Acteoside-mediates chemoprevention of experimental liver carcinogenesis through STAT-3 regulated oxidative stress and apoptosis

ABSTRACT In the absence of an effective therapy against Hepatocellular Carcinoma (HCC), chemoprevention remains an important strategy to circumvent morbidity and mortality. Here, we examined chemopreventive potential of Acteoside (ACT), a plant derived phenylethanoid glycoside against an environment...

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Published in:Environmental toxicology 2016-07, Vol.31 (7), p.782-798
Main Authors: Peerzada, Kaiser J., Faridi, Aamir H., Sharma, Love, Bhardwaj, Subhash C., Satti, Naresh K., Shashi, Bhushan, Tasduq, Sheikh A.
Format: Article
Language:English
Subjects:
acteoside
Animals
Anticarcinogenic Agents - pharmacology
Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis - drug effects
Carcinogens - antagonists & inhibitors
Carcinogens - toxicity
Cell Line, Tumor
chemoprevention
Cytokines - metabolism
diethyl nitrosamine
Diethylnitrosamine - antagonists & inhibitors
Diethylnitrosamine - toxicity
Glucosides - pharmacology
hepatocellular carcinoma (HCC)
Hepatocytes - drug effects
Hepatocytes - pathology
Liver Neoplasms, Experimental - chemically induced
Liver Neoplasms, Experimental - pathology
Liver Neoplasms, Experimental - prevention & control
Male
Oxidative Stress - drug effects
Phenols - pharmacology
rat
Rats
Rats, Wistar
STAT3 Transcription Factor - drug effects
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Summary:ABSTRACT In the absence of an effective therapy against Hepatocellular Carcinoma (HCC), chemoprevention remains an important strategy to circumvent morbidity and mortality. Here, we examined chemopreventive potential of Acteoside (ACT), a plant derived phenylethanoid glycoside against an environmental and dietary carcinogen, diethylnitrosamine (DEN)‐induced rat hepatocarcinogenesis. ACT treatment (0.1 and 0.3% supplemented with diet) started 2 weeks before DEN challenge and continued for 18 weeks thereafter, showed a remarkable chemopreventive activity. ACT treatment resulted in reduced HCC nodules. Histopathology showed progressive tissue damage, necrosis (5 weeks), hepatocytic injury (10 weeks), anisonucleosis with presence of prominent nucleoli, sinusidal dilations, and lymphomono nuclear inflammation (18 weeks). Biochemical analysis showed hepatocytic injury (raised ALT, p 
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22089