| First Author | Ye B | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 434 |
| Issue | 3 | Pages | 547-51 |
| PubMed ID | 23583384 | Mgi Jnum | J:201859 |
| Mgi Id | MGI:5515873 | Doi | 10.1016/j.bbrc.2013.03.112 |
| Citation | Ye B, et al. (2013) Absence of NF-kappaB subunit p50 ameliorates cold immobilization stress-induced gastric ulcers. Biochem Biophys Res Commun 434(3):547-51 |
| abstractText | Stress ulcers are a common complication in critically ill patients, but the underlying mechanism is little known. This study characterized the function of the p50 subunit of NF-kappaB in an experimental model of cold immobilization stress-induced gastric ulcers. Stress-induced gastric mucosal inflammation and gastric injury were examined in wild-type and NF-kappaB p50-deficient mice. When subjected to cold immobilization stress, NF-kappaB was rapidly activated in the gastric mucosa in WT mice whereas the majority of kappaB DNA-binding activity was abrogated from p50(-/-) mice. Deficiency of p50 ameliorated stress-induced expression of TNF-alpha, MIP-2, and ICAM-1, resulting in reduced mucosal accumulation of neutrophils and gastric injury. These data indicated a critical role for the p50 in the gastric mucosal inflammatory response to cold restraint stress. |
