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作 者:王正宇[1] 朱云[1] 杨小中[1] 杨刚[1] 朱卫文[1] 马涛[1] 张健[1]
机构地区:[1]重庆医科大学附属第一医院骨科,重庆400016
出 处:《细胞与分子免疫学杂志》2015年第2期145-148,共4页Chinese Journal of Cellular and Molecular Immunology
基 金:国家自然科学基金(81071490)
摘 要:目的探讨瘦素对可溶性核因子κB配体的受体活化因子(sRANKL)诱导RAW264.7巨噬细胞向破骨细胞分化的影响及其机制。方法抗酒石酸酸性磷酸酶(TRAP)染色检测瘦素对sRANKL诱导RAW264.7向破骨细胞分化的形态学影响;实时荧光定量PCR检测TRAP及过氧化物酶体增殖物激活受体γ(PPARγ)的mRNA表达;Western blot法检测TRAP及PPARγ的蛋白表达。结果瘦素和sRANKL联合处理组与单独sRANKL组相比,TRAP染色破骨细胞数目明显减少;TRAP的mRNA和蛋白表达量明显降低;PPARγ的mRNA和蛋白表达量明显降低,且与瘦素浓度呈梯度相关。结论瘦素可能通过抑制PPARγ的表达来抑制RAW264.7细胞向破骨细胞分化。Objective To investigate the effects of leptin on the differentiation of RAW264.7 cells into osteoclasts induced by soluble receptor activator of nuclear factor-κB ligand (sRANKL) and its possible mechanism. Methods The effects of leptin on the differentiation from osteoclast precursor cells into osteoclasts were detected by tartrate-resistant acid phosphatase (TRAP) staining. The mRNA expressions of TRAP and peroxisome proliferator-activated receptor γ (PPARγ) in osteoclast precursor cells were measured by real-time quantitative PCR (qRT-PCR). The protein expressions of TRAP and PPARγ were detected by Western blotting. Results Compared with sRANKL treatment group, the differentiation from osteoclast precursor cells into osteoclasts was significantly inhibited in sRANKL combined with leptin treatment groups. Additionally, the mRNA and protein expressions of both TRAP and PPARγ significantly decreased in sRANKL combined with leptin treatment groups compared with the sRANKL treatment alone. Furthermore, the expression of PPARγ was reduced in a dose-dependent manner. Conclusion Leptin could inhibit the differentiation of RAW264. 7 cells into osteoclasts via inhibiting the expression of PPARγ.
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