Effects of LBPs on intestinal I/R injury
Intestinal I/R is a frequently occurring condition during abdominal and thoracic vascular surgery, small bowel transplantation, hemorrhagic shock, and surgery using cardiopulmonary bypass, with high morbidity and mortality.74 Intestinal I/R is associated with intestinal barrier function loss, which facilitates bacterial translocation into the circulation, thereby triggering systemic inflammation. Moreover, reperfusion of ischemically damaged intestinal tissue further aggravates tissue damage and is considered to be an effector of local as well as distant inflammation and multiple organ failure, which remains the leading cause of death in critically ill patients.74
In a recent study, Yang et al75 examined the effects and potential mechanisms of LBPs on intestinal I/R injury in rats. A common I/R model was used to induce intestinal injury by clamping and unclamping the superior mesenteric artery in rats. Changes in the MDA, tumor necrosis factors (TNF)-α, activated NF-κB, intercellular adhesion molecule (ICAM)-1, E-selectin, and related antioxidant enzyme levels, polymorphonuclear neutrophil accumulation, intestinal permeability, and intestinal histology were monitored. LBPs showed marked inhibitory effect against free radicals and lipid peroxidation in vitro.75 LBPs increased the levels of antioxidant enzymes and reduced intestinal oxidative injury in animal models of intestinal I/R. In addition, LBPs inhibited polymorphonuclear neutrophil accumulation and ICAM-1 expression, and ameliorated changes in the TNF-α level, NF-κB activation, intestinal permeability, and histology.75 These results indicate that LBPs protect against I/R-induced intestinal injuries, possibly through inhibiting I/R-induced oxidative stress, cytokine production, and inflammation.