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通过调节破骨细胞和成骨细胞分化发挥的 Leaf 正己烷馏分的抗骨质疏松作用。

Anti-Osteoporosis Effect of Leaf Hexane Fraction through Regulating Osteoclast and Osteoblast Differentiation.

机构信息

Division of Biochemistry, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand.

Unit of Excellence in Research to Develop Lanna Herbs against Osteoporosis, University of Phayao, Phayao 56000, Thailand.

出版信息

Molecules. 2022 Jan 26;27(3):824. doi: 10.3390/molecules27030824.

DOI:10.3390/molecules27030824
PMID:35164085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8840259/
Abstract

Osteoporosis is the result of an imbalance in the bone-remodeling process via an increase in osteoclastic activity and a decrease in osteoblastic activity. Our previous studies have shown that seed meal has anti-osteoclastogenic activity. However, the role of perilla leaf hexane fraction (PLH) in osteoporosis has not yet been investigated and reported. In this study, we aimed to investigate the effects of PLH in osteoclast differentiation and osteogenic potential using cell-based experiments in vitro. From HPLC analysis, we found that PLH contained high luteolin and baicalein. PLH was shown to inhibit RANKL-induced ROS production and tartrate-resistant acid phosphatase (TRAP)-positive multi-nucleated osteoclasts. Moreover, PLH significantly downregulated the RANKL-induced MAPK and NF-κB signaling pathways, leading to the attenuation of NFATc1 and MMP-9 expression. In contrast, PLH enhanced osteoblast function by regulating alkaline phosphatase (ALP) and restoring TNF-α-suppressed osteoblast proliferation and osteogenic potential. Thus, luteolin and baicalein-rich PLH inhibits osteoclast differentiation but promotes the function of osteoblasts. Collectively, our data provide new evidence that suggests that PLH may be a valuable anti-osteoporosis agent.

摘要

骨质疏松症是由于破骨细胞活性增加和成骨细胞活性降低导致骨重塑过程失衡的结果。我们之前的研究表明,芝麻粕具有抗破骨细胞生成活性。然而,紫苏叶己烷部分(PLH)在骨质疏松症中的作用尚未得到研究和报道。在这项研究中,我们旨在通过体外细胞实验研究 PLH 对破骨细胞分化和成骨潜能的影响。通过 HPLC 分析,我们发现 PLH 含有丰富的木犀草素和黄芩素。PLH 被证明可以抑制 RANKL 诱导的 ROS 产生和抗酒石酸酸性磷酸酶(TRAP)阳性多核破骨细胞。此外,PLH 显著下调了 RANKL 诱导的 MAPK 和 NF-κB 信号通路,从而减弱了 NFATc1 和 MMP-9 的表达。相比之下,PLH 通过调节碱性磷酸酶(ALP)增强成骨细胞功能,并恢复 TNF-α抑制的成骨细胞增殖和成骨潜能。因此,富含木犀草素和黄芩素的 PLH 抑制破骨细胞分化,但促进成骨细胞的功能。综上所述,我们的数据提供了新的证据,表明 PLH 可能是一种有价值的抗骨质疏松药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/02d78745fa7e/molecules-27-00824-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/a0a7102f4e11/molecules-27-00824-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/0a88f7f4a22f/molecules-27-00824-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/300a7d91a0f5/molecules-27-00824-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/5510b06208e7/molecules-27-00824-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/2c75bcbee6cf/molecules-27-00824-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/02d78745fa7e/molecules-27-00824-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/a0a7102f4e11/molecules-27-00824-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/cc2718d96a67/molecules-27-00824-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/0a88f7f4a22f/molecules-27-00824-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/d14130f565ca/molecules-27-00824-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/300a7d91a0f5/molecules-27-00824-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/5510b06208e7/molecules-27-00824-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/2c75bcbee6cf/molecules-27-00824-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c145/8840259/02d78745fa7e/molecules-27-00824-g008.jpg

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