Endotoxin protects rat heart of myocardial reperfusion by inducing expression of lrg

AIM: To explore the protective mechanism of endotoxin in myocardial ischemia-reperfusion injury. METHODS: The total of 30 SD rats were subject to ischemia-reperfusion. Pentobarbital sodium (40 mg/kg) was intraperitoneally injected to anaesthetize rats, and threading ligation of left anterior descending coronary artery was performed to induce myocardial ischemia-reperfusion model. 10 rats were pretreated with endotoxin, another 10 received surgery, and the rest 10 were used as the controls. Western blot and image analysis software were employed to semi-quantitatively calculate the dynamic changes of lrg expression level. The changes of plasma CGRP, ET-1 and TNF-α concentration were measured by radioimmunoassay. With triphenyl tetrazolium chloride (TTC) staining and computer image analysis system, the area of myocardial infarction was calculated. RESULTS: In endotoxin-pretreated group, the levels of plasma ET-1 and serum TNF-α and the myocardial infarct size were significantly reduced at 1.5 h following ischemia-reperfusion, compared with those in the control group (P<0.01), whereas the expression of lrg and level of plasma CGRP were significantly increased (P<0.01). CONCLUSION: Endotoxin pretreatment can upregulate lrg expression to significantly reduce ET-1 level, increasing CGRP concentration and reducing myocardial infarct size of acute myocardial infarction, which suggests endotoxins protective effect in myocardial reperfusion.