Protective effects of carbon monoxide releasing molecule‑2 on pancreatic function in septic mice.

The present study aimed to investigate the effect of carbon monoxide (CO)‑releasing molecule‑2 (CORM‑2) on pancreatic function in sepsis‑model mice. To perform the present investigation, mice were rendered septic by cecal ligation and puncture (CLP). Then, mice were either treated with or without CORM‑2 (8 mg/kg, intravenous) for different durations (6, 12 and 24 h) immediately following CLP. The levels of serum amylase and lipase, tumor necrosis factor α, interleukin‑1β and interleukin‑6 in addition to myeloperoxidase (MPO) activity in pancreatic tissues were determined at 6, 12 and 24 h post‑CLP. Histological scores and the expression of intercellular adhesion molecule 1 (ICAM‑1), vascular cell adhesion molecule 1 (VCAM‑1), nuclear factor‑κB (NF‑κB) and phosphorylated inhibitor of κB (p‑IκB‑α) in the pancreas were also evaluated at 24 h post‑CLP. The results of the present study revealed that compared with CLP‑alone group, CORM‑2 treatment significantly (P<0.05) reduced the levels of serum amylase, lipase and pro‑inflammatory cytokines. In parallel, the severity of pancreatic histology, MPO activity and the expression levels of ICAM‑1 and VCAM‑1 in the pancreas of CORM‑2 treated CLP mice were substantially decreased compared with the untreated group. Furthermore, CORM‑2 treatment inhibited the expression levels of NF‑κB and P‑IκB‑α in the pancreas of mice following CLP compared with the untreated group. CORM‑2‑liberated CO exerted protective effects on the pancreatic function of septic mice, and the beneficial effects may be due to the suppression of NF‑κB activation and subsequent regulation of NF‑κB‑dependent expression of cytokines.