# Protective Effects and Mechanisms of Taxus cuspidata Seed Oil on CCl4-Induced Hepatic Fibrosis in Mice

## TL;DR

This study shows that Taxus cuspidata seed oil protects mice from liver damage and fibrosis caused by toxic chemicals, offering potential for new natural treatments.

## Contribution

The study demonstrates the novel protective effects of Taxus cuspidata seed oil against hepatic fibrosis in mice.

## Key findings

- TCSO reduces liver enzyme levels and fibrosis markers in CCl4-treated mice.
- TCSO enhances antioxidant activity and reduces oxidative stress in the liver.
- TCSO suppresses fibrosis-related proteins like TGF-β1, MMP-2, and TIMP-1.

## Abstract

This study aimed to discover new approaches to combat liver fibrosis. We focused on investigating whether oil extracted from the seeds of Taxus cuspidata (abbreviated as TCSO) possesses liver-protective effects. The experimental results show that TCSO can effectively reduce liver damage in mice caused by toxic chemicals. It primarily works through three pathways: reducing liver cell damage, enhancing the liver’s own antioxidant defenses, and preventing excessive scar tissue formation. This research confirms that TCSO significantly improves liver fibrosis in animal models. It provides an important scientific basis for the future development of natural ingredient-based liver protective products or drugs, offering new hope for patients with liver disease.

This study aimed to investigate the effect and underlying mechanism of Taxus cuspidata seed oil (TCSO) on carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. A mouse model of hepatic fibrosis was established by CCl4 induction, and the model mice were subsequently treated orally with high dose or low dose TCSO for eight weeks. The degree of liver fibrosis and the mechanism of action were assessed through organ indices, serum biochemical markers, oxidative stress levels, histopathological examination, and molecular biological analyses. The results demonstrated that TCSO significantly reduced serum levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Concurrently, it decreased the concentrations of liver fibrosis markers, including procollagen III (PC III), collagen IV (IV-C), hyaluronic acid (HA), and laminin (LN), and reduced hepatic collagen deposition. Furthermore, TCSO enhanced the activities of the antioxidants superoxide dismutase (SOD) and glutathione (GSH) while inhibiting the production of the lipid peroxidation product malondialdehyde (MDA), and it ameliorated histopathological alterations in liver tissue. Additionally, TCSO markedly downregulated the expression of key fibrogenic proteins, such as transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinases-1 (TIMP-1), thereby effectively suppressing the progression of hepatic fibrosis. In conclusion, TCSO ameliorates hepatic fibrosis in mice by reducing hepatotoxic enzyme activity and collagen deposition, enhancing antioxidant capacity, and downregulating the expression of fibrosis-related proteins.