大鼠肝缺血/再灌注损伤时TNF-α和ICAM-1在心肌组织中的表达及意义

The expression of TNF-α and ICAM-1 in myocardial tissue after liver ischemia-reperfusion in rats

目的:观察大鼠肝缺血/再灌注损伤(ischemia/reperfusioninjury,I/RI)过程中肝组织TNF-α和心肌组织TNF-α、ICAM-1的表达;探讨肝脏缺血/再灌注过程对心脏的影响以及其机制。方法:选健康雄性Wistar大鼠48只,建立肝脏缺血/再灌注动物模型,每组8只,共分6组。应用免疫组织化学方法测定肝组织TNF-α和心肌组织中TNF-α、ICAM-1的表达。结果:在肝缺血/再灌注过程中,TNF-α在肝脏中的表达在I/R组就有升高(P<0.05),在I/R1h组增高明显,I/R2h、I/R4h组虽然略有波动,但I/R2h组与I/R1h组,I/R4h组与I/R2h组比较差异无统计学意义(P>0.05)。TNF-α在心肌组织中的表达随着再灌注时间的延长逐渐升高,I/R1h组与I/R组、I/R4h组与I/R1h组相比差异有统计学意义(P<0.05),但I/R2h组与I/R1h组、I/R4h组与I/R2h组差异均无统计学意义(P>0.05)。心肌组织ICAM1的表达随着再灌注时间的延长逐渐升高,I/R1h组与I/R组相比、I/R4h组与I/R2h组比较差异均有统计学意义(P<0.05)。肝组织TNF-α和心肌组织TNF-α的表达呈正相关(r=0.844,P<0.01),心肌组织TNF-α与ICAM-1的表达呈正相关(r=0.7544,P<0.01)。肝HE染色切片见I/R导致肝明显的损伤,随着再灌注时间的延长,肝细胞水肿,炎性细胞浸润,甚至肝细胞坏死。心肌HE染色见心肌部分横纹不清楚。

Objective: To observe the expression of tumor necrosis factor-α (TNF-α)and intercellular adhesion molecule-1 (ICAM-1)induced by liver ischemia/reperfusion injury in Wistar rats, and study its mechanism. Methods: A model of liver ischemia/reperfusion injury was established by imitation. Forty-eight male Wistar rats were randomly divided into 6 groups as follows: the control group (the group of sham operation), simply ischemia 30 min without reperfusion (I group), reperfusion following ischemia 30 min (I/R group), 1 hour reperfusion following ischemia 30 min (I/R 1h group), 2 hours reperfusion following ischemia 30 min (I/R 2 h group) and 4 hours reperfusion following ischemia 30 min (I/R 4 h group). TNF-α and ICAM-1 were detected by immunohistochemical staining in myocardial tissue. Results: The expression of TNF-α in liver tissue was significantly increased, especially in I/R 1 h group (P<0.05), but there were not significant changes in I/R 2 h group and I/R 4 h group. The expression of TNF-α and ICAM-1 in myocardial tissue were similar . The expressionss of TNF-α presented a positive correlation in liver tissue,compared with in myocardial tissue (r=0.844,P<0.01). And also there was a positive correlation between the expression of TNF-α and ICAM-1 in myocardial tissue (r=0.7544, P<0.01). At the same time, it can be found that there was hepatic cell edema, inflammatory cellular infiltration, even cellular necrosis following the process of liver ischemia/reperfusion injury through observing HE staining slice and in myocardial tissue, there were inflammatory cellular infiltration, myocardial fibre tumefaction. Conclusions: The expression of TNF-α formed in liver tissue following the process of liver ischemia/reperfusion injury can lead to the increasing expression of TNF-α in myocardial tissue ,and the later promoted high changes of ICAM-1 in myocardial tissue. The results suggested that TNF-α and ICAM-1 involved in the forming of myocardial tissue injury after liver ischemia/reperfusion.