Carbon Monoxide Releasing Molecule-2 (Corm-2)-Liberated Co Ameliorates Acute Pancreatitis

The purpose of the present study was to investigate the effect of carbon monoxide (CO) released from CO-releasing molecule 2 (CORM-2) on mice with acute pancreatitis (AP). To perform the investigation, a mouse AP model was established using caerulein. The mice were treated with or without CORM-2. The survival rate of the mice in the different groups was analyzed, and serum amylase and lipase levels were measured to assess the degree of pancreatic injury. The severity of AP was also evaluated by histological examination, and histopathological scoring of the pancreatic damage was performed. Pancreatic cell apoptosis was analyzed using a terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling assay. The function of the lung and liver was also assessed in the present study. Furthermore, the role of CORM-2 on oxidative stress, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) expression, pro-inflammatory cytokine production, and nuclear factor (NF)-kappa B activation in the pancreas of AP mice was determined. The results demonstrated that CORM-2 reduced the mortality, pancreatic damage, and lung and liver injury of AP mice. CORM-2 administration also reduced systemic and localized inflammatory cell factors. Furthermore, treatment with CORM-2 inhibited the expression of ICAM-1 and VCAM-1, and the activation of NF-kappa B and phosphorylated inhibitor of NF-kappa B subunit alpha, in the pancreas of AP mice. These results indicated that CO released from CORM-2 exerted protective effects on AP mice, and the beneficial effects were likely due to inhibition of NF-kappa B pathway activation.