After operations such as organ transplantation or cardiopulmonary bypass complicated with is-chemia/reperfusion injury,activated inflammatory cells can express and secret HMGB1,and cooperate with other inflammation factor to induce tissue damage.The mechanism is HMGB1 actives such receptors as TLRs,RAGE,TM,and NF-κB transcription factor,P38MAPK pathway,induce releasing of HMGB1 itself and other inflammation factors.Different with sepsis,HMGB1 emerges much earlier,lasting longer.Inter-ference therapy of HMGB1 could effectively decrease secretion of HMGB1 after ischemia/reperfusion injury.