Cantharidin-induced liver injuries in mice and the protective effect of vitamin C supplementation

• VC enhances hepatofunction in cantharidin-treated mice.
• VC mitigates cantharidin-mediated liver damages.
• VC inhibits cantharidin-induced oxidative stress.
• VC blocks cantharidin-derived liver inflammation.
• VC protects against hepatotoxicity.

Cantharidin, a promising anti-cancer medication, is limitedly prescribed due to the risk of hepatic toxicity. Our previous study has shown that vitamin C (VC) acts as a potential hepatoprotective agent against chemical liver damage. Here we implemented further experiments to investigate the benefits of VC on cantharidin-induced liver injuries in mice. The findings showed that VC mitigated cantharidin-mediated hepatic impairments via reducing liver enlargement, as well as lowering elevated serum concentrations of glutamic-pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT), whereas the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), sodium-potassium ATPase (Na+K+-ATPase) in the liver was increased. In addition, the count of intrahepatic TNF-α positive cells was lowered. The mRNAs of TLR4 and NF-κB pro-inflammatory mediators were down-regulated. Moreover, the phosphorylation of IkB level was decreased in the hepatocytes, while the Mn-SOD (SOD2) expression was up-regulated. Overall, these observations demonstrate that vitamin C has pre-clinical benefits against cantharidin-induced liver injury, possibly through attenuating inflammatory response and oxidative stress.