The protective effects of adenosine deaminase inhibitor and ouercetin against hepatocellular carcinoma induced by thioacetamide in male rats via downregulation of iNOS, Ki67 and Pan-CK

The liver is the largest and most vulnerable organ in the body, several factors can cause liver cirrhosis and the onset of hepatocellular carcinoma. This study aims to investigate the possibility for adenosine deaminase inhibitor (EHNA) which reduces liver injury, neutrophil infiltration and the levels of proinflammatory cytokines and also it is considering as a target of liver cirrhosis and beginning of hepatocellular carcinoma protective, quercetin which is one of the most common flavonoids has an antioxidant, antitumor and chemopreventive effect on the liver-induced preneoplastic lesions and their combination against thioacetamide as a hepatotoxic and a carcinogenic compound. Biochemical, histopathological and immunohistochemical studies were carried out on male albino rats model to evaluate this possibility. Thioacetamide-treated rats showed a significant increase in liver function tests, alpha-fetoprotein level, expression of inducible Nitric Oxide Synthesis (iNOS), Ki67 and Pan-Cytokeratin (Pan-CK) in hepatic tissue of rats. The results of the present study show that treatment with quercetin, EHNA or their combination attenuated changes in liver functions, histopathological changes, reduced collagen deposition and decreased the expression of iNOS, Ki67 and Pan-CK induced by thioacetamide

Hepato and neuro-protective influences of biopropolis on thioacetamide-induced acute hepatic encephalopathy in rats

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome ultimately occurs as a complication of acute or chronic liver failure; accompanied by hyperammonemia. This study aimed to evaluate the potential of biopropolis as a hepato and neuroprotective agent using thioacetamide (TAA)-induced acute HE in rats as a model. Sixty Wistar rats were divided into five groups: Group 1 (normal control) received only saline and paraffin oil. Group 2 (hepatotoxic control) received TAA (300 mg/kg, once). Groups 3, 4 and 5 received TAA followed by vitamin E (100 mg/kg) and biopropolis (100 and 200 mg/kg), respectively, daily for 30 days. Evidences of hepatic encephalopathy were clearly detected in TAA-hepatotoxic group including significant elevation in the serum level of ammonia, liver functions, increased oxidative stress in liver and brain, apoptotic DNA fragmentation and overexpression of iNOS gene in brain tissue. The findings for groups administered biopropolis, highlighted its efficacy as a hepato and neuro-protectant through improving the liver functions, oxidative status and DNA fragmentation as well as suppressing the brain expression of iNOS gene. In conclusion, bioproplois, at a dose of 200 mg/kg/day protected against TAA-induced HE through its antioxidant and antiapoptotic influence; therefore, it can be used as a protective natural product.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author