| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2540443 | International Immunopharmacology | 2015 | 6 Pages |
•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.
