Carbon monoxide releasing molecule‑2 (CORM‑2)‑liberated CO ameliorates acute pancreatitis
- Yishu Liu
- Xu Wang
- Xiaohan Xu
- Weiting Qin
- Bingwei Sun
Affiliations: Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China, Department of Oncology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China, Department of Burns and Plastic Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China
- Published online on: April 19, 2019 https://doi.org/10.3892/mmr.2019.10173
Copyright: © Liu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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)‑κB 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‑κB and phosphorylated inhibitor of NF‑κB subunit α, 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‑κB pathway activation.