论文部分内容阅读
目的探讨鲫鱼卵唾液酸糖蛋白(Carassius auratus sialoglycoproteins,Ca-SGP)对核因子κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)诱导形成的破骨细胞的抑制作用及机制。方法初断乳ICR雄性小鼠,无菌取股骨,分离骨髓造血细胞并诱导其分化为破骨细胞。分别检测Ca-SGP对破骨细胞及其前体细胞活力、抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)活性及分化成熟过程的影响,测定破骨细胞形成过程中核因子κB(Nuclear factor,NF-κB)和丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)信号通路关键因子的表达。结果 Ca-SGP可有效抑制由RANKL诱导的破骨细胞分化及成熟,降低细胞TRAP活性及其表达,抑制骨吸收陷窝形成;分子机制方面,Ca-SGP可明显降低信号传导关键蛋白TRAP6的活性,进而抑制NF-κB和MAPKs信号通路关键因子mRNA的表达,达到抑制破骨细胞分化成熟的效果。结论 Ca-SGP可通过NF-κB和MAPKs信号通路抑制由RANKL诱导的破骨细胞形成和分化成熟。
Objective To investigate the inhibitory effect of Carassius auratus sialoglycoproteins (Ca-SGP) on osteoclasts induced by receptor activator of NF-κB ligand (RANKL) and its mechanism. Methods Weanling ICR male mice were randomly divided into three groups: osteoblasts and osteoblasts were isolated from bone marrow hematopoietic cells. The effects of Ca-SGP on the viability of osteoclasts and their precursors, the activity of tartrate-resistant acid phosphatase (TRAP) and the differentiation and maturation of osteoclasts and their precursors were detected respectively. The effects of nuclear factor kappa B , NF-κB) and mitogen-activated protein kinases (MAPK) signaling pathway. Results Ca-SGP could effectively inhibit the differentiation and maturation of osteoclasts induced by RANKL, reduce the activity of TRAP and its expression, and inhibit the formation of bone resorption lacuna. Ca-SGP could obviously decrease the activity of signal transduction key protein TRAP6 in molecular mechanism , And then inhibit the expression of key factor mRNAs of NF-κB and MAPKs signaling pathway to inhibit osteoclast differentiation and maturation. Conclusion Ca-SGP can inhibit osteoclast formation and differentiation induced by RANKL through NF-κB and MAPKs signaling pathways.