Dept. of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahwaz, Iran.
Dept. of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahwaz, Iran; Ahvaz Physiology Research center, Ahvaz Jundishapur University of Medical Sciences, Ahwaz, Iran; Atherosclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahwaz, Iran.
Biomed Pharmacother. 2017 Dec;96:612-618. doi: 10.1016/j.biopha.2017.10.014. Epub 2017 Oct 13.
Diabetic rats are more susceptible to myocardial ischemia-reperfusion injury than control rats. The aim of the present study was to evaluate the cardioprotective effect of gallic acid (GA) on isolated rat hearts with alloxan-induced diabetes mellitus. Adult male Sprague-Dawley rats were divided randomly into three groups: control, untreated diabetic and diabetic animals treated with (GA, 25mg/kg). Diabetes was induced by 120mg/kg alloxan injection. Eight weeks after GA administration, the hearts were isolated and exposed to myocardial ischemia-reperfusion. The body weight, blood glucose, hypertrophy index, left ventricular function, infarct size, cardiac markers and oxidative stress were measured. In the diabetic group, body weight, cardiac contractility (±dp/dt), glutathione peroxidase (GPx) level (p<0.001), left ventricular developed pressure (LVDP), rate pressure product (RPP), superoxide dismutase (SOD) and catalase (CAT) levels (p<0.01) as well as the heart weight (p<0.05) significantly reduced. However, blood glucose, infarct size, hypertrophy index, lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB, p<0.001) and troponin-I (cTnI) levels (p<0.05) significantly increased in the diabetic rats compared with the control group. Nevertheless, administration of GA improved significantly LVDP, ±dp/dt, infarct size, LDH, CK-MB (p<0.001), blood glucose, the heart weight (p<0.01), body weight, RPP, hypertrophy index, antioxidant enzyme and cTnI levels (p<0.05) in the diabetic rats. The results of this study indicated that in the diabetic rats, left ventricular dysfunction and hypertrophy significantly induced possibly by oxidative stress. Moreover, GA as a potent antioxidant improved both left ventricular dysfunction and hypertrophy.
糖尿病大鼠比正常大鼠更容易发生心肌缺血再灌注损伤。本研究旨在评估没食子酸(GA)对链脲佐菌素诱导的糖尿病大鼠离体心脏的保护作用。成年雄性 Sprague-Dawley 大鼠随机分为三组:对照组、未治疗的糖尿病组和用 GA(25mg/kg)治疗的糖尿病组。用 120mg/kg 链脲佐菌素注射诱导糖尿病。GA 给药 8 周后,分离心脏并暴露于心肌缺血再灌注。测量体重、血糖、肥大指数、左心室功能、梗死面积、心脏标志物和氧化应激。在糖尿病组中,体重、心脏收缩力(±dp/dt)、谷胱甘肽过氧化物酶(GPx)水平(p<0.001)、左心室发展压(LVDP)、压力速率产物(RPP)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)水平(p<0.01)以及心脏重量(p<0.05)显著降低。然而,与对照组相比,糖尿病大鼠的血糖、梗死面积、肥大指数、乳酸脱氢酶(LDH)、肌酸激酶-MB(CK-MB,p<0.001)和肌钙蛋白 I(cTnI)水平(p<0.05)显著升高。然而,GA 的给药显著改善了糖尿病大鼠的 LVDP、±dp/dt、梗死面积、LDH、CK-MB(p<0.001)、血糖、心脏重量(p<0.01)、体重、RPP、肥大指数、抗氧化酶和 cTnI 水平(p<0.05)。本研究结果表明,在糖尿病大鼠中,左心室功能障碍和肥大显著诱导,可能是由氧化应激引起的。此外,GA 作为一种有效的抗氧化剂,改善了左心室功能障碍和肥大。