| 引用本文: | 林忠,孙渊,金慧,洪盾,朱敏,杨建苗,林建群,丁亭亭.淫羊藿苷抑制亮氨酸拉链蛋白表达调节糖皮质激素诱导的MC3T3-E1成骨基因的表达失衡[J].中国现代应用药学,2014,31(8):926-933. |
| LIN Zhong,SUN Yuan,JIN Hui,HONG Dun,ZHU Min,YANG Jianmiao,LIN Jianqun,DING Tingting.Icraiin Regulating Expression Imbalance of Glucocorticoid-induced Osteogenesis Genes by Inhibiting GILZ Expression in MC3T3-E1[J].Chin J Mod Appl Pharm(中国现代应用药学),2014,31(8):926-933. |
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| 摘要: |
| 目的 考察成骨细胞MC3T3-E1中亮氨酸拉链蛋白(GILZ)的表达与淫羊藿苷(icraiin，ICR)和糖皮质激素地塞米松(dexamethasone，DEX)之间的关系以及对部分成骨相关基因的表达影响。方法 将诱导成熟分化的MC3T3-E1细胞分为3组，分别为DEX组、ICR组以及ICR+DEX组，通过Real-Time RT-PCR来检测不同组中GILZ、骨保护素(OPG)、破骨细胞分化因子(RANKL)、骨钙素(OC)和碱性磷酸酶(ALP)mRNA表达。结果 DEX能够提升GILZ、RANKL和ALP的表达，降低OPG、OC的表达，提高RANKL/OPG表达比率。ICR能够抑制GILZ、RANKL和ALP的表达，提升OPG、OC的表达，降低RANKL/OPG表达比率。并且ICR能够抑制DEX诱导的GILZ、RANKL和ALP表达升高，逆转DEX诱导的OPG、OC的表达抑制。同时显著降低了RANKL/OPG表达比率。结论 ICR通过抑制GILZ的mRNA表达，降低RANKL/OPG的表达比率，抑制破骨细胞成熟激活。ICR通过抑制ALP表达和提高OC表达提高成骨细胞的增殖能力。 |
| 关键词: 淫羊藿苷 亮氨酸拉链蛋白 糖皮质激素 MC3T3-E1 |
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| 基金项目:恩泽科研基金(12EZD34)；台州医院青蓝人才培养工程 |
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| Icraiin Regulating Expression Imbalance of Glucocorticoid-induced Osteogenesis Genes by Inhibiting GILZ Expression in MC3T3-E1 |
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LIN Zhong, SUN Yuan, JIN Hui, HONG Dun, ZHU Min, YANG Jianmiao, LIN Jianqun, DING Tingting
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Clinical Pharmacy Experimental Center of Taizhou Hospital in Zhejiang Province, Taizhou 317000, China
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| Abstract: |
| OBJECTIVE To investigate the icraiin regulating expression imbalance of glucocorticoid-induced osteogenesis genes by inhibiting GILZ expression in MC3T3-E1. METHODS Mature induced differentiation of MC3T3-E1 were divided into 3 groups, respectively dexamethasone(DEX) group, icraiin(ICR) group and ICR+DEX group. The mRNA expression lever of GILZ, osteoprotegerin(OPG), osteoclast differentiation factor(RANKL), osteocalcin (OC) and alkaline phosphatase (ALP) from different groups were detected by Real-Time RT-PCR. RESULT On the one hand, increase of GILZ by DEX improved the expression lever of RANKL, ALP and the ratio of RANKL/OPG in a dose-dependent manner in MC3T3-E1, but inhibited OPG and OC. On the other hand, inhibition of GILZ by ICR increased expression lever of OPG and OC, but inhibited RANKL, ALP and the ratio of RANKL/OPG also in a dose-dependent manner. Further more, enhancing of GILZ, RANKL, ALP and the ratio of RANKL/OPG induced by DEX could be inhibited in the presence of ICR, but the expression lever of OPG and OC were increased. CONCLUSION Inhibition of GILZ by ICR reduced the ratio of RANKL/OPG, suggesting a physiological role in inhibiting osteoclast maturation. Inhibition of ALP and increase of OC by ICR may improve proliferation of osteoblasts. |
| Key words: icraiin GILZ glucocorticoid MC3T3-E1 |
