# Lagerstroemia speciosa Pers. (Lythraceae) Ethanolic Extract Attenuates Isoniazid-Induced Oxidative Stress and Hepatic Inflammation in Rats

## TL;DR

This study shows that an extract from banaba leaves can protect rat livers from damage caused by isoniazid, a drug used to treat tuberculosis.

## Contribution

The novel contribution is demonstrating the hepatoprotective effect of Lagerstroemia speciosa ethanolic extract against isoniazid-induced liver injury in rats.

## Key findings

- Ethanolic banaba leaf extract reduced isoniazid-induced liver enzyme elevation and oxidative stress in rats.
- The extract mitigated proinflammatory markers and restored antioxidant levels in liver tissue.
- Histopathological analysis confirmed the protective effect of the extract against liver damage.

## Abstract

Background

Drug-induced liver injury is a common cause of acute liver failure. Isoniazid (INH) is used as a first-line treatment for tuberculosis. Clinical and experimental studies have reported abnormal liver function after INH therapy. Lagerstroemia speciosa Pers., commonly known as banaba, has been traditionally used to treat various ailments including diabetes and obesity due to its antioxidant and anti-inflammatory properties.

Aim

To investigate the hepatoprotective effect of ethanolic banaba leaf extract (EBLE) against INH-induced hepatotoxicity in rats.

Materials and methods

A total of 30 male Wistar albino rats (150 - 200 g) were divided into five groups (n = 6). Group I rats were served as a control and were administered dimethyl sulfoxide for the first 30 days and water for the next 30 consecutive days. Group II rats were administered INH (50 mg/kg, p.o.) once in the first 30 consecutive days and sacrificed at Day 30. Group III rats were administered INH for 30 consecutive days and left without treatment for the next 30 days. In Groups IV and V, rats were post-treated orally with EBLE 250 and 500 mg/kg, p.o. (0.3 ml/rat) for 30 days after INH administration. At the end of Day 60, the remaining group of animals were sacrificed. The blood and liver tissues were collected. The marker enzymes of hepatotoxicity, oxidative stress markers, inflammatory markers, and histopathology were analyzed.

Results

INH administration induced significant elevation of marker enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, bilirubin, gamma-glutamyl transpeptidase) of hepatotoxicity in the serum. This treatment also increased lipid peroxidation and proinflammatory marker expression (tumor necrosis factor-alpha, transforming growth factor-beta, and nuclear factor kappa B (NF-κB) except inhibitor of NF-κB) and decreased antioxidants such superoxide dismutase, catalase, and glutathione in the liver tissue. All these abnormalities were significantly mitigated after treatment with EBLE.

Conclusion

The results of this study suggest that EBLE can be used for INH-induced hepatotoxicity.