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夏枯草通过激活 Smad 通路保护糖皮质激素诱导的骨髓间充质干细胞成骨抑制作用。

Prunella vulgaris L protects glucocorticoids-induced osteogenesis inhibition in bone marrow mesenchymal stem cells through activating the Smad pathway.

机构信息

Department of Orthopaedic Surgery, Xijing Hospital, The Fourth Military Medical University, Xian, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 May;24(10):5691-5696. doi: 10.26355/eurrev_202005_21360.

DOI:10.26355/eurrev_202005_21360
PMID:32495904
Abstract

OBJECTIVE

To elucidate the role of Prunella vulgaris L (PVL) in protecting glucocorticoids (GC)-induced osteogenesis inhibition, thereafter, protecting the deterioration of osteoporosis (OP).

MATERIALS AND METHODS

Cell Counting Kit-8 (CCK-8) assay was conducted to assess the influence of PVL treatment on MSCs viability. Osteogenesis in MSCs was induced by Dexamethasone (DEX) stimulation. Regulatory effects of PVL on osteogenesis-related gene expressions, ALP activity, and mineralization ability in DEX-induced MSCs were determined. At last, protein levels of p-Smad1/5/9 and total-Smad1/5/9 influenced by DEX and PVL were measured by Western blot.

RESULTS

PVL treatment did not pose a time- or dose-dependent influence on MSCs viability. DEX induction in MSCs downregulated ALP, RUNX2, Bglap, and Osterix. ALP activity and mineralization in DEX-induced MSCs were suppressed. Downregulated osteogenesis-related genes decreased ALP activity and mineralization in MSCs undergoing DEX stimulation were partially reversed by PVL treatment. Moreover, the downregulated p-Smad1/5/9 level in DEX-induced MSCs was elevated by PVL treatment, while total-Smad1/5/9 was not affected.

CONCLUSIONS

PVL alleviated GC-induced suppression in MSCs osteogenesis by activating the Smad pathway, thereafter, protecting the deterioration of OP.

摘要

目的

阐明夏枯草(PVL)在保护糖皮质激素(GC)诱导的成骨抑制、进而保护骨质疏松(OP)恶化中的作用。

材料与方法

通过细胞计数试剂盒-8(CCK-8)测定法评估 PVL 处理对间充质干细胞(MSCs)活力的影响。用地塞米松(DEX)刺激诱导 MSCs 成骨。测定 PVL 对 DEX 诱导的 MSCs 中成骨相关基因表达、碱性磷酸酶(ALP)活性和矿化能力的调节作用。最后,通过 Western blot 测定 DEX 和 PVL 影响的 p-Smad1/5/9 和总-Smad1/5/9 蛋白水平。

结果

PVL 处理对 MSCs 活力没有时间或剂量依赖性影响。DEX 诱导 MSCs 下调 ALP、RUNX2、Bglap 和 Osterix。DEX 诱导的 MSCs 中 ALP 活性和矿化受到抑制。下调的成骨相关基因使 DEX 刺激的 MSCs 中的 ALP 活性和矿化减少,PVL 处理部分逆转了这种情况。此外,DEX 诱导的 MSCs 中下调的 p-Smad1/5/9 水平被 PVL 处理上调,而总-Smad1/5/9 不受影响。

结论

PVL 通过激活 Smad 通路缓解 GC 诱导的 MSCs 成骨抑制,进而保护 OP 的恶化。

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