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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。
Objective To investigate the relationship between the expression of leucine zipperin (GILZ) and icariin (ICR) and dexamethasone (DEX) in osteoblast MC3T3-E1, Related gene expression effects. Methods The mature and differentiated MC3T3-E1 cells were divided into 3 groups: DEX group, ICR group and ICR + DEX group. Real-time RT-PCR was used to detect GILZ, osteoprotegerin (OPG) Osteoblast differentiation factor (RANKL), osteocalcin (OC) and alkaline phosphatase (ALP) mRNA expression. Results DEX increased the expression of GILZ, RANKL and ALP, decreased the expression of OPG and OC, and increased the ratio of RANKL / OPG expression. ICR can inhibit the expression of GILZ, RANKL and ALP, enhance the expression of OPG and OC, and decrease the ratio of RANKL / OPG. And ICR can inhibit DEX-induced GILZ, RANKL and ALP expression increased reverse DEX-induced inhibition of OPG, OC expression. While significantly reducing the RANKL / OPG expression ratio. Conclusion ICR can inhibit the activation of osteoclasts by inhibiting the mRNA expression of GILZ, reducing the expression of RANKL / OPG. ICR enhances osteoblast proliferation by inhibiting ALP expression and increasing OC expression.