Carbon tetrachloride-induced acute liver injury
A mouse study100 on the protective effect of LBPs was conducted in carbon tetrachloride (CCl4)-induced acute liver injury. Mice were intraperitoneally injected with CCl4 to induce acute hepatotoxicity and were orally fed with LBPs 2 hours before the CCl4 injection. The results showed that LBPs reduced necroinflammation and oxidative stress induced by CCl4. The protective effects of LBPs against CCl4-induced hepatotoxicity were partly through the downregulation of NF-κB activity.100 NF-κB plays a key role in regulating the immune response to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, and infection.101 While in an inactivated state, NF-κB is located in the cytosol complexed with the inhibitory protein IκBα. The activated NF-κB will be translocated into the nucleus where it binds to specific sequences of DNA called response elements. The DNA/NF-κB complex then recruits other proteins such as coactivators and RNA polymerase to trigger gene expression.101
Ahn et al102 investigated whether Lycium chinense (LC) fruit extract and its component betaine could affect CCl4-induced hepatotoxicity in rats. The treatment of L. chinense fruit extract significantly suppressed the increase of serum alanine aminotransferase and AST in CCl4-injured rats; restored the decreased levels of anti-oxidant enzymes, such as total antioxidant capacity, SOD, CAT, and GPx; and suppressed the expression of inflammatory mediators including inducible nitric oxide synthase and cyclooxygenases.102 Betaine showed hepatoprotective effects as that of L. chinense fruit extract. These findings imply that LC fruit extract reduced CCl4-induced hepatic injury via increasing antioxidative activity and decreasing inflammatory mediators including inducible nitric oxide synthase and cyclooxygenases.