Chemoprotective Effect of Decalactone on Hepatic Cancer via Diminishing the Inflammatory Response and Oxidative Stress
Article ID: ess22033
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Article ID: ess22033
Hepatocellular Carcinoma (HCC) is the 5th most common type of cancer in all types of cancers, globally. It is well known that the frequency of inflammatory reaction and oxidative stress increases during the HCC. The goal of this study was to see if decalactone could prevent rats against HCC caused by diethylnitrosamine (DEN). Single intraperitoneal administration of DEN (200 mg/kg) used as inducer and weekly intraperitoneal injection of phenobarbital (8 mg/kg) was used as promotor for induction the HCC in rats. Serum alpha fetoprotein (AFP) was used for the confirmation of HCC. Different doses of decalactone (5, 10 and 15 mg/kg) were orally administered to the rats. The body weight was determined at regular time. The hepatic, non-hepatic, antioxidant markers and inflammatory mediators were scrutinized. All groups of animals were scarified and macroscopically examination of the liver tissue was performed and the weight of organ (hepatic tissue) were estimated. Decalactone increased body weight while also suppressing hepatic nodules and tissue weight. Decalactone treatment reduced AFP, total bilirubin, and direct bilirubin levels while increasing albumin and total protein levels in a dose-dependent manner. Decalactone reduced lipid peroxidation (LPO) and increased catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), and superoxide dismutase (SOD) levels significantly (p < 0.001) (SOD). Decalactone lowered the levels of significantly (p < 0.001) inflammatory cytokines and inflammatory markers in the liver. Based on the findings, we may conclude that decalactone inhibited HCC in DEN-induced HCC animals via reducing oxidative stress and inflammatory mediators.
