Abstract

Natural oils are traditional medicinal herbs, which have attracted interests for its potential anti-inflammatory and anticancer activities. The present work is aimed at evaluating the protective effect of garlic oil and cinnamon oil on diethylnitrosamine- (DENA-) and 2-acetylaminofluorene- (2-AAF-) induced p53 gene mutation and hepatocarcinogenesis in rats. Forty male albino rats were divided into 4 equal groups: control, hepatocellular carcinoma (HCC), garlic oil-HCC, and cinnamon oil-HCC. The HCC-induced group showed a significant decrease in the body mass and a significant elevation in the liver weight, alpha-fetoprotein (AFP), liver enzymes, hepatic malondialdehyde (MDA), and p53 protein expression levels as well as genetic mutations in intron 5 of p53 gene in the form of Single-Nucleotide Polymorphisms (SNPs) and insertions. In addition, the glutathione (GSH) level and superoxide dismutase (SOD) activities were increased. While HCC rats pretreated with garlic oil or cinnamon oil were significantly reversed, these destructive actions increased GSH and SOD levels. The HCC-induced group showed histopathological features of liver cancer including hypercellularity, nuclear hyperchromasia, mitotic figures, and preneoplastic foci. On the other hand, HCC rats pretreated with garlic oil or cinnamon oil revealed partial reversal of normal liver architecture. The present findings proposed that these natural oils have the ability to improve liver function, significantly reduced the liver toxicity and HCC development. However, further sophisticated studies are recommended before their use as conventional therapeutics for HCC treatment.

Highlights

  • Hepatocellular carcinoma (HCC) is one of the most prevalent and deadliest malignancies worldwide

  • On the first 2 weeks, the HCC-induced group showed a slight decrease in the body weight began to show a very slow increase in the growth rate from 3rd to 14th weeks

  • At the end of 21 weeks, the body weight of rats in the control group was increased to about 1.35-fold of the initial value, while that of rats in the HCC-induced group was decreased by 0.5%

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Summary

Introduction

Hepatocellular carcinoma (HCC) is one of the most prevalent and deadliest malignancies worldwide It is the second leading cause of cancer-related mortalities and accounts for 70–85% of the primary malignant liver neoplasms [1]. Prominent risk factors associated with HCC development include cirrhosis, ingestion of aflatoxin B1-contaminated food, chronic alcohol consumption, and hepatitis B as well as C viral infections [3]. The danger of this devastating cancer is expected to increase further in coming years, due to rising incidence at alarming rates, late diagnosis, lack of definitive treatment, and poor prognosis [4]. Various genes are involved in HCC pathogenesis which can be divided into four main groups: genes regulating DNA damage response (p53), genes involved in cell cycle control (RB1, P16 INK4A, and Cyclin D), genes involved in growth inhibition and apoptosis (TGF-β, M6P/1GF2R, SMAD2, and SMAD4), and genes responsible for cell-cell interaction and signal transduction (APC/βcatenin pathway and E-cadherin) [5]

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