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IJAREM: Current Issue (Volume 08 - No. 11, 2022)

 

1. The Study on the Relation between Neutrophil Respiration Burst Activity and Oxidative Tissue Injury during Ischemia- Reperfusion
Chen Wei
Abstract
During the ischemia-reperfusion,ROS are produced in the cells of the ischemic or reperfused tissue or organ by the route of mitochondria, xanthine oxidase, catecholamine-self oxidation, especially by xanthine oxidase route. ROS can activate endothelia cells to release P-Selectin or express de novo a series of CAMs, such as E-Slectin, VCAM and ICAM through inducement of the production of TNF-α or through oxidation-reduction sensitive factors such as NF-KB、AP-1. At the same time endothelia cells also set free chemotactic factors, such as IL-8, MIPs etc, which can activate Integrins on the membrane of Neutrophils. The de novo CAMs that endothelia cells express and activated integrins, such as αLβ2(CD-11a, LFA-1), αMβ2, αXβ2 result in the fixed adhesion of neutrohils to endothelial cells, which at last does much harm to blood vessels and tissues by respiratory burst activity or obstructing the blood vessel. During exercise and recovery period after exercise, the ischemia and reperfusion of tissues or organs also exists, but because of the distinct increase of IL-1ra, sTNF-R, IL-10 and IL-6, the amount of TNF-α in blood is small. What is more, IL-6, IL-8 and especially enzymes released during the course of respiratory burst activity, work together to make CD-11b on the neutrohils shed or down-regulate. so it is evident that oxidative injury caused by exercise-induced ischemia/reperfusion differs from what is caused during the general ischemia/reperfusion, that is to say, oxidative injury caused by exercise-induced ischemia/reperfusion seems to have nothing to do with the neutrophils or their respiratory burst activities.

 

 

 

 

 

 

 

 

 

 

 

 

 

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