Evaluation of hepatoprotective potential of selected schiff bases (SW8/SB & SW10/SB) against gentamicin-induced hepatotoxicity

Drug-induced hepatotoxicity is a usual way that the liver can suffer harm regardless of the advantageous roles of liver. Gentamicin-induced hepatotoxicity is a significant clinical disadvantage. It is believed that gentamicin- induced hepatotoxicity is due to formation of free radicals. Like other synthetic antioxidant compounds, Schiff bases also have the ability to scavenge free radicals. This study emphasizes the hepatoprotective potential of Schiff bases (Designated as compound A and compound B) in a gentamicin-induced hepatotoxicity animal model. Thirty mices were randomly divided into six groups of five each. Group 1 was injected with 0.9% normal saline intraperitoneally (I.P.) per day and served as control while group 2 received gentamicin I.P. at a dose level of 100mg/kg/day. Group 3 received gentamicin 100mg/kg/day I.P. and compound SW8/SB at a dose level of 25mg/kg/day orally. Group 4 was injected with gentamicin 100mg/kg/day I.P. and SW8/SB at a dose level of 50mg/kg/day orally. Similarly group 5 received gentamicin 100mg/kg/day I.P. and SW10/SB at a dose level of 25mg/kg/day orally. Group 6 received 100mg/kg/day of gentamicin I.P. and 50mg/kg/day of SW10/SB orally. The said procedure lasted for eight days. Then liver function was evaluated by measurement of biomarkers of the liver, including total bilirubin, alkaline phosphatase, and alanine aminotransferase. İn addition to this, histological studies were performed to point out pathological changes in liver. Gentamicin administration elevated serum level of alanine aminotransferase, alkaline phosphatase and total bilirubin as well as gentamicin treatment also caused histopathological alterations. However, administration of Schiff bases reduced both serum level of hepatic biomarkers and histopathological changes. The 50mg/kg of compound SW10/SB showed almost normal histoarchitecture. It is concluded that Schiff bases have the ability to reduce gentamicin-induced hepatotoxicity in mice. However, further studies are still required to further determine the safety and physiological mechanisms behind this effect.