关键词: α7烟碱型乙酰胆碱受体, 单核细胞, 核因子κB, 信号传导与转录激活因子3

Abstract: Objective To investigate the effect of α7 nicotinic acetylcholine receptor (α7nAChR) agonists agent PNU282987 on bone cement particles stimulated secretion of inflammatory cytokines in blood monocytes and its molecular mechanism. Methods Mouse peripheral blood monocytes were isolated and the inflammatory response were induced by PMMA particles. TNF-α, IL-1β and IL-6 concentration in culture supernatant were measured by ELISA. TNF-α, IL-1β and IL-6 mRNA expression were measured by RT-PCR. P-p65, p65, p-JAK2, JAK2, p-STAT3, STAT3, and β-actin expression were detected by Western blot. NF-?B DNA binding activity were measured by ELISA. Results After stimulation of PMMA particles, TNF-α, IL-1β and IL-6 concentration in culture supernatant were significantly increased (P<0.05), TNF-α, IL-1β and IL-6 mRNA expression were significantly increased (P<0.05), p-p65, p-JAK2 and p-STAT3 expression and NF-κB DNA binding activity were also increased significantly (P<0.05). However, after PNU282987 treatment, TNF-α, IL-1β and IL-6 concentration in culture supernatant were decreased in a concentration gradient way (P<0.05), TNF-α, IL-1β and IL-6 mRNA expression were decreased in a concentration gradient way (P<0.05), p-p65, p-JAK2 and p-STAT3 expression and NF-κB p65 DNA binding activity were also decreased in a concentration gradient way (P<0.05). Conclusion A7nAChR agonist PNU282987 significantly inhibited PMMA bone cement particles induced secretion of inflammatory cytokines in blood mononuclear cells of mice.

Key words: α7nAChR, monocyte, NF-κB, STAT3