Role of neuroinflammation in pathogenesis of cognitive disorders after aortocoronary bypass grafting

Abstract

Here we present the study aimed to identify dynamic quantitative changes in NSE, NGF, IL-1β, IL-10, IL-6 in patients with postoperative cognitive dysfunction after coronary artery bypass grafting. There were enrolled 44 patients aged 62 to 75 years after coronary artery bypass grafting. MoСA test data allowed to subdivide patients into two groups: group I – 22 patients with MoСA test data changed by less than 3b score before surgery and on day 7 after surgery, no postoperative cognitive dysfunction; Group II – 22 patients with deteriorated MoСA test score by more than 3b, with postoperative cognitive dysfunction. Level of NSE, NGF, IL-1β, IL-10, IL-6 was measured by using enzyme-linked immunosorbent assay (RD Systems, USA) at four time points: before surgery, after surgery, 24 hours and 7t day after surgery. Mean values were compared by using non-parametric Mann–Whitney test. Significance level was set at p 0.05. It was found that patients with postoperative cognitive disorders contained higher level of serum NSE before surgery, immediately postsurgery and 24 hours after surgery, evidences about a role for neuron-specific enolase in the pathogenesis of early postoperative cognitive complications. A pronouncedly increased level of serum nerve growth factor in patients from group II was revealed 24 hours after surgery and elevated concentration on day 7 after surgery, which may be related to compensatory processes in response to damaging factors. Patients from group II were noted to have more marked and prolonged pro-inflammatory response confirmed by dynamic changes in IL-6 level paralleled with elevated amount of serum IL-10. It might be linked to some IL-10-mediated pro-inflammatory properties or more extensive reaction to pronounced pro-inflammatory response. The association between increased NSE and IL-10 levels was revealed. Of interest, the level of IL-1β smoothly declined at all stages in group II patients potentially reflecting impaired anti-inflammatory response, despite the fact that IL-1β is a pro-inflammatory interleukin, or its lack contributes to developing postoperative cognitive disorders, due to disturbed neural plasticity and hippocampus functioning.