Hepatic injury is a worldwide health problem. This study aimed to evaluate the possible hepatoprotective potential of Artichoke (Cynara scolymus) extract (CSE) in albino rats using the thioacetamide (TAA) a model of liver injury. Acclimatized 42 rats were divided randomly into seven groups, each consists of six rats, and subjected to different treatments. Hepatic injury model was induced by administration of TAA at a dose of 100 mg per kg, intraperitoneally, twice weekly for 8 weeks (+ve control); test groups rats received CSE at doses of 100 or 200 mg/kg BW, orally, daily for 8 weeks adjunct with TAA; standard group rats received Silymarin at a dose of 100 mg per kg, orally, daily for 8 weeks adjunct with TAA; other 2 groups of rats received only CSE at the same dose levels; while -ve control rats received only the vehicles. Blood and liver tissue samples were collected at the end of the experimental course for different assessments. Results revealed that CSE exhibited dose-dependent hepatoprotection indicated by nearly normalized parameters, including enzymatic liver function parameters (AST, ALT, GGT & ALP with potential % of 94.06, 86.96, 85.93, 64.85, respectively, after large dose when standardized by Silymarin); non-enzymatic parameters (total protein, albumin, globulins, total bilirubin, conjugated bilirubin, unconjugated bilirubin, TAGs, Cholesterol, HDL, LDL & VLDL with potential % of 83.42, 85.9, 83.44, 98.1, 77.41, 91.5, 97.51, 97.46, 81.41, 88.52 & 89.4, respectively, after large dose when standardized by Silymarin). The underlying mechanism of the observed hepatoprotection of CSE was attributed to impeding the oxidative stress-mediated by TAA, indicated by reduced hepatocyte lipid peroxidation product MDA (95.96 % of Silymarin), and improved antioxidative enzymes in liver homogenate, namely, GPx, Catalase & SOD with potentials of 95.44, 87.02 & 81.48 % of Silymarin, respectively. Macroscopic and microscopic pathological pictures were supportive to the biochemical findings, where the pathological lesions caused by TAA as congestion and dilatation of central and portal veins with perivascular fibrous connective tissue proliferation admixed with few mononuclear leukocytes plus necrotic hepatocytes and hyperplastic biliary epithelium, were ameliorated dose-dependently when CSE was administered together with TAA. The present study's data may suggest CSE as a natural source for promising hepatoprotective and antioxidant drug preparations.

Drug-induced hepatotoxicity is a frequent cause of liver injury worldwide. The present study was designed to evaluate the possible hepato-protective potential Agaricus bisporus extract (ABE; a type of mushrooms) in albino rats using Carbon tetrachloride (CCl4)-model of liver injury. Forty-two albino rats were utilized in this experiment arranged randomly in seven groups, six rats each, of different treatments. He-patic injury model was induced by administration of CCl4 (25% in corn oil) at a dose of 2.5 ml/kg, interperitoneally, twice weekly for 8 weeks (+ve control); test group rats received ABE at escalating doses of 200 or 400 mg/kg, orally, daily for 8 weeks with exposure to CCl4; standard group rats received Silymarin at dose of 100 mg/kg, orally, daily for 8 weeks along with CCl4; further 2 groups of rats received only ABE at the same dose levels; while rats of -ve control group received only the vehicles of the used drugs. Blood and liver tissue sam-ples were picked out at the end of the experimental course for different assays. Biochemical analysis revealed that ABE exhibited dose-dependent hepatoprotection indicated by almost normalized biomarkers, including, enzymatic liver function parameters, namely, AST, ALT, GGT & ALP with potential % of 93.1, 58.2, 65.2, 68.9, respectively, after ABE large dose when standardized by Silymarin; non-enzymatic parameters, namely, total protein, albumin, globulins, total bilirubin, conjugated bilirubin, unconjugated bilirubin, TAGs, Cholesterol, HDL, LDL & VLDL with potential % of 59.3, 54.5, 57.3, 81.8, 81.0, 80.0, 75.5, 90.4, 80.8, 84.5 & 78.7, respectively, after ABE large dose when standardized by Silymarin. The mechanism of the obtained hepatoprotection of ABE may be based on impeding the oxidative stress mediated by the used hepatotoxin, indicated by reduced MDA (37.9 % of Silymarin), and restored SOD, Catalase & GPx in liver homogenate with potentials of 94.9, 63.0 & 88.4 % of Silymarin, respectively. Pathological findings, both macroscopic and microscopic, were supportive to the biochemical findings, where the pathological lesions caused by CCl4 as fatty degeneration of hepatocytes with vacuolated cytoplasm, proliferated fibrous connective tissue with eosinophilic edematous fluid cells plus focal and diffuse necrotic areas and hyperplastic biliary epithelium, were ameliorated dose-dependently when ABE was administered together with CCl4. Data of the present study may suggest ABE as a good natural source for promising hepatoprotective and antioxidative remedies.