The hepatotoxicity induced by
APAP is caused by the excessive production of N-acetyl-
para-benzoquinone imine (
NAPQI), which, when reacting with hepatic
proteins proved to cause irreversible lesions. Associated with this process, an intense inflammatory process is also evidenced, characterized by the increased cell influx and production/release of inflammatory mediators.
Trans anethole, an aromatic compounds has been showed anti-inflammatory efficacy by inhibit the cellular recruitment and synthesis/releases of many proinflammatory mediators such as
prostaglandin (
PGE2),
cytokines (TNF, IL-1) and nitrico
oxide (NO). The aim of this study is to investigate the effect of
trans anethole on some inflammatory parameters that are involved in hepatotoxicity induced by high doses of
acetaminophen. Our results demonstrate that treatment with AN at doses 125 and 250mg/kg once a day for seven days prevented the changes caused by the
APAP overdose, showing less intensity in the histological changes (
necrosis, size of hepatocyte area and inflammatory infiltration), and corroborating the findings of serum activities of
transaminases and
phosphatases and the activity of the
enzyme myeloperoxidase. In addition, the treatment prevented the up-regulation of proinflammatory mediators such as NO, TNF, IL-1α, MIP-1α and MCP-1 and induced the up-regulation of anti-inflammatory
cytokines (IL-4 and IL-10). Thus, our results demonstrate a possible protective effect of
trans anethole on the hepatotoxicity induced by
APAP.