Osthole Improves Acute Pancreatitis Injury By Regulating Nf-Kappa B, Nuclear Factor Pathway

We have investigated the protective role of osthole in tissue injury in experimentally induced acute pancreatitis in a rat model. Acute pancreatitis causes moderate to severe interstitial edema, extensive infiltration of inflammatory cells, marked vacuolation of pancreatic acinar cells, necrosis and hemorrhage in pancreatic tissues. Also, the levels of amylase and lipase, diagnostic markers of acute pancreatitis, are elevated with concurrent rise in the pro-inflammatory cytokines-tumor necrosis factor-alpha, interleukin-6, and interleukin-1 beta. The levels of capase-3, caspase-9, cleaved-caspase-3 and cleaved-caspase-9 were also elevated. The phosphorylation of p65 and I kappa B alpha was upregulated and the expression of I kappa B alpha was downregulated. There was a diminution in all of the aforementioned changes following osthole administration. In conclusion, the results of this study demonstrated that osthole prevents tissue injury in acute pancreatitis through inhibition of the activation of NF-kappa B pathway, providing a new insight to potential treatment.