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目的建立大鼠心肌缺血-再灌注损伤模型,观察阿托伐他汀预处理对心肌缺血再灌注损伤的保护作用,并探讨其可能的作用机制。方法将36只健康雄性SD大鼠随机分为假手术(S)组、缺血再灌注(I/R)组和阿托伐他汀干预(AT+I/R)组,每组12只。采用冠状动脉左前降支结扎法制备大鼠心肌缺血再灌注损伤模型。通过Evans蓝和四氮唑(TTC)染色评估各组大鼠心肌梗死面积;采用放射免疫法测定大鼠缺血未梗死区心肌组织中肿瘤坏死因子α(TNF-α)、丙二醛(MDA)、髓过氧化物酶(MPO)含量及总超氧化物歧化酶(TSOD)活性;采用比色法测定一氧化氮(NO)含量及总一氧化氮合酶(NOS)、诱导型NOS(iNOS)活性。结果 AT+I/R组心肌梗死区与缺血区(缺血未梗死区+梗死区)面积比值低于I/R组[(29.4±8.4)%vs(57.7±6.5)%,P<0.001];AT+I/R组梗死面积与左室面积的比值也低于I/R组[(15.9±5.6)%vs(29.0±8.9)%,P<0.05]。AT+I/R组及I/R组左室非梗死区域心肌TNF-α、MDA、MPO、NO含量及NOS、iNOS活性均高于S组(P<0.05),而TSOD活性则低于S组(P<0.05);与I/R组比较,AT+I/R组心肌TNF-α、MDA、MPO、NO含量及NOS、iNOS活性均降低(P<0.05),TSOD含量升高(P<0.05)。结论阿托伐他汀对缺血再灌注损伤心肌具有保护作用,机制可能与其降低炎性反应、激活抗氧化反应、提高机体清除氧自由基能力有关,且iNOS在其中的作用值得重视。
Objective To establish a rat model of myocardial ischemia-reperfusion injury and observe the protective effect of atorvastatin preconditioning on myocardial ischemia-reperfusion injury and to explore its possible mechanism. Methods Thirty - six healthy male Sprague - Dawley rats were randomly divided into sham operation (S) group, ischemia / reperfusion (I / R) group and AT + I / R group. Rat model of myocardial ischemia reperfusion injury was established by ligation of the left anterior descending coronary artery. The area of myocardial infarction in each group was assessed by Evans blue and tetrazolium (TTC) staining. The levels of tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) in myocardium were measured by radioimmunoassay ), Myeloperoxidase (MPO) and total superoxide dismutase (TSOD) activity were determined. The content of nitric oxide (NO), total nitric oxide synthase (NOS) and inducible NOS iNOS) activity. Results The area ratio of infarction area to ischemic area (ischemic non-infarct area + infarct area) in AT + I / R group was lower than that in I / R group [(29.4 ± 8.4)% vs (57.7 ± 6.5)%, P <0.001 ]. The ratio of infarct size to left ventricular area in AT + I / R group was also lower than that in I / R group [(15.9 ± 5.6)% vs (29.0 ± 8.9)%, P <0.05]. The levels of TNF-α, MDA, MPO, NO and the activity of NOS and iNOS in AT + I / R group and I / R group were significantly higher than those in S group (P < (P <0.05). Compared with I / R group, the content of TNF-α, MDA, MPO, NO and the activity of NOS and iNOS in AT + <0.05). Conclusions Atorvastatin has a protective effect on myocardial ischemia-reperfusion injury, and its mechanism may be related to its ability to reduce inflammatory reaction, activate anti-oxidation reaction and improve the ability of scavenging oxygen free radicals. And the role of iNOS in it should be emphasized.