Hepatoprotective Effects of Biochanin A Against Acetaminophen-induced Liver Toxicity in Mice

Acetaminophen (APAP), a common analgesic agent, is hepatotoxic in overdose. N-acetylcysteine (NAC), as an APAP antidote, shows anaphylactic reactions and has low efficacy in APAP poisoning in high doses.

This study was designed to examine the hepatoprotective effect of biochanin A (BA) in a mice model of acetaminopheninduced hepatotoxicity.

To evaluate APAP-induced oxidative stress, the liver tissue level of malondialdehyde (MDA) and glutathione (GSH) and the activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), catalase, and superoxide dismutase (SOD) were measured. Histological analysis was performed.

APAP-induced hepatotoxicity was manifested by inflammation, acinar hepatic necrosis, and fatty degeneration, as well as an increase in the levels of ALP, ALT, AST, MDA, and a decrease in the SOD, catalase (CAT), and GSH. Pre-treatment with BA at low doses (10 and 20 mg/kg) reduced ALT, AST, and MDA levels and raised the SOD, GSH, and CAT levels. Moreover, it normalized the structure of liver tissue.

The results of this study indicated that BA protected the liver from APAP-induced injury. Protection may be due to the inhibition of oxidative stress, which reduces liver inflammation.