血清白细胞介素8和白细胞介素10在心肌缺血预处理中的变化及意义

Significance and changes of serum interleukin-8 and 10 in human myocardium ischemic preconditioning

目的:探讨缺血预处理(IP)对心肌细胞的保护机制。方法:收集2004年4月-12月期间36例在我科行瓣膜置换手术的病人资料,根据是否采取缺血预处理分为预处理组(IP,20例)和对照组(control,16例),比较2组炎症因子白细胞介素-8(IL-8)、白细胞介素-10(IL-10)和心肌细胞Bcl-2、caspase-3的变化情况,分析IP对机体炎症反应的影响。结果:2组病人细胞因子IL-8、IL-10均在主动脉开放6h时达到高峰,术后5d均恢复到术前水平。预处理组开放后6h、术后1d、术后2dIL-8水平明显低于对照组(P<0.05),IL-10水平显著高于对照组(P<0.05)。复灌后对照组心肌细胞Bcl-2蛋白表达轻度提高,与阻断前比较,无差异;而复灌后IP组心肌细胞Bcl-2蛋白表达明显提高,与阻断前和对照组比较,差异显著(P<0.05);并与IL-10呈正相关性,与IL-8呈负相关性。对照组复灌后心肌细胞caspase-3蛋白表达显著提高,IP组心肌细胞中caspase-3蛋白表达也增高,但比对照组降低,2组间有显著差异(P<0.05)。结论:缺血预处理可能通过降低机体的炎症反应途径达到心肌细胞保护的效果。

AIM： To explore the mechanism of myocardium protection after ischemia/reperfusion （I/R） injury by preconditioning with ischemia in human. METHODS： Thirty - six patients underwent valve replacement were divided into ischemic preconditioning group （ IP group, 20 cases） and non - ischemic preconditioning group （ control group, 16 cases） according to whether they were given single cycle reperfusion before cardioplegia or not. Serum levels of interleukin - 8 and 10 were measured with ELISA. Expressions of myocardial Bcl -2 and caspase- 3 were analyzed. RESULTS： The inflammatory factors IL - 8 and IL - 10 increased to the highest level in serum at 6 h after declamping and recovered to normal level on 5 d after declamping. On 6 h, 1 d and 2 d after declamping, serum level of IL - 8 was significantly lower in IP group than that in control group （ P 〈 0. 05 ）, but serum level of IL - 10 was higher in IP group （ P 〈 0. 05 ）. Expression of myocardial Bcl - 2 and caspase - 3 increased in both groups after reperfusion, and Bcl - 2 was lower in the control group than that in IP group while the level of caspase - 3 was higher （P 〈 0.05）. Expression of myocardial Bcl - 2 had positive correlation with IL - 10 and negative correlation with IL - 8. CONCLUSION ： Ischemic preconditioning has the effect of protection of human myocardial cells after ischemia/reperfusion injury through decreasing systemic inflammatory response following ischemia reperfusion injury.