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目的:探讨脂联素(Adiponectin,APN)是否能够抑制糖尿病心肌病大鼠心肌间质纤维化,该效应是否通过抗氧化机制而实现。方法:取60只6周龄的清洁级雄性wister大鼠,随机分为APN组、DETC+APN组、Saline组,每组20只。所有大鼠禁食12h后一次性腹腔注射链腺佐菌素(STZ,55mg/kg)制作糖尿病模型,于造模后每组每天分别给予腹腔注射APN、DETC+APN、Saline(APN:1.5×10~3μg/kg;DETC:750mg/kg),持续至造模后第16周末。16周末评定糖尿病发病率,造模72小时后血糖>16.7mol/L;尿糖(+++～++++);且具有多饮、多食、多尿现象为糖尿病成模;测定心脏超声评估心功能;取心脏病理切片进行Masson’s染色以测定心肌纤维化情况;心脏病理切片进行DHE染色以评估氧化应激情况。结果:Saline组和DETC+APN组至16周末分别死亡4只和2只,发生糖尿病大鼠分别为14只(87.5%)和10只(55.5%);而APN组无死亡,6只发生糖尿病(30.0%)。与Saline组大鼠相比,APN组和DETC+APN组大鼠左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)、左心室舒张末期容积(LVEDV)和左心室收缩末期容积(LVESV)均显著减少(P<0.05),短轴缩短率(FS)和射血分数(EF)显著升高(P<0.05),左室胶原容量分数(CVF)显著减少(P<0.05),反映氧化应激情况的DHE染色相对发光值显著减弱(P<0.05)。与APN组大鼠相比,DETC+APN组大鼠LVEDD、LVESD、LVEDV和LVESV均显著增加(P<0.05),FS和EF显著降低(P<0.05),CVF显著增加(P<0.05),氧化应激显著增强(P<0.05)。结论:APN能够通过抗氧化应激效应抑制大鼠糖尿病心肌病心肌纤维化。
Aims: To investigate whether Adiponectin (APN) can inhibit myocardial interstitial fibrosis in diabetic cardiomyopathy rats and whether this effect is mediated by anti-oxidative mechanism. Methods Sixty clean male Wister rats of 6 weeks old were randomly divided into APN group, DETC + APN group and Saline group, with 20 rats in each group. All rats were fasted for 12 hours and then given a single intraperitoneal injection of streptozotocin (STZ, 55mg / kg) to make diabetic model. Each group was given intraperitoneal injection of APN, DETC + APN and Saline (APN: 1.5 × 10 ~ 3μg / kg; DETC: 750mg / kg), until the end of the 16th week after modeling. 16 weekend assessment of the incidence of diabetes, modeling 72 hours after the blood glucose> 16.7mol / L; urinary sugar (+++ ~ ++++); and have a multi-drink, eat more, polyuria phenomenon of diabetes mellitus; determination of the heart Cardiac function was assessed by echocardiography; Masson’s staining was performed on cardiac sections to determine myocardial fibrosis; and DHE staining was performed on cardiac sections to assess oxidative stress. Results: In the Saline group and the DETC + APN group, 4 and 2 diabetic rats died at the end of the 16th week, respectively. There were 14 (87.5%) and 10 (55.5%) diabetic rats, while no deaths and 6 diabetes mellitus (30.0%). The left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were significantly decreased (P <0.05), short axis shortening (FS) and ejection fraction (EF) were significantly increased (P <0.05), and left ventricular fractional volume The relative luminescence value of DHE staining, which reflects oxidative stress, was significantly weaker (P <0.05). Compared with APN group, the levels of LVEDD, LVESD, LVEDV and LVESV in DETC + APN group were significantly increased (P <0.05), the FS and EF were significantly decreased (P <0.05), the CVF was significantly increased Oxidative stress was significantly increased (P <0.05). Conclusion: APN can inhibit myocardial fibrosis in diabetic cardiomyopathy rats through anti-oxidative stress.