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缺血预适应对SD大鼠缺血/再灌注血清TNF-α、IL-8和心肌IL-10水平的影响 被引量:2

Effect of ischemic preconditioning on tumor necrosis factor-α interleukin-8 and interleukin-10 in Spraque-Dawley rats following myocardial ischemia and reperfusion
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摘要 目的观察缺血预适应对SD大鼠心肌缺血/再灌注期血清中肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)及心肌组织中的白细胞介素-10(IL-10)的影响,并探讨其心肌保护机制。方法36只SD大鼠随机分成3组:①缺血预适应(IPC)组:缺血5 min+再灌注5 min反复4次后,缺血60 min+再灌注120 min;②缺血/再灌注(IRI)组:大鼠开胸后,继续观察40 min,然后予以缺血60 min+再灌注120 min;③假手术组(SO):仅开胸,分离血管,不予缺血与再灌注剌激,只进行同样长时间的观察。3组实验结束取右心房血及心肌组织,批量测定血清TNF-α和IL-8及心肌组织IL-10浓度。结果IRI组血清TNF-α和IL-8含量分别为(1 009±277)和(334±187)ng/L,IPC组血清TNF-α和IL-8含量分别为(778±178)和(229±90)ng/L,较IRI组显著降低(P<0.05);IRI组心肌组织IL-10含量为(6.8±2.6)ng/g,IPC组心肌组织IL-10含量为(9.4±4.1)ng/g,较IRI组显著升高(P<0.05)。结论缺血预适应不仅可减少心肌缺血/再灌注病理过程中促炎细胞因子TNF-α和IL-8的产生,还可促进抗炎细胞因子IL-10的产生,而发挥抗炎作用,提示缺血预适应具有保护再灌注心肌抗炎作用的新机制。 AIM To observe the effects of ischemic preconditioning on the production of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and interleukin-10 (IL-10) following myocardial ischemia and reperfusion and to investigate its mechanism. METHODS Thirty-six Spraque-Dawley rats were randomly divided into three groups: ischemic preconditioning group (group IPC, n = 12) was subjected to a 5 min occlusion of left anterior descending coronary artery ( LAD), followed by reperfusion for 5 min four times and then elicited by l h occlusion and 2 h reperfusion; ischemia reperfusion group (group IRI, n = 12) was observed for 40 min and then elicited by 1 h occlusion and 2 h reperfusion; sham-operated group (group SO, n = 12) was only observed for 40 min. At the end of the experiment, the right atrium myocardial blood and myocardial tissue were obtained and the serum TNF-α, IL-8 mass and myocardial tissue concentrations of IL-10 were detected. RESULTS In group IRI, the serum levels of TNF-α and IL-8 were (1 009 ± 277) and (334 ± 187) ng/L and inn group IPC, the serum levels of TNF-α and IL-8 were (778 ± 178) and (229 ± 90) ng/L, significantly lower than those in IRI group (P 〈0. 05). In group IRI, the myocardial IL-10 was (6. 8 ±2.6) ng/g and in group IPC, the myocardial IL-10 was (9.4 ± 4. 1 ) ng/g, significantly higher than those in IRI group ( P 〈 0.05 ). CONCLUSION Ischemic preconditioning not only reduces the myocardial ischemia-reperfusion pathological process of proinflammatory cytokines TNF-α and the IL-8 produce, but also promotes the anti-inflammatory cytokines IL-10, suggesting that the protective effect of ischemic preconditioning on myocardial reperfusion injury through anti-inflammatory mechanism.
出处 《心脏杂志》 CAS 2008年第5期517-520,共4页 Chinese Heart Journal
基金 广东省自然科学基金项目资助(20010783)
关键词 缺血预适应 肿瘤坏死因子-α 白细胞介素-8 白细胞介素-10 心肌缺血/再灌注 ischemic preconditioning tumor necrosis factor-α interleukin-8 interleukin-10 myocardial ischemia-reperfusion
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共引文献17

同被引文献23

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