# Betaine Mitigates Paclitaxel‐Induced Hepatotoxicity in Rats by Regulating Oxidative Stress, Inflammation, Apoptosis, and Autophagy

## TL;DR

This study shows that betaine can protect rat livers from damage caused by the chemotherapy drug paclitaxel.

## Contribution

This is the first study to show betaine's protective effect against paclitaxel-induced liver injury in rats.

## Key findings

- Betaine improved liver antioxidant levels and reduced liver damage markers like AST and ALT.
- Betaine reduced inflammation and apoptosis while enhancing autophagy in PTL-treated rats.
- Betaine modulated key proteins like Nrf2, NF-κB, and LC3-II/LC3-I to protect the liver.

## Abstract

Paclitaxel (PTL) is widely used in chemotherapy; however, its efficacy is compromised by the risk of liver toxicity. This is the first study to investigate the protective effect of betaine (BTN) against PTL‐induced liver injury. Rats were randomly divided into five experimental groups (n = 7 per group): control (saline), BTN (100 mg/kg/day), PTL (2 mg/kg/day), PTL + BTN (2 and 50 mg/kg/day), and PTL + BTN (2 and 100 mg/kg/day). After the rats received 2 mg/kg body weight PTL intraperitoneally for the first five consecutive days, BTN was administered orally for 10 days. Our results indicate that BTN restores liver antioxidant levels (SOD, FRAP, and GSH), improves liver function by lowering AST and ALT levels, and attenuates PTL‐induced lipid peroxidation. In the livers of PTL‐treated rats, BTN significantly decreased the levels of NF‐κB and TNF‐α proteins and the ratio of caspase‐3/pro‐caspase‐3, whereas it increased the levels of Nrf2, LC3‐II/LC3‐I, and Bcl‐2. In summary, the results of this study suggest that BTN may ameliorate PTL‐induced liver injury by regulating oxidative stress, inflammation, apoptosis, and autophagy.

This study investigated the protective effect of betaine (BTN) against paclitaxel (PTL)‐induced liver injury in rats. The results showed that betaine reduced PTL‐induced liver injury by improving antioxidant levels, reducing inflammation, apoptosis, and regulating autophagy.