福辛普利钠预处理对缺血后适应大鼠心肌组织Toll样受体表达及炎症因子的影响

Abstract

To observe the effects of ischemic post-conditioning (IPoC) on Toll-like receptor expression and myocardial inflammatory infiltration in myocardial tissue of rats with ischemic reperfusion (I/R) injury and fosinopril sodium pre-treatment, a total of 60 Sprague-Dawley rats were randomly assigned to the following groups: sham (suture around left anterior descending coronary artery was not tied), ischemic reperfusion (30 min<italic> in situ</italic> transient occlusion of the left anterior descending artery, followed by 1 h reperfusion), IPoC (30-min occlusion of left anterior descending artery, followed by three cycles of 10-s reperfusion/10-s ischemia prior to 1-h reperfusion), and fosinopril sodium +IPoC (fosinopril sodium pre-treatment, 0.9 mg/kg, for 14 d, followed by 2-h I/R after last gavage, and IPoC treatment during I/R). Arterial blood and heart samples were extracted after 1-h reperfusion. Serum cTnT levels were measured using the colorimetric method, myocardial infarct size was measured using nitrotetrazolium blue/chloride staining, TNF-α and MCP-1 levels in myocardial tissue were measured by ELISA. TLR2 and TLR4 expression in myocardial tissue was analyzed using immunohistochemistry, and infiltrating cells were detected by hematoxylin-eosin staining. Compared with the I/R group, myocardial enzyme cTnT levels and infarct size significantly decreased in the IPoC group (<italic>P</italic> < 0.01). In addition, MCP-1 and TNF-α levels, as well as the number of infiltrating cells in myocardial tissue, significantly decreased (<italic>P</italic> < 0.05, <italic>P</italic> < 0.01, respectively). TLR2 and 4 expressions also significantly decreased in the IPoC group (<italic>P</italic> < 0.05, <italic>P</italic> < 0.01, respectively). Compared with the IPoC group, the combination of fosinopril sodium and IPoC further reduced infarct size (<italic>P</italic> < 0.05), as well as TNF-α levels in myocardial tissue (<italic>P</italic> < 0.01). TLR2 and 4 expressions and infiltration of inflammatory cells were also significantly decreased (<italic>P</italic> < 0.05). Therefore, fosinopril sodium enhanced the protective effect of IPoC in a rat model of myocardial I/R injury. These mechanisms could be related to inhibition of the TLR signal pathway and chemotactic factor reactions.