ORIGINAL ARTICLE The healing effect of Curcuma longa on liver in experimental acute hepatic encephalopathy of rat Mojtaba Farjam & Davood Mehrabani & Farah Abbassnia & Nader Tanideh & Mohammad Hadi Imanieh & Sara Pakbaz & Mohammad Javad Ashraf & Mohammad Reza Panjehshahin & Sudabeh Dehdab Received: 15 June 2013 /Accepted: 7 January 2014 # Springer-Verlag London 2014 Abstract Hepatic encephalopathy (HE) is a potentially re- versible spectral neuropsychiatric state that complicates liver disease and negatively affects the prognosis. This study eval- uated the effect of Curcuma longa in acute HE in rat and determined the behavioral, biochemical, and histological changes. Forty male Sprague Dawley rats were randomly divided into the control and three experimental groups. Thioacetamide (TAA, 300 mg/kg) was administered intraper- itoneally to induce acute HE. Curcumin was administered orally at doses of 200, 300, and 400 mg/kg. The animals’ behavior, levels of ammonia, alkaline phosohatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) enzymes were evaluated. The livers were evaluated histologically too. TAA could successfully induce inflamma- tion and necrosis in hepatic tissue. Regarding the behavioral score, an increase in the dose of curcumin was correlated with a significant decrease in behavioral score. Ammonia, ALP, ALT, and AST levels were significantly lower among curcumin-receiving groups when compared with the control group, which was dose dependent. Histologically, curcumin was shown to reduce inflammation and necrosis in hepatic tissue, which was dose dependent too. Our findings revealed that curcumin could successfully prevent acute HE, which may happen due to a reduction in release of free radicals in the liver. Keywords Curcuma longa . Acute hepatic encephalopathy . Liver . Rat Introduction Hepatic encephalopathy (HE) is a potentially reversible spec- tral neuropsychiatric state that complicates liver disease and negatively affects the prognosis (Seyan et al. 2010). Both acute and chronic liver dysfunctions may show clinical fea- tures of encephalopathy, but the mortality rate is different in these conditions. In acute liver failure (ALF), 80 % of patients die without liver transplantation (Sherlock and Dooley, 2002). Fulminant hepatic failure (FHF) is the accepted terminology for this condition (Chadipiralla et al. 2012). Unfortunately, the critical condition of the patient suffering from acute HE as well as few livers available for transplantation are major practical problems that physicians face in saving patients with acute HE. To increase the patients’ survival, many aspects of the pathogenesis must be clarified. Although the pathogenic mechanism is not fully understood, the pharmacological in- tervention to protect the brain and spinal cord against hazard- ous toxins which are supposed to escape the acutely affected liver may be a fruitful strategy. Although the role of ammonium intoxication, inflamma- tion, and infection is commonly accepted (Bemeur et al. 2010; Shawcross and Jalan 2005), there are incontrovertible pieces of evidence for the role of oxidative stress in the pathogenesis of HE (Gorg et al. 2010; Lemberg and Fernandez 2009; Schliess et al. 2006). Based on animal studies, considerable reductions in the activities of glutathione peroxidase and superoxide dismutase enzymes in the liver and brain exposed M. Farjam : N. Tanideh : M. R. Panjehshahin Department of Pharmacology, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran D. Mehrabani (*) : N. Tanideh : S. Pakbaz : M. J. Ashraf Stem Cell Research and Transgenic Technology Research Center, Department of Pathology, Shiraz University of Medical Sciences, PO Box: 71345–1744, Shiraz, Iran e-mail: mehrabad@sums.ac.ir F. Abbassnia : S. Dehdab Islamic Azad University, Fars Science Research Branch, Shiraz, Iran M. H. Imanieh Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran Comp Clin Pathol DOI 10.1007/s00580-014-1883-0