高血糖介导炎性反应加重大鼠急性心肌缺血损伤的作用

Role of hyperglycemia-mediated inflammatory response in aggravating acute myocardial ischemia injury in rats

目的探讨NF-κB和TNF-α等炎性因子在高血糖大鼠急性心肌缺血组织的加重损伤机制。方法选择SPF级雄性SD大鼠48只,按随机数字表法分为假手术组、高血糖合并急性心肌梗死(AMI)组(高血糖AMI组)、正常血糖AMI组,每组16只。采用分光光度法和酶联免疫吸附法检测各组大鼠心肌组织髓过氧化物酶(myeloperoxidase,MPO)、白细胞介素(IL)-1β和IL-6水平,Western blot法检测缺血心肌组织NF-κB和TNF-α表达。结果与假手术组比较,高血糖AMI组MPO、IL-1β、IL-6水平明显升高,差异有统计学意义(P<0.05)。与高血糖AMI组比较,正常血糖AMI组MPO、IL-1β、IL-6水平明显降低,差异有统计学意义(P<0.05)。与假手术组比较,高血糖AMI组NF-κB和TNF-α表达明显升高(P<0.01)。与高血糖AMI组比较,正常血糖AMI组NF-κB和TNF-α表达明显降低(1.231±0.245 vs 1.743±0.383,1.109±0.247 vs 1.624±0.413,P<0.01)。结论高血糖介导的炎性因子MPO、IL-1β、IL-6、NF-κB和TNF-α表达增加可能是加重急性心肌缺血损伤的主要机制之一。

Objective To study the mechanism of inflammatory factors such as NF-κB and TNF-α in aggravating acute myocardial ischemia(AMI) injury in hyperglycemia rats.Methods Forty-eight SPF male SD rats were randomly divided into sham operation group(n=16),hyperglyce-mia+AMI group(n=16) and normal blood glucoe+AMI group(n=16).Their serum levels of MPO,IL-1β and IL-6 in ischemic myocardial tissue were measured by spectrophotography and ELISA respectively.The expressions of NF-κB and TNF-α in ischemic myocardial tissue were detected by Western blot.Results The serum levels of MPO,IL-1β and IL-6 were significantly higher in hyperglycemia+AMI group than in sham operation group(P<0.05) and significantly lower in normal blood glucoe+AMI group than in hyperglycemia+AMI group(P<0.05).The expression levels of NF-κB and TNF-α were significantly higher in hyperglycemia+AMI group than in sham operation group(P<0.01) and significantly lower in normal blood glucoe+AMI group than in hyperglycemia+AMI group(1.231±0.245 vs 1.743±0.383,1.109±0.247 vs 1.624±0.413,P<0.01).Conclusion Hyperglycemia-mediated high expression level of MPO,IL-1β,IL-6,NF-κB,TNF-α is one of the mechanisms of inflammatory factors in aggravating AMI injury in rats.