Objective To detect the expression of developmental endothelial locus-1(DEL-1)in human coronary atherosclerotic plaques,to investigate the mechanism of its involvement in the development of coronary heart disease.Methods Fifty-eight human coronary artery specimens were divided into coronary heart disease group(CHD,25 cases)and control group(CON,33 cases).The left anterior descending branch was taken as the object of study.The structural changes of coronary arteries were evaluated by HE staining on coronary artery intima thickness,fibrous cap thickness and lumen stenosis degree.The expression levels of DEL-1,interleukin-17(IL-17),glycogen synthase kinase-3β(GSK-3β),phosphorylated glycogen synthase kinase-3β(p-GSK-3β)and CCAAT enhanced binding proteinβ(C/EBPβ)in coronary arteries were detected by Western blot.The expression and distribution of DEL-1,GSK-3β,C/EBPβ,and IL-17 in atherosclerotic plaques were detected by immunohistochemical staining,and the correlation between DEL-1 expression and coronary artery structure was analyzed by Pearson moment correlation coefficient test.Results HE results showed that compared with the CON group,the intima of vessels in the CHD group was thickened,the degree of lumen narrowing increased,and the thickness of the fibrous cap thinned(P<0.05);immunohistochemical staining results showed that DEL-1 was mainly expressed in the cytoplasm and nucleus of foam cells within the plaques in the CHD group,whereas IL-17,GSK-3β,and C/EBPβwere mainly expressed in the cytoplasm.Western blot results indicated the expression levels of DEL-1,IL-17,GSK-3β,p-GSK-3β,and C/EBPβ were elevated in the CHD group compared with CON group(P<0.05).Pearson moment correlation coefficients showed that the protein expression level of DEL-1 was positively correlated with intima-media thickness and luminal stenosis,and negatively correlated with fibrous cap thickness(r=0.693,0.733;P<0.05),and negatively correlated with thickness of the fibrous cap(r=-0.432,P<0.05).Conclusion DEL-1 expression is increased within human atherosclerotic plaques and might be involved in the development of coronary heart disease by regulating the intraplaque inflammatory response through the GSK-3β/C-EBPβ pathway.