Wednesday, 17 April 2019

Journal of Health Research and Reviews-Lupine Publishers




Intestinal ischemia-reperfusion (I-R) injury is a severe condition resulting from acute mesenteric ischemia, small bowel transplantation, abdominal aortic aneurysm, hemorrhage, trauma, septic shock, or severe burns. Various chemical and cellular mediators have been implicated in the pathogenesis of intestinal ischemia/reperfusion, such as reactive oxygen, cytokines, endotoxins, and neutrophils [1]. Following adhesive interactions among neutrophils and endothelial cells, neutrophil accumulation in the intestinal mucosa contributes to intestinal ischemia/ reperfusion injury via production of reactive oxygen metabolites and proteases. Leukocyte accumulation is a complex phenomenon that also involves endothelium-based adhesion molecules as well as leukocyte chemotaxis factors such as interleukin-8 (IL-8) [2,3]. Intercellular adhesion molecules are normally expressed at a low basal level, but their expression can be enhanced by several inflammatory cytokines such as IL-1β and tumour necrosis factor-α (TNF-α). A variety of cytokines, including TNF-α, interferon-γ, and IL-1β, are released from post-ischemic tissues [4]. To know more click on below link.


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