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目的:探讨血清高速泳动族蛋白B1(HMGB1)水平与2型糖尿病(DM)患者急性冠状动脉综合征(ACS)发生的关系。方法:选取218例ACS患者,其中不稳定型心绞痛(UAP)95例,急性心肌梗死(AMI)123例。健康体检者234名作为对照;采用酶联免疫吸附法(ELISA)检测血清HMGB1、高敏C反应蛋白(hsCRP)和肿瘤坏死因子α(TNF-α)的水平。并对血清HMGB1水平与TNF-α、hsCRP和血糖水平进行相关性分析。结果:与对照组相比,AMI组、UAP组血清HMGB1[(12.70±6.72)μg/L、(7.68±3.63)μg/L比(3.83±1.72)μg/L,P<0.01]、hsCRP[(3.30±2.97)mg/L、(1.46±1.37)mg/L比(0.83±0.69)mg/L,P<0.05]和TNF-α[(71.04±38.34)ng/L、(52.69±24.76)ng/L比(43.27±20.56)ng/L,P<0.01]水平均明显升高。在对照组、UAP组和AMI组的亚组中,DM患者血清HMGB1水平均高于非DM者(均P<0.05)。血清HMGB1水平与hsCRP,TNF-α、血糖水平均呈正相关(均P<0.05)。结论:ACS患者HMGB1水平显著升高,且合并DM的ACS患者HMGB1水平高于非DM患者,表明HMGB1有可能参与ACS的发生、发展过程,且在糖尿病时对ACS的病理生理过程影响更大。
Objective: To investigate the relationship between serum high-speed motility protein B1 (HMGB1) and acute coronary syndrome (ACS) in type 2 diabetes mellitus (DM). Methods: A total of 218 patients with ACS were enrolled, including 95 patients with unstable angina pectoris (UAP) and 123 patients with acute myocardial infarction (AMI). 234 healthy subjects were taken as control. Serum levels of HMGB1, hsCRP and TNF-α were detected by enzyme linked immunosorbent assay (ELISA). The correlation between serum HMGB1 levels and TNF-α, hsCRP and blood glucose levels was analyzed. Results: Compared with the control group, the serum levels of HMGB1 [(12.70 ± 6.72) μg / L, (7.68 ± 3.63) μg / L) in AMI group and UAP group were significantly higher than those in control group (3.83 ± 1.72 μg / L, L, (3.30 ± 2.97) mg / L, (1.46 ± 1.37) mg / L vs 0.83 ± 0.69 mg / L, P <0.05] and TNF-α [(71.04 ± 38.34) ng / L (43.27 ± 20.56) ng / L, P <0.01]. In the subgroups of control group, UAP group and AMI group, serum HMGB1 levels in DM patients were higher than those in non-DM patients (all P <0.05). Serum HMGB1 levels were positively correlated with hsCRP, TNF-α and blood glucose (all P <0.05). CONCLUSIONS: The level of HMGB1 is significantly elevated in patients with ACS, and the level of HMGB1 in ACS patients with DM is higher than that in non-DM patients, indicating that HMGB1 may be involved in the development and progression of ACS and has a greater impact on the pathophysiology of ACS during diabetes.