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山奈酚通过JNK和p38-MAPK信号通路改善地塞米松对MC3T3-E1细胞成骨作用的抑制活性。

Kaempferol Ameliorates the Inhibitory Activity of Dexamethasone in the Osteogenesis of MC3T3-E1 Cells by JNK and p38-MAPK Pathways.

作者信息

Xie Baocheng, Zeng Zhanwei, Liao Shiyi, Zhou Chenhui, Wu Longhuo, Xu Daohua

机构信息

Guangdong Key Laboratory for Research and Development of Natural Drugs, The Public Service Platform of South China Sea for R&D Marine Biomedicine Resources, Marine Biomedical Research Institute, Guangdong Medical University, Zhanjiang, China.

Department of Pharmacy, Affiliated Dongguan Hospital, Southern Medical University, Dongguan, China.

出版信息

Front Pharmacol. 2021 Oct 5;12:739326. doi: 10.3389/fphar.2021.739326. eCollection 2021.

DOI:10.3389/fphar.2021.739326
PMID:34675808
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8524096/
Abstract

Kaempferol has been reported to exhibit beneficial effect on the osteogenic differentiation in mesenchymal stem cells (MSC) and osteoblasts. In our previous study, dexamethasone (DEX) demonstrated inhibitory effect on MC3T3-E1 cells differentiation. In this study, we mainly explored the protective effect of kaempferol on the inhibitory activity of DEX in the osteogenesis of MC3T3-E1 cells. We found that kaempferol ameliorated the proliferation inhibition, cell cycle arrest, and cell apoptosis and increased the activity of alkaline phosphatase (ALP) and the mineralization in DEX-treated MC3T3-E1 cells. Kaempferol also significantly enhanced the expression of osterix (Osx) and runt-related transcription factor 2 (Runx2) in MC3T3-E1 cells treated with DEX. In addition, kaempferol attenuated DEX-induced reduction of cyclin D1 and Bcl-2 expression and elevation of p53 and Bax expression. Kaempferol also activated JNK and p38-MAPK pathways in DEX-treated MC3T3-E1 cells. Furthermore, kaempferol improved bone mineralization in DEX-induced bone damage in a zebrafish larvae model. These data suggested that kaempferol ameliorated the inhibitory activity of DEX in the osteogenesis of MC3T3-E1 cells by activating JNK and p38-MAPK signaling pathways. Kaempferol exhibited great potentials in developing new drugs for treating glucocorticoid-induced osteoporosis.

摘要

据报道，山奈酚对间充质干细胞（MSC）和成骨细胞的成骨分化具有有益作用。在我们之前的研究中，地塞米松（DEX）对MC3T3-E1细胞分化表现出抑制作用。在本研究中，我们主要探讨了山奈酚对DEX抑制MC3T3-E1细胞成骨活性的保护作用。我们发现，山奈酚改善了DEX处理的MC3T3-E1细胞的增殖抑制、细胞周期阻滞和细胞凋亡，并增加了碱性磷酸酶（ALP）活性和矿化作用。山奈酚还显著增强了DEX处理的MC3T3-E1细胞中osterix（Osx）和 runt相关转录因子2（Runx2）的表达。此外，山奈酚减弱了DEX诱导的细胞周期蛋白D1和Bcl-2表达的降低以及p53和Bax表达的升高。山奈酚还激活了DEX处理的MC3T3-E1细胞中的JNK和p38-MAPK信号通路。此外，山奈酚改善了斑马鱼幼虫模型中DEX诱导的骨损伤中的骨矿化。这些数据表明，山奈酚通过激活JNK和p38-MAPK信号通路改善了DEX对MC3T3-E1细胞成骨的抑制活性。山奈酚在开发治疗糖皮质激素诱导的骨质疏松症的新药方面具有巨大潜力。

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