Sodium butyrate protects against myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats

Abstract

High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been reported that it could inhibit HMGB1 expression. This study investigated the effect of sodium butyrate on myocardial I/R injury in rats. Anesthetized male rats were once treated with sodium butyrate (100 or 300 mg/kg, i.p.) 30 min before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. After 4 h reperfusion, pretreatment of sodium butyrate (300 mg/kg) could significantly inhibit the infarct size and the levels of LDH and CK (all P < 0.05). Sodium butyrate (300 mg/kg) could also inhibit significantly the increase of the MDA level and the decrease of the SOD level (both p < 0.05). Sodium butyrate (300 mg/kg) could also inhibit significantly the expression of HMGB1 induced by I/R. The present study suggested that pretreatment of sodium butyrate could protect against myocardial I/R injury by inhibiting HMGB1 expression.