Tephrosia purpurea (Linn.) attenuates progression of acute liver failure by reducing oxidative stress and inflammation via modulating cytoprotective enzyme hemoxygenase-1 activity

Abstract Background: Acute liver failure (ALF), often associated with elevated oxidative stress and sustained inflammation, is one of the major clinical manifestations of liver disease with limited therapeutic options. Tephrosia purpurea is mentioned in Ayurvedic literature to be effective against various health problems. Additionally, this plant with various unknown bioactive components has not been fully explored against acute organ injury, especially against D-galactosamine and lipopolysaccharide induced acute hepatitis. Thus, we aimed to characterize and investigate the efficacy of hydroethanolic extract of Tephrosia purpurea to attenuate ALF progression. Methods: Different doses of Tephrosia purpurea extract (50, 100 and 200 mg/kg) were administered orally once a day for 6 days. In vivo injury was induced via intraperitoneal injection of D-galactosamine (300 mg/kg) followed by lipopolysaccharide (50 μg/kg). Presence of bioactive compounds, functional groups, nature and size of particles, thermal properties of the extract were determined. Results: Levels of lipid peroxidation, proinflammatory cytokines were significantly elevated after D-galactosamine and lipopolysaccharide administration that were restored by the administration of Tephrosia purpurea via modulating hemoxygenase-1 enzyme. Tephrosia purpurea alleviated serum transaminase levels, hematological variables and markedly reduced histological and ultrastructural alterations. Tephrosia purpurea reduced iron overload and maintained glutathione homeostasis (P£ 0.05). Not only that, it also eliminated lipid droplets, restored biomacromolecule homeostasis, maintained stability of the membrane, cellular organelles and the DNA. Conclusions: These findings provided novel insights into the anti-inflammatory and antioxidative mechanisms of Tephrosia purpurea and suggested its use as a potential therapeutic candidate against ALF.