# Components Changes in Fresh Ginseng Pulp Treated With Commercial Sterilization and Its Potential Therapeutic in CTX‐Induced Liver Injury via Apoptosis and Nrf2‐MAPKs/NF‐κB Pathways

## TL;DR

This study shows that sterilized ginseng pulp can protect the liver from chemotherapy drug side effects by reducing oxidative stress and harmful pathways.

## Contribution

The study reveals that sterilization increases beneficial ginsenosides and shows SGP's protective effects on CTX-induced liver injury.

## Key findings

- Sterilization increases total and minor ginsenosides and antioxidant capacity in ginseng pulp.
- Both fresh and sterilized ginseng pulp reduce CTX-induced liver injury biomarkers and oxidative damage in mice.
- SGP shows superior liver protection by modulating apoptosis and Nrf2-MAPKs/NF-κB pathways.

## Abstract

Ginseng, as an important dietary supplement, possesses physiological activities including antitumor, immunoregulatory, and antioxidative effects. Ginsenosides are important components that play a physiological role, while minor ginsenosides exhibit stronger functions. Sterilization is the most effective method to increase the minor ginsenosides' contents, and it is also a prevalent technique in food processing. However, it is still unclear whether ginsenosides have protective effects on cyclophosphamide (CTX)‐induced liver injury, and the potential mechanism is still unclear. This research has found that sterilization treatment enhances the contents of total and minor ginsenosides, and also improves its antioxidant capacity, which is significant for the development of healthy food. CTX, a commonly used chemotherapy drug, has inevitable side effects, particularly serious damage to the liver. The purpose of this research is to investigate the improvement effects of fresh ginseng pulp (FGP) and sterilized ginseng pulp (SGP) on CTX‐induced liver injury in mice. Both FGP and SGP could reverse the increase of liver injury biomarkers induced by CTX, and also improve the equilibrium of essential antioxidant enzymes within the redox system, reducing the malondialdehyde (MDA) level. At the same time, FGP and SGP alleviated CTX‐induced liver oxidative damage by inhibiting the MAPKs, Nf‐κB signaling pathways and apoptosis, while enhancing the Nrf2/HO‐1/NQO1 antioxidant defense system. More importantly, SGP exhibits a superior effect in alleviating CTX‐induced liver injury. Cumulatively, SGP has the potential to become a functional food ingredient for alleviating the side effects of CTX‐induced liver injury, offering an important theoretical foundation for its development.

SGP alleviated CTX‐induced liver injury via apoptosis and Nrf2‐MAPKs/NF‐κB pathways.