Gallic acid against hepatocellular carcinoma: An integrated scheme of the potential mechanisms of action from in vivo study

The global burden of hepatocellular carcinoma is increasing; actually, it is estimated as 750,000 new cases annually. This study was initiated to emphasize the possibility that gallic acid could alleviate hepatocarcinogenesis in vivo. In this study, 40 rats were enrolled and distributed as follows;...

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Published in:Tumor biology 2017-06, Vol.39 (6), p.1010428317699127-1010428317699127
Main Authors: Aglan, Hadeer A, Ahmed, Hanaa H, El-Toumy, Sayed A, Mahmoud, Nadia S
Format: Article
Language:English
Subjects:
alpha-Fetoproteins - biosynthesis
Animals
Antioxidants
Antitumor activity
Apoptosis
Apoptosis - drug effects
Authorship
Biomarkers, Tumor - biosynthesis
Biomarkers, Tumor - genetics
Carcinoma, Hepatocellular - chemically induced
Carcinoma, Hepatocellular - drug therapy
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - pathology
Cell cycle
Chromatography
Deoxyribonucleic acid
Diethylnitrosamine
Diethylnitrosamine - toxicity
DNA
Doxorubicin
Drug dosages
Gallic Acid
Gene expression
Gene Expression Regulation, Neoplastic
Glycoprotein gp96
Glypicans - biosynthesis
Heat shock proteins
Heparan sulfate proteoglycans
Hepatocellular carcinoma
Humans
Inflammation
Intoxication
Liver - pathology
Liver cancer
Liver Neoplasms - chemically induced
Liver Neoplasms - drug therapy
Liver Neoplasms - genetics
Liver Neoplasms - pathology
Males
Medical prognosis
Membrane Glycoproteins - genetics
NMR
Nuclear magnetic resonance
Rats
Research centers
Rodents
Serum levels
Signal transduction
Spectrum analysis
STAT3 Transcription Factor - biosynthesis
Supplements
Transcription
α-Fetoprotein
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Summary:The global burden of hepatocellular carcinoma is increasing; actually, it is estimated as 750,000 new cases annually. This study was initiated to emphasize the possibility that gallic acid could alleviate hepatocarcinogenesis in vivo. In this study, 40 rats were enrolled and distributed as follows; group 1 was set as negative control, while all of groups 2, 3, and 4 were orally received N-nitrosodiethylamine for hepatocellular carcinoma induction. Group 2 was left untreated, whereas groups 3 and 4 were orally treated with gallic acid and doxorubicin, respectively. The current data indicated that gallic acid administration in hepatocellular carcinoma bearing rats yielded significant decline in serum levels of alpha-fetoprotein, glypican-3, and signal transducer and activator of transcription 3 along with significant enhancement in serum suppressors of cytokine signaling 3 level. Also, gallic acid–treated group displayed significant downregulation in the gene expression levels of hepatic gamma glutamyl transferase and heat shock protein gp96. Intriguingly, treatment with gallic acid remarkably ameliorated the destabilization of liver tissue architecture caused by N-nitrosodiethylamine intoxication as evidenced by histopathological investigation. In conclusion, this study demonstrates that the hepatocarcinogenic effect of N-nitrosodiethylamine can be abrogated by gallic acid supplementation owing to its affinity to regulate signal transducer and activator of transcription 3 signaling pathway through its outstanding bioactivities including antioxidant, anti-inflammatory, apoptotic, and antitumor effects.
ISSN:1010-4283
1423-0380
DOI:10.1177/1010428317699127