alleviates CCl-induced acute liver injury by regulating hepatic S100A8 and S100A9.

Objective: Acute liver injury (ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride (CCl) is a possible environmental toxicant that can induce ALF. (PO) is one of the most popular edible herbs and has several biological activities such as antioxidant, antimicrobial, anti-inflammatory effects. We explored the significance of PO in regulating inflammatory function in animal models and cultured hepatocytes during liver damage caused by CCl.

Methods: The effect of PO on ALF was evaluated by CCl-induced mice models . Hepatic levels of transaminase activities and inflammatory factors were examined. The gene and protein expression of S100A8 and S100A9 were measured by RT-PCR and Western blot analysis. Meanwhile, the efficacy of PO was certified by HepG2 cells . The transaminase activities, inflammatory factors, and the protein expression of S100A8 and S100A9 were also detected.

Results: Animal tests showed that pretreatment with PO reduced the liver pathological tissue damage and the serum levels of ALT, AST, ALT and LDH, as well as reducing the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) secretion in CCl-induced liver injury mice. Simultaneously, HepG2 cells pretreated with PO exhibited a significant decrease in the activities of ALT and AST. Moreover, PO resulted in a significant downregulation of the pro-inflammatory markers S100A8, S100A9 gene and protein expression on CCl induced acute liver injury was demonstrated entirely and experiments.

Conclusion: PO may down-regulate S100A8 and S100A9 and inhibit pro-inflammatory cytokines' release, indicating a potential clinical effect for controlling the disease.