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目的观察胰高血糖素样多肽-1(GLP-1)对大鼠2型糖尿病性心肌病心肌损伤的影响。方法采用高脂高糖膳食合并链脲佐菌素(40 mg/kg)诱导的方法建立2型糖尿病大鼠模型。将糖尿病大鼠模型随机分为模型组和GLP-1组,采取皮下包埋缓释泵,分别给两组大鼠连续灌注生理盐水或GLP-1 30 pmol/(kg·min 1),7 d后,处死取心脏,利用Langendorff离体心脏灌流系统进行心脏功能检测和心肌细胞形态学观察。结果糖尿病大鼠在建模成功后第10天出现左心室功能异常。3周后,与正常相比,左室发展压(LVDP)、心率–左心室发展压乘积值(RPP)、dp/dtmax、m-dp/dtmax分别降低40.80%、51.50%、50.87%、52.81%;心肌组织炎性细胞浸润增加,血管周围及心肌细胞间纤维化增加,心肌细胞凋亡指数增加。GLP-1处理组LVDP、RPP、dp/dtmax、m-dp/dtmax分别较模型组增加25.36%、10.90%、22.62%、30.07%,心肌细胞炎症、凋亡减少,心肌组织间及血管周围纤维化降低,差异具有统计学意义(P<0.05)。结论糖尿病可直接诱发以间质性纤维化、代偿性纤维化、炎症细胞浸润和凋亡细胞增多为特点的心肌组织损伤,形成糖尿病性心肌病。体内持续释放GLP-1可缓解糖尿病引发的心肌组织损伤,对其心肌组织有保护作用。
Objective To investigate the effect of GLP-1 on myocardial injury in type 2 diabetic cardiomyopathy rats. Methods The rat model of type 2 diabetes was induced by high fat and sugar diet combined with streptozotocin (40 mg / kg). The diabetic rat model was randomly divided into model group and GLP-1 group. Subcutaneous injection of sustained-release pump was used to treat rats in both groups. Rats in both groups were given saline or GLP-1 30 pmol / (kg · min 1) Afterward, the heart was sacrificed and the heart function and myocardial morphology were observed by Langendorff’s ex vivo cardiac perfusion system. Results Diabetic rats developed left ventricular dysfunction on the 10th day after successful modeling. After 3 weeks, LVDP, RPP, dp / dtmax and m-dp / dtmax decreased by 40.80%, 51.50%, 50.87%, 52.81 %. The infiltration of inflammatory cells in myocardium increased, the perivascular and myocardial fibrosis increased, and the apoptotic index increased. Compared with model group, LVDP, RPP, dp / dtmax and m-dp / dtmax in GLP-1 treatment group increased by 25.36%, 10.90%, 22.62% and 30.07%, respectively, and decreased in cardiomyocyte inflammation, apoptosis, myocardial tissue and perivascular fibers Decreased, the difference was statistically significant (P <0.05). Conclusion Diabetes mellitus can directly induce myocardial injury characterized by interstitial fibrosis, compensatory fibrosis, infiltration of inflammatory cells and increase of apoptotic cells, resulting in the development of diabetic cardiomyopathy. Sustained release of GLP-1 in vivo can relieve the damage of myocardial tissue induced by diabetes and protect the myocardial tissue.