Wang Ying, Qi Xiuru, Wang Chunliang, Zhao Danning, Wang Hongjie, Zhang Jianxin
Department of Anesthesiology, Affiliated Hospital of Hebei University, Baoding, Hebei 071000, P.R. China.
Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang, Hebei 050021, P.R. China.
Biomed Rep. 2017 Jan;6(1):69-74. doi: 10.3892/br.2016.805. Epub 2016 Nov 9.
The current study aimed to examine the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) in rats with type-2 diabetes mellitus (T2DM) and to assess the role of inflammatory mediators. Fifty healthy male adult Sprague-Dawley rats were randomly divided into the sham, ischemia-reperfusion (IR), IR plus low, middle and high-dose (6, 12 and 24 mg/kg/h, intravenous) propofol groups. The rats of all the groups were fed a high-sugar and high-fat diet for 8 weeks and streptozotocin (30 mg/kg, intraperitoneally) was used to establish the T2DM model. Apart from the sham group rats, MIRI was induced by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 2 h. Heart rate (HR), left ventricular systolic pressure (LVSP), and the rate of left ventricular pressure increase in early systole (± dp/dt) were recorded. Levels of cardiac troponin T (cTnT), nitric oxide (NO), endothelin-1 (ET-1), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were also measured. Myocardial lesions were observed under light microscopy and scanning electron microscopy. Compared with levels prior to arterial occlusion, HR, LVSP, and ± dp/dt were significantly reduced (P<0.05) following occlusion for 30 min and reperfusion for 2 h. The administration of propofol ameliorated the cardiac function of rats as reflected by the increase in HR, LVSP and ± dp/dt. In addition, the administration of propofol increased the serum NO concentration, and reduced ET-1 and cTnT levels, as well as levels of inflammatory mediators including IL-1β, IL-6 and TNF-α. Thus, propofol exerts protective effects against MIRI in T2DM rats by increasing NO and reducing ET-1 and the inflammatory mediators.
本研究旨在探讨丙泊酚对2型糖尿病（T2DM）大鼠心肌缺血再灌注损伤（MIRI）的影响，并评估炎症介质的作用。将50只健康成年雄性Sprague-Dawley大鼠随机分为假手术组、缺血再灌注（IR）组、IR加低、中、高剂量（6、12和24mg/kg/h，静脉注射）丙泊酚组。所有组的大鼠均给予高糖高脂饮食8周，并用链脲佐菌素（30mg/kg，腹腔注射）建立T2DM模型。除假手术组大鼠外，通过结扎左冠状动脉前降支30分钟，然后再灌注2小时诱导MIRI。记录心率（HR）、左心室收缩压（LVSP）和左心室早期收缩压上升速率（±dp/dt）。还测量了心肌肌钙蛋白T（cTnT）、一氧化氮（NO）、内皮素-1（ET-1）、白细胞介素（IL）-1β、IL-6和肿瘤坏死因子（TNF）-α的水平。在光学显微镜和扫描电子显微镜下观察心肌病变。与动脉闭塞前水平相比，闭塞30分钟和再灌注2小时后，HR、LVSP和±dp/dt显著降低（P<0.05）。丙泊酚给药改善了大鼠的心功能，表现为HR、LVSP和±dp/dt增加。此外，丙泊酚给药增加了血清NO浓度，降低了ET-1和cTnT水平，以及包括IL-1β、IL-6和TNF-α在内的炎症介质水平。因此，丙泊酚通过增加NO并降低ET-1和炎症介质对T2DM大鼠的MIRI发挥保护作用。
