Hepatocellular carcinoma (HCC), one of the most common
cancers in the world, is a leading cause of cancerrelated mortality. HCC develops most frequently in the background of oxidative stress and chronic hepatic
inflammation due to
viral infections,
alcohol abuse as well as exposure to environmental and dietary
carcinogens. As the prognosis of HCC is extremely poor and mostly unresponsive to current chemotherapeutic treatment regimens, novel preventive approaches like
chemoprevention are urgently needed. We have recently found that
resveratrol, a dietary
polyphenol present in grapes, berries, peanuts as well as red wine, prevents
diethylnitrosamine (DENA)-initiated hepatocarcinogenesis in rats through suppression of
inflammation and oxidative stress. As
cytokines are considered to be important
mediators of inflammation, the objective of the present study was to investigate the effects of
resveratrol on hepatic
cytokines during DENA-initiated hepatocarcinogenesis in rats. Liver samples were harvested from our previous study in which
resveratrol (50, 100 and 300 mg/kg) was found to exert a chemopreventive action against rat liver
tumorigenesis induced by DENA. The levels of proinflammatory
cytokines, namely
tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and
interleukin- 6 (IL-6), were measured using
enzyme-linked
immunosorbent assays. The
mRNA expression of these
cytokines was studied by
reverse transcriptase-polymerase chain reaction for comparison.
Resveratrol treatment reversed the DENAinduced alteration of the level and expression of hepatic TNF-α, IL-1β and
IL-6. From the current results in conjunction with our previous findings, it can be concluded that
resveratrol-mediated
chemoprevention of rat liver
carcinogenesis is related to alteration of proinflammatory
cytokines.