CAJ | 학술논문

目的：检测高迁移率族蛋白1(HMGB1)在大鼠心肌中的表达,验证脑利钠肽(BNP)后处理是否能够减少心肌损伤。方法给予麻醉后的大鼠30 min心肌缺血,再灌注前静注BNP15 min,然后再灌注4 h。记录乳酸脱氢酸(LDH)、心肌磷酸激酶(CK),肿瘤坏死因子α(TNF α),白介素(IL 6)等指标的变化,通过免疫印迹法评估 HMGB1的表达。结果 BNP后处理在4 h再灌注后可以显著减少心肌损伤大小和 LDH,CK的表达(P<0.05),明显减少 TNF α,IL 6的增长。同时,在心肌损伤中可以明显抑制HMGB1的表达。结论 BNP后处理可以通过抑制 HMGB1的表达来保护心肌缺血再灌注损伤。
목적：검측고천이솔족단백1(HMGB1)재대서심기중적표체,험증뇌리납태(BNP)후처리시부능구감소심기손상。방법급여마취후적대서30 min심기결혈,재관주전정주BNP15 min,연후재관주4 h。기록유산탈경산(LDH)、심기린산격매(CK),종류배사인자α(TNF α),백개소(IL 6)등지표적변화,통과면역인적법평고 HMGB1적표체。결과 BNP후처리재4 h재관주후가이현저감소심기손상대소화 LDH,CK적표체(P<0.05),명현감소 TNF α,IL 6적증장。동시,재심기손상중가이명현억제HMGB1적표체。결론 BNP후처리가이통과억제 HMGB1적표체래보호심기결혈재관주손상。
Objective To explore the effect of B type natriuretic peptide (BNP)preconditioning on myocardial ischemia reperfusion (I/R)injury and the expression of high mobility group box 1 protein (HMGB1)in rats.Methods Anesthetized male rats were ische-mia for 30 min,and then were treated with BNP in 15 min before reperfusion until the end of reperfusion,and fol owed by reperfusion for 4 hours.Lactate dehydrogenase (LDH),creatine kinase (CK),tumor necrosis factor α(TNF α),interleukin 6(IL 6)and in-farct size were measured.HMGB1 expression was assessed by immunoblotting.Results The Results showed that treatment of BNP post conditioning could significantly decrease the infarct size and the levels of LDH and CK after 4 h reperfusion (al P<0.05). BNP post conditioning could also significantly inhibit the increases of TNF αand IL 6 (both P<0.05).Meanwhile,BNP post conditioning could significantly inhibit HMGB1 expression induced by I/R.Conclusion The present study suggested that post con-ditioning of BNP could protect against myocardial I/R injury which might be associated with inhibiting HMGB1 expression.