摘要
目的观察吡格列酮对培养的大鼠破骨细胞样细胞(OLC)活性的影响,探讨过氧化物酶体增殖剂激活受体(PPAR)γ2活化与破骨细胞之间的关系。方法用核因子κB受体活化因子配体(RANKL)及巨噬细胞集落刺激因子(M-CSF)诱导大鼠骨髓单个核细胞向OLC分化,同时加入不同浓度盐酸吡格列酮(终浓度0、1、5、10μmol/L)干预,用流式细胞仪(FCM)检测培养3、5及7dOLC整合素β3(CD61)表达量,比较不同浓度吡格列酮对OLC活性的影响。结果培养早期(3及5d)吡格列酮10μmol/L及5μmol/L干预组OLCCD61表达量及平均荧光强度明显下调(P<0.05,P<0.01),表明吡格列酮在OLC分化早期可抑制其骨吸收活性。结论吡格列酮激活PPARγ2转录活性可部分抑制大鼠骨髓破骨细胞早期的融合聚集活性,这对骨质疏松具有潜在的治疗价值。
Objective To study the effect of pioglitazone on the expression of integrin β3 of osteodast-like cells（OLC） of rats,and probe the relationship between altimted PPAR T2 and osteeclast. Methods In the first day of osteeclast-like cells formation from nonadherent （BMCs）obtained from rats induced by M-CSF and RANKL.Pioglitazone hydrochloride with different concentration（final concentration in 1 μmol/L、5 μmol/L and 10 μmol/L） were added. The expression on integrin β3 （CD61） of OLC were measured by flow cytometry in day 3.5 and 7 of cultural process. Results The expression and mean fluorescence intensity of CD61 were down regulated in groups of pioglitazone 5 μmol/L and 10 μmol/L （P〈0.05,P〈0.01）,which indicated that pioglitazone may suppress the activity of osteeclast in the nonage of differentiation. Conclusions Activation of PPAR T2 pathway by pioglitazone could partly inhibit function of OLC derived from rats BMCs and may have potential therapeutic value of osteoporosis.
出处
《中国药物与临床》
CAS
2006年第5期353-356,F0003,共5页
Chinese Remedies & Clinics
