The Effects of HMGB1 on Ischemia-Reperfusion Injury in the Rat Heart.

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BackgroundCoronary ischemia-reperfusion (I/R) injury proceeds to cause cardiomyocyte necrosis. The pathogenesis of I./R injury is a multi-step process including an inflammatory reaction. A recent study has suggested that high-mobility group boxl (HMGB1) is a late mediator of lethal sepsis and an early mediator of inflammation and necrosis following I/R injury. A neutralizing monoclonal antibody (mAb) for HMGB1 was used to clarify the role of HMGB1 in cardiac I/R injury. Methods and resultsRats underwent 30 min of left coronary artery occlusion followed by 60 min reperfusion. Rats were administered an intravenous injection of anti-HMGB1 mAb or control IgG just before reperfusion. The infarct size was enlarged in the anti-HMGB1 mAb group in comparison to the control group (p<0.05). The treatment of anti-HMGB1 mAb significantly increased the plasma troponin T (TpT) and norepinephrine (NE) content in the heart in comparison to the control (p<0.05). Moreover, the production of DHPG was reduced in the anti-HMGB1-treated group (p<0.05).ConclusionThis study showed for the first time the effects of treatment with neutralizing anti-HMGB1 mAb on I/R injury in rat heart. These findings supported the novel view that I/R-induced HMGB1 may be an important factor to modulate interstitial NE.