Sun Guoqiang, Li Yubo, Ji Zhiyong
Department of Emergency, The First Hospital of Jilin University Changchun, Jilin, China.
Changchun Medical College Changchun, Jilin, China.
Int J Clin Exp Med. 2015 Sep 15;8(9):14837-45. eCollection 2015.
The role of atorvastatin in inflammation and oxidative stress induced by ischemia/reperfusion is currently not well understood. The aim of this study was toinvestigate whether atorvastatin modulates neutrophil accumulation, TNF-α induction and oxidative stress and to examine the possible role of the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway in an ischemia/reperfusion injured rat heart model. Rats were randomly assigned into tosham operation group, myocardial ischemia/reperfusion (MI/R) group, MI/R + atorvastatin group. Myocardial infarct area, myeloperoxidase (MPO), serum creatinine kinase (CK) and lactate dehydrogenase (LDH) levels were monitored. The results indicate that compared to MI/R, atorvastatin reduced myocardial infarction area, MPO level, serum CK and LDH levels, and both serum and myocardial TNF-αproduction. In addition, atorvastatin increased SOD and GSH-PX activity and decreased MDA content. Atorvastatin also enhanced levels of Nrf2 and heme oxygenase-1. In summary, our data suggests that atorvastatin exerts significant cardioprotective effects following myocardial ischemia, possibly through the activation of the Nrf2/ARE signaling pathway.
目前，阿托伐他汀在缺血/再灌注诱导的炎症和氧化应激中的作用尚不清楚。本研究的目的是调查阿托伐他汀是否调节中性粒细胞聚集、肿瘤坏死因子-α（TNF-α）诱导和氧化应激，并研究核因子红细胞2相关因子2（Nrf2）/抗氧化反应元件（ARE）途径在缺血/再灌注损伤大鼠心脏模型中的可能作用。将大鼠随机分为假手术组、心肌缺血/再灌注（MI/R）组、MI/R + 阿托伐他汀组。监测心肌梗死面积、髓过氧化物酶（MPO）、血清肌酸激酶（CK）和乳酸脱氢酶（LDH）水平。结果表明，与MI/R组相比，阿托伐他汀减少了心肌梗死面积、MPO水平、血清CK和LDH水平，以及血清和心肌TNF-α的产生。此外，阿托伐他汀增加了超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-PX）活性，降低了丙二醛（MDA）含量。阿托伐他汀还提高了Nrf2和血红素加氧酶-1的水平。总之，我们的数据表明，阿托伐他汀在心肌缺血后发挥显著的心脏保护作用，可能是通过激活Nrf2/ARE信号通路实现的。
