# Label-free proteomic analysis reveals the hepatoprotective mechanism of gypenosides in liver injury rats

## TL;DR

This study uses proteomics to uncover how gypenosides protect the liver in injured rats, identifying key proteins involved in the process.

## Contribution

The study reveals novel therapeutic targets and mechanisms of gypenosides in liver injury through label-free proteomics and PRM validation.

## Key findings

- 2104 differentially expressed proteins associated with liver injury were identified using label-free proteomics.
- GPs treatment reversed 1508 proteins, with eight key targets validated including Lgals3, Psat1, and Cyp3a9.
- GPs restored metabolic processes like valine, leucine, isoleucine degradation, and steroid hormone biosynthesis.

## Abstract

Chronic liver disease, a long-term condition resulting from various causes such as alcohol abuse, metabolic disorders, and viral hepatitis, is becoming a significant global health challenge. Gypenosides (GPs), derived from the traditional Chinese medicine Gynostemma pentaphyllum (Thunb.) Makino, exhibited hepatoprotective properties in recent years, yet the precise therapeutic mechanism remains unclear. In this study, label-free and parallel reaction monitoring (PRM) proteomics were used to elucidate the hepatoprotective mechanism of GPs in liver injury rats. Through label-free proteomics, we identified 2104 differentially expressed proteins (DEPs) associated with liver injury, along with 1974 DEPs related to the effects of GPs. Bioinformatics analysis revealed that GPs primarily restored metabolic processes involving valine, leucine, and isoleucine degradation, as well as propanoate and butanoate metabolism, and steroid hormone biosynthesis during liver injury. Subsequently, overlapping the two groups of DEPs identified 1508 proteins reversed following GPs treatment, with key targets further validated by PRM. Eight target proteins were identified for GPs treatment of liver injury, including Lgals3, Psat1, Phgdh, Cyp3a9, Cyp2c11, Cyp4a2, Glul, and Ces1d. These findings not only elucidated the hepatoprotective mechanism of GPs, but may also serve as potential therapeutic targets of chronic liver disease.