A3 adenosine receptor agonist, CF102, protects against hepatic ischemia/reperfusion injury following partial hepatectomy

Ischemia/reperfusion (IR) injury during clinical hepatic procedures is characterized by inflammatory conditions and the apoptosis of hepatocytes. Nuclear factor-kappa B (NF-kappa B), nitric oxide and the expression levels of inflammatory cytokines, tumor necrosis factor-alpha and interleukin-1 were observed to increase following IR and mediate the inflammatory response in the liver. CF102 is a highly selective A(3) adenosine receptor (A3AR) agonist, and has been identified to induce an anti-inflammatory and protective effect on the liver via the downregulation of the NF-kappa B signaling pathway. The present study aimed to determine the effect of CF102 on protecting the liver against IR injury. The potential protective effect of CF102 (100 mu g/kg) was assessed using an IR injury model on 70% of the liver of Wistar rats, which was induced by clamping the hepatic vasculature for 30 min. The regenerative effect of CF102 was assessed by the partial hepatectomy of 70% of the liver during 10 min of IR. CF102 reduced the levels of liver enzymes following IR injury. A higher regeneration rate in the CF102 treatment group was observed compared with the control group, suggesting that CF102 had a positive effect on the proliferation of hepatocytes following hepatectomy. CF102 had a protective effect on the liver of Wistar rats subsequent to IR injury during hepatectomy. This may be due to an anti-inflammatory and anti-apoptotic effect mediated by the A(3)AR.