ABSTRACT

Objective: To investigate the hepatoprotective effect and underlying mechanisms of β-Aescin in Isoniazid (INH)-induced liver damage.

Methodology: This experimental study was carried out at the Pharmacology department and Postgraduate Laboratory of Isra University Hyderabad with the collaboration of Sindh Agricultural University Tando Jam. Forty adult Albino Wister rats, weighing between 200 and 250 grams were taken under a well-ventilated & hygienic environment at 26◦C of room temperature and light/dark cycle of 12 hours and divided into 5 groups, each group containing 8 rats. After experiment animals were sacrificed via midline incision, the heart was identified and blood was drawn by cardiac puncture into a plain vial. The blood was allowed to clot and serum separated and stored at 20○C till further use. The liver was identified, removed and rinsed with normal saline and weighed. Serum levels of alanine aminotransferase (ALT), aspartate amino- transferase (AST) and bilirubin total were assessed using a commercially available kit. All the data were collected via study proforma, and analysis was done using SPSS version 26.

Results: A total of 40 animals after dividing in 5 groups as per study protocol were studied; to observe the hepatoprotective effect of β-Aescin in Isoniazid (INH)-induced liver damage. The body weight of the animal was significantly decreased in Isoniazid (INH) control group, experimental group C and D, while it was cured by β-Aescin 3.6 mg/kg. The findings are showing that the Isoniazid (INH) drug also significantly decreased the body weight and β-Aescin 3.6 mg/kg showed the significant protective effects in the body weight. The weight of the liver was significantly increased in Isoniazid (INH) group and experimental group C and D in contrast to the normal control (p-0.001), while experiment group E (β-Aescin 3.6 mg/kg) showed almost equal liver weight compared to the control normal group (p-0.345). β-Aescin 3.6 mg/kg showed the significant protective effects of hepatotoxicity induced by Isoniazid (INH), as the average of ALT, AST, total bilirubin and direct bilirubin were significant decreased almost near to control normally in the β-Aescin 3.6 mg/kg treated group (p-0.001).

Conclusion: As per study conclusion the β-Aescin 3.6 mg/kg was observed to be a protective agent against Isoniazid (INH)-induced hepatic toxicity. It was observed as the antioxidative and anti-inflammatory and antifibrotic to cure the liver. Hence, it can be used as a promising hepatoprotective agent.