Wang Ying, Zhang Kecheng, Qi Xiuru, Yang Guang, Wang Hongjie, Zhang Zhe, Yang Baofeng
Department of Anesthesiology, Affiliated Hospital of Hebei University, Baoding, Hebei 071000, P.R. China.
Department of Medicine, Hebei University, Baoding, Hebei 071000, P.R. China.
Exp Ther Med. 2020 Apr;19(4):2441-2448. doi: 10.3892/etm.2020.8499. Epub 2020 Feb 7.
To investigate the effects of propofol on myocardial ischemia reperfusion in rats with type 2 diabetes, male adult rats were divided into five groups: Sham-operation (CC), ischemia-reperfusion (CI), low-dose propofol (LP), moderate-dose propofol (MP) and high-dose propofol (HP). The LP, MP and HP groups were administered with 6, 12 and 24 mg/kg/h propofol, respectively, prior to occlusion. Heart rate (HR), left ventricular systolic pressure (LVSP) and the rate (dp/dt max) of left ventricular pressure rise in early systole (±dp/dt max) were recorded. The role of autophagy was also studied by measuring the levels of superoxide dismutase (SOD), malondialdehyde (MDA), autophagy marker protein LC3II, mammalian target of rapamycin (mTOR)/phosphorylate (p)-mTOR and cardiac troponin T (cTnT). The myocardial morphological features were assessed using light and electron microscopy. The present results demonstrated that the HR, LVSP, +dp/dt and -dp/dt levels in the propofol groups (LP, MP and HP) were significantly increased (P<0.05) when compared with the CI group. The myocardial cells in the MP group showed mild edematous changes and partially dissolved mitochondrial cristae and membrane rupture. SOD, cTnT and MDA levels were significantly decreased (P<0.05), mTOR expression decreased significantly (P<0.05) and p-mTOR expression increased significantly in the MP group (P<0.05). The present study demonstrated the protective effects of propofol in T2DM rats exhibiting MIRI, with an optimal protective effect at an infusion rate of 12 mg/kg/h. Additionally, the results revealed that propofol led to significant reductions in LC3II and mTOR serum levels and the inhibition of autophagy in myocardial cells.
为研究丙泊酚对2型糖尿病大鼠心肌缺血再灌注的影响，将成年雄性大鼠分为五组：假手术组（CC）、缺血再灌注组（CI）、低剂量丙泊酚组（LP）、中剂量丙泊酚组（MP）和高剂量丙泊酚组（HP）。在阻断前，LP、MP和HP组分别以6、12和24mg/kg/h的速度输注丙泊酚。记录心率（HR）、左心室收缩压（LVSP）以及左心室压力上升速率（±dp/dt max）。通过检测超氧化物歧化酶（SOD）、丙二醛（MDA）、自噬标记蛋白LC3II、雷帕霉素靶蛋白（mTOR）/磷酸化（p）-mTOR和心肌肌钙蛋白T（cTnT）水平来研究自噬的作用。采用光镜和电镜评估心肌形态学特征。目前的结果表明，与CI组相比，丙泊酚组（LP、MP和HP）的HR、LVSP、+dp/dt和-dp/dt水平显著升高（P<0.05）。MP组心肌细胞出现轻度水肿改变，线粒体嵴部分溶解，膜破裂。MP组SOD、cTnT和MDA水平显著降低（P<0.05），mTOR表达显著降低（P<0.05），p-mTOR表达显著升高（P<0.05）。本研究证明了丙泊酚对2型糖尿病合并心肌缺血再灌注损伤大鼠具有保护作用，输注速率为12mg/kg/h时保护效果最佳。此外，结果显示丙泊酚可显著降低LC3II和mTOR血清水平，并抑制心肌细胞自噬。
