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咖啡酸衍生物 MPMCA 抑制破骨细胞生成并促进破骨细胞凋亡:在治疗骨质疏松症中的意义。

Caffeic acid derivative MPMCA suppresses osteoclastogenesis and facilitates osteoclast apoptosis: implications for the treatment of bone loss disorders.

机构信息

Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.

School of Chinese Medicine, China Medical University, Taichung, Taiwan.

出版信息

Aging (Albany NY). 2024 Aug 26;16(16):11926-11938. doi: 10.18632/aging.206067.

DOI:10.18632/aging.206067
PMID:39189924
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11386915/
Abstract

Osteoclast activity plays a crucial role in the pathological mechanisms of osteoporosis and bone remodeling. The treatment of these disorders involves the use of pharmacological medicines that work by inhibiting the activity of osteoclasts. Nevertheless, the prevalent and infrequent negative consequences of current antiresorptive and bone anabolic treatments pose significant drawbacks, hence restricting their prolonged administration in patients, particularly those who are elderly and/or suffer from many medical conditions. We are currently in the process of creating a new molecule called N-(4-methoxyphen) methyl caffeamide (MPMCA), which is a derivative of caffeic acid. This compound has shown potential in preventing the production of osteoclasts and causing existing osteoclasts to undergo cell apoptosis. Our investigation discovered that MPMCA hinders osteoclast function via suppressing the MAPK pathways. The expectation is that the findings of this study will stimulate the advancement of a novel approach to treating anti-resorption.

摘要

破骨细胞的活性在骨质疏松症和骨重塑的病理机制中起着关键作用。这些疾病的治疗涉及使用药理学药物,通过抑制破骨细胞的活性来发挥作用。然而,目前抗吸收和骨合成治疗的普遍和不频繁的负面后果带来了重大的缺点,因此限制了它们在患者中的长期使用,特别是那些年老和/或患有多种疾病的患者。我们目前正在开发一种名为 N-(4-甲氧基苯)甲基咖啡酰胺(MPMCA)的新分子,它是咖啡酸的衍生物。该化合物已显示出预防破骨细胞生成和诱导现有破骨细胞细胞凋亡的潜力。我们的研究发现,MPMCA 通过抑制 MAPK 通路来抑制破骨细胞的功能。我们希望本研究的结果将激发一种治疗抗吸收的新方法的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/4490c36aa8db/aging-16-206067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/a53bf36e386e/aging-16-206067-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/1b93ccac8243/aging-16-206067-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/b1cb572f49ed/aging-16-206067-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/95f8f5bb4ff1/aging-16-206067-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/19e0f61e626b/aging-16-206067-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/af3ebee3b636/aging-16-206067-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/0f7c591de6a0/aging-16-206067-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/4490c36aa8db/aging-16-206067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/a53bf36e386e/aging-16-206067-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/1b93ccac8243/aging-16-206067-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/b1cb572f49ed/aging-16-206067-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/95f8f5bb4ff1/aging-16-206067-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/19e0f61e626b/aging-16-206067-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/af3ebee3b636/aging-16-206067-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/0f7c591de6a0/aging-16-206067-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c41d/11386915/4490c36aa8db/aging-16-206067-g008.jpg

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