Effect of Acacia hydaspica R. Parker extract on lipid peroxidation, antioxidant status, liver function test and histopathology in doxorubicin treated rats.

Doxorubicin (DOX) is an anthracycline agent mostly prescribed for various cancers. However, its treatment is contiguous with toxic effects. Acacia hydaspica prevented drug-induced hepatic-toxicity in animals with anti-oxidative mechanisms. We intended to study the efficacy of A. hydaspica ethyl acetate extract (AHE) for inhibiting DOX- induced liver damage.Normal control group received saline; Drug control group received 3 mg/kg b.w. dose of DOX for 6 weeks (single dose/week, intraperitoneal injection) to study the effect of chronic DOX treatment. In co-treatment groups, 200 and 400 mg/kg b.w AHE was given orally for 6 weeks in concomitant with DOX (3 mg/kg b.w, i.p. injection per week). The standard drug group received silyamrin 100 mg/kg b.w (2 doses/week: 12 doses/6 weeks) in conjunction with DOX (single dose/week). Lipid profile, liver function tests (LFTs), antioxidant enzymes, oxidative stress enzymes and morphological alterations were studied to evaluate the hepatoprotective potential of AHE.DOX treatment inhibits body weight gain and upturn liver index. DOX considerably upset serum cholesterol, triglycerides and LDL concentration. On the contrary, it reduced serum HDL amount. DOX induced marked depreciation in serum LFTs, diminish hepatic antioxidant enzymes; however, raised tissue oxidative stress markers accompanied by morphological damages. Co-treatment with AHE dose dependently adjusted DOX-prompted fluctuations in lipid profile, AST, ALP, ALT, total bilirubin, and direct bilirubin concentrations and hepatic weight. Likewise, AHE usage enhanced total protein and hepatic tissue antioxidant enzyme quantities whereas declined oxidative stress markers in hepatic tissue. Correspondingly histopathological examinations aid the biochemical results. The influence of AHE 400 mg/kg b.w dose is analogous to silymarin.Acacia hydaspica possibly serve as adjuvant therapy that hampers DOX inveigled liver damage due to the underlying antioxidant mechanism of secondary metabolites.