低浓度乙醇抑制糖尿病大鼠心肌损伤和NF-κB炎症信号通路活化

Low concentration ethanol inhibits myocardial injury and activation of NF-κB inflammation signaling pathway in diabetic rats

目的探讨低浓度乙醇对糖尿病心肌保护作用与NF-κB和TNF-α表达的关系。方法选取8周、体重140~160g的健康雄性SD大鼠30只,随机分为对照组、糖尿病组、糖尿病+低浓度乙醇组(每组10只)。通过单次腹腔内注射链脲佐菌素(STZ)制备糖尿病大鼠模型。造模成功后1周给予糖尿病+低浓度乙醇组大鼠2.5%乙醇日常饮用,1周后改为5%的乙醇持续至造模成功后第8周,对照组和糖尿病组大鼠均日常饮水。8周后取大鼠腹主动脉血进行肌酸激酶(CK)及乳酸脱氢酶(LDH)检测,取大鼠离体心肌行HE染色观察心肌细胞的形态学改变,免疫组织化学检测心肌细胞NF-κB蛋白的免疫反应性表达,酶联免疫吸附法(ELISA)检测大鼠心肌细胞中TNF-α含量。结果与对照组相比,糖尿病组大鼠的血液中CK和LDH显著升高,心肌细胞排列紊乱,NF-κB和TNF-α水平增加;糖尿病+低浓度乙醇组CK及LDH水平的升高、心肌细胞排列紊乱及结构损伤程度、NF-κB及TNF-α增加幅度均不如糖尿病组明显。结论低浓度乙醇可能通过调节糖尿病大鼠心肌细胞中NF-κB和TNF-α的表达发挥心脏保护作用。

Objective To study the relationship between the protective effect of low concentration ethanol on diabetic myocardiumand the expression of NF-κB and TNF-α.Methods Thirty8-week-old healthy male SD rats each weighing140~160g wererandomly divided into three groups:the control group,diabetes group,and diabetes with low concentration ethanol group(DM+ETOH),ten rats each group.The diabetic model was prepared by single intraperitoneal injection of streptozotocin(STZ),a week aftersuccessful modeling,the DM+ETOH group was fed with2.5%ethanol daily,and another week later with5%ethanol,continue to theeighth week the control and the diabetic groups were given water only.After eight weeks,the abdominal aortic blood was collectedfor creatine kinase(CK)and lactate dehydrogenase(LDH)detection,the morphological changes of myocardial cells were observed byHE staining,the expression of NF-κB protein in myocardial cells was determined by immunohistochemistry,and the content of tumornecrosis factor-αin myocardial cells was detected by ELISA.Results Compared with the control group,blood CK and LDH increasedsignificantly in the diabetic rats,myocardial cells were irregularly arranged,and the levels of NF-κB and TNF-αalso increased;thesechanges were less significant in the DM+EtOH group.Conclusion Low concentration ethanol protects the myocardium of diabetic ratspossibly by inhibiting the expression of NF-κB and TNF-αin myocardial cells.