The role of HMGB1 in ischemia-reperfusion injury in the rat small intestine

Abstract

DOI of original article: 10.1016/j.jss.2012.0 * Corresponding author. Uniformed Services MD 20814, USA. Tel.: þ1 301 295 2552; fax: þ E-mail address: hassan_tetteh@hks09.ha 0022-4804/$ e see front matter a 2013 Elsev doi:10.1016/j.jss.2012.04.004 Kojima et al. highlight the High Mobility Group Box Chromosomal Protein 1 (HMGB1) and its potential role in response to ischemia-reperfusion injury in the small intestine [1]. Their results suggest that HMGB1 is an importantmediator in the rat model of ischemia-reperfusion injury, and that therapeutic agents may be developed for targeted therapy in ischemiarelated injury to the small intestine. Several studies have previously explored the impact and role ofHMGB1 inacute lung injuryand ischemia-reperfusion injuryof the kidney, heart, brain, and liver [2e5]. This current studyby the authors appears to be the first report that investigates HMGB1 in the intestinal rat model of ischemia-reperfusion injury, and it offers three unique perspectives that may create opportunity for further investigation and innovation in the treatment of ischemia-reperfusion injury. First, the study demonstrated that increased serum HMGB1 concentration and its localization in damaged intestinal tissue were identified after reperfusion injury. Second, the study suggests that there is strong expression of HMGB1 in the damaged cells of terminal protein of the villi of small intestine. Finally, the administration of anti-HMGB1 antibody appears to ameliorate local disturbances and improve survival in the study subjects over controls. The authors’