Evaluation of the Ethanolic Leaf Extract of Abutilon indicum on Isonicotinic Acid Hydrazide-Induced Proinflammatory Marker Gene Expression Changes.

Background: Abutilon indicum, widely found in India, Sri Lanka, and parts of America and Malaysia, is renowned for its rich bioactive compounds including alkaloids, flavonoids, and sesquiterpene lactones. Due to its diverse pharmacological potential, it has garnered significant attention in traditional medicine. In particular, the ethanolic leaf extract of Abutilon indicum (ELEAI) has demonstrated anti-inflammatory effects, notably targeting the 5-lipoxygenase enzyme pivotal in inflammatory responses.

Objective: This study aimed to elucidate the impact of the ELEAI on proinflammatory marker gene expression induced by isoniazid (INH).

Methods: A total of 36 rats were systematically divided into six experimental groups. The control group received DMSO orally for the initial 30 days followed by distilled water for the subsequent 30 days. The INH group received a daily dose of INH (30 mg/kg b.w., i.p.) for 30 days and the rats were then sacrificed on day 30. The ELEAI (250 mg/kg) group was administered INH daily for 30 days, followed by daily post-treatment with ELEAI (250 mg/kg) for another 30 days. Similarly, the ELEAI (500 mg/kg) group received INH daily for 30 days, followed by daily post-treatment with ELEAI (500 mg/kg) for another 30 days. The silymarin (SIL) group was given INH daily for 30 days, followed by post-treatment with SIL at a dose of 100 mg/kg body weight daily for the subsequent 30 days. Finally, the ELEAI (500 mg/kg) alone group was administered distilled water orally for the first 30 days and then received ELEAI at a dose of 500 mg/kg b.w. orally once daily for the next 30 days.

Results: Continuous INH exposure for a month led to a pronounced increase in proinflammatory genes like TNF-α, TGF-β, and NF-kB and a decrease in the IkB gene in rat liver tissues. Subsequent treatment with SIL (100 mg/kg) and ELEAI (250 and 500 mg/kg) post-INH exposure resulted in a marked decrease in proinflammatory genes and a surge in IkB expression.

Conclusion: The findings suggest that the ELEAI exerts a dose-responsive influence on proinflammatory activities. Notably, A. indicum counteracts inflammation, especially that triggered by bradykinin and prostaglandins. The ELEAI showcases promising therapeutic potential, exhibiting both pro and anti-inflammatory properties and antiproliferative characteristics.