Effects of icariin on microRNAs expression in bone microvascular endothelial cells in steroids-induced femoral head lesions / 中国组织工程研究

ABSTRACT

BACKGROUND:MicroRNAs (miRNAs) are widely involved in regulation of physiological processes, such as human development, cel proliferation, differentiation, and apoptosis, angiogenesis and lipid metabolism. MiRNAs also play an important regulating role in the pathological process of femoral head necrosis. At present, the research about the effect of icarin on miRNA expression in glucocorticoid- induced avascular necrosis is stil in the exploratory stage, and the specific targets, possible regulation mechanism and signaling pathway remain unclear. OBJECTIVE:To explore the effect of icarin on miRNA expression of bone microvascular endothelial cels in steroids-induced human femoral head lesionsin vitro. METHODS: Bone microvascular endothelial cels in cancelous bone of the femoral head were isolated and harvested in vitro. Icarin preconditioning preceded establishment of models of glucocorticoid-induced bone microvascular endothelial cel injury. Differential expression profiles and transcriptomes in glucocorticoid and normal groups were tested by miRNA microarrays. The most differentialy expressed miR-23b and miR-339 in microarray analysis were further confirmed by real-time quantitative PCR, Meanwhile the effects of icarin on the expression of miR-23b-5p and miR-339-5p were detected. RESULTS AND CONCLUSION:According to the microarray analysis, one miRNA was up-regulated and four mi RNAs were down-regulated in the glucocorticoid group (fold > 2,P < 0.05). Results of RT-qPCR revealed that miR-23b was down-regulated and miR-339 up-regulated in the glucocorticoid group, which were in agreement with the microarray analysis (P < 0.05). Icarin pretreatment effectively prevented the imbalances of miR-23b expression induced by glucocorticoid (P < 0.01). These findings indicate that Icarin may participate in the pathological process of steroid-induced femoral head necrosis through regulating the expression of miR-23b.