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红曲菌素通过调节丝裂原活化蛋白激酶(MAPKs)信号通路,消除RAW264.7细胞中核因子κB受体活化因子配体(RANKL)介导的破骨细胞生成。

Monascin abrogates RANKL-mediated osteoclastogenesis in RAW264.7 cells via regulating MAPKs signaling pathways.

作者信息

Cheng Yin, Liu Haixia, Li Jing, Ma Yujie, Song Changheng, Wang Yuhan, Li Pei, Chen Yanjing, Zhang Zhiguo

机构信息

Institute of Basic Theory, China Academy of Chinese Medical Sciences, Beijing, China.

Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering, Chinese Academy of Medical Sciences; Beijing Key Laboratory of New Drug Development and Clinical Trial of Stem Cell Therapy (BZ0381), Beijing, China.

出版信息

Front Pharmacol. 2022 Jul 15;13:950122. doi: 10.3389/fphar.2022.950122. eCollection 2022.

DOI:10.3389/fphar.2022.950122
PMID:35910375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9337785/
Abstract

Osteoclasts (OCs) are multinucleated cells that play a major role in osteolytic diseases such as osteoporosis. Monascin (Ms) is one of the active substances in the traditional Chinese medicine red yeast rice. Studies have found that red yeast rice can maintain bone health. In this study, the anti-osteoclastogenesis effects of Ms on RANKL-induced RAW264.7 cells were assessed, and the underlying mechanism was investigated. Ms exhibited inhibitory effects on OC differentiation and formation in a dose-dependent manner and suppressed the bone-resorbing activity of mature OCs. Ms blocked OCs-typical genes (c-Fos, NFATc1, CSTK, MMP-9, TRAP, ITG-β3, OSCAR and DC-STAMP). Furthermore, Ms treatment considerably inhibited the activation of MAPKs, JNK and p38. Taken together, Ms suppresses RANKL-induced osteoclastogenesis of RAW264.7 cells by restraining MAPKs signaling pathways and is a potential therapeutic option as a novel OC inhibitor to mitigate bone erosion.

摘要

破骨细胞(OCs)是多核细胞,在骨质疏松症等溶骨性疾病中起主要作用。莫纳辛(Ms)是中药红曲米中的活性物质之一。研究发现,红曲米可以维持骨骼健康。在本研究中,评估了Ms对RANKL诱导的RAW264.7细胞的抗破骨细胞生成作用,并研究了其潜在机制。Ms对OC分化和形成呈剂量依赖性抑制作用,并抑制成熟OC的骨吸收活性。Ms阻断了OC典型基因(c-Fos、NFATc1、CSTK、MMP-9、TRAP、ITG-β3、OSCAR和DC-STAMP)。此外,Ms处理显著抑制了MAPKs、JNK和p38的激活。综上所述,Ms通过抑制MAPKs信号通路抑制RANKL诱导的RAW264.7细胞破骨细胞生成,作为一种新型OC抑制剂减轻骨侵蚀是一种潜在的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/9128d4d83d67/fphar-13-950122-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/9a132c8db530/fphar-13-950122-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/3f5b0c8b8748/fphar-13-950122-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/13e4bf13dc59/fphar-13-950122-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/c4b74d696795/fphar-13-950122-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/aa0919662e86/fphar-13-950122-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/9128d4d83d67/fphar-13-950122-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/9a132c8db530/fphar-13-950122-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/3f5b0c8b8748/fphar-13-950122-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/13e4bf13dc59/fphar-13-950122-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/c4b74d696795/fphar-13-950122-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/aa0919662e86/fphar-13-950122-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfb/9337785/9128d4d83d67/fphar-13-950122-g006.jpg

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