investigate the protective effect of geraniol (GNL) against HIRI in a rat model.

Wistar rats were randomly divided into seven groups and subjected to 45 min of hepatic ischemia, followed by either 60 min or 6 h of reperfusion. Immediately before reperfusion, graded doses of geraniol (50 and 100 mg/kg) were administered intraperitoneally. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured to evaluate liver function. Antioxidant enzyme activities were assessed in liver homogenates. The concentrations of TNF-α, IL-1β, Bax, and Bcl2 mRNA and proteins in liver tissue were measured using RT-PCR and enzyme-linked immunosorbent assay (ELISA). The expression of Bcl2 and caspase-3 in liver tissue was evaluated by immunohistochemistry. In addition, liver tissue histopathology was examined under a light microscope.

The results demonstrated that liver damage significantly increased after repeated HIRI. However, treatment with GNL reduced hepatic enzyme levels and mitigated pathological changes resulting from repeated HIRI. Additionally, GNL treatment led to a decrease in apoptotic factors.

GNL may be a potential therapeutic agent for preventing or treating hepatic fibrosis caused by ischemia–reperfusion injury.