Introduction Hepatic fibrosis is caused by chronic liver injury and repeated repair with scar tissue accumulation in the liver. It is the last reversible stage before liver cirrhosis and hepatocellular carcinoma (HCC). Cordyceps cicadae is a well-known Chinese herbal medicine for treating palpitations and eye diseases. Recent research indicates that C. cicadae contains large quantities of adenosine, N6-(2-hydroxyethyl)-adenosine (HEA) and polysaccharides, which are reported to have anti-oxidation and anti-inflammatory activities. This study investigated the effect of C. cicadae and its active constitutions on carbon tetrachloride (CCl4)-induced liver fibrosis in BALB/c mice
Method Male mice were injected 0.5 µL/g CCl4 (in corn oil) 3 times a week for 4 weeks to induce hepatic fibrosis and treated with C. Cicadae mycelium, adenosine, HEA, and polysaccharides daily for 6 weeks. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) indicated liver function. The collagen levels were determined by serum procollagen-III-peptide (PIIIP), liver hydroxyproline (HYP) and picrosirius red (PSR) stained paraffin-embedded tissue sections. The anti-oxidative enzymes and thiobarbituric acid reactive substances (TBARS) were measured.
Results AST, ALT and ALP levels were reduced significantly by treatment of C. Cicadae mycelium, adenosine, HEA, and polysaccharides compared with the CCl4 group. Moreover, serum PIIIP, liver HYP, and relative liver weight were decreased in all of the sample groups. Furthermore, TBARS levels were decreased by C. Cicadae mycelium, adenosine, HEA, and polysaccharides. However, after CCl4 administration, superoxide dismutase (SOD) and catalase (CAT) activities were increased compared with the control group and treatment of C. Cicadae mycelium, adenosine, HEA, and polysaccharides promoted higher levels of SOD and CAT to protect oxidative damage by reactive oxygen species (ROS).
Conclusion C. Cicadae mycelium, adenosine, HEA, and polysaccharides had potential to prevent hepatic fibrosis via anti-oxidation in CCl4-induced hepatic fibrosis.
Disclosure of Interest None Declared
- Liver Fibrosis