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从 中分离得到的异佛手柑内酯对体外破骨细胞和成骨细胞的影响。

Effect of Ishophloroglucin A Isolated from on In Vitro Osteoclastogenesis and Osteoblastogenesis.

机构信息

Chuncheon Center, Korea Basic Science Institute (KBSI), Chuncheon 24341, Republic of Korea.

Department of Medical Biomaterials Engineering, College of Biomedical Sciences, Kangwon National University, Chuncheon 24341, Republic of Korea.

出版信息

Mar Drugs. 2023 Jun 26;21(7):377. doi: 10.3390/md21070377.

DOI:10.3390/md21070377
PMID:37504908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10381815/
Abstract

The balance between bone-resorbing osteoclasts and bone-forming osteoblasts is essential for the bone remodeling process. This study aimed to investigate the effect of Ishophloroglucin A (IPA) isolated from on the function of osteoclasts and osteoblasts in vitro. First, we demonstrated the effect of IPA on osteoclastogenesis in receptor activator of nuclear factor κB ligand (RANKL)-induced RAW 264.7 cells. IPA inhibited the tartrate-resistant acid phosphatase (TRAP) activity and osteoclast differentiation in RANKL-induced RAW 264.7 cells. Moreover, it inhibited the RANKL-induced osteoclast-related factors, such as TRAP, matrix metalloproteinase-9 (MMP-9), and calcitonin receptor (CTR), and transcription factors, such as nuclear factor of activated T cells 1 (NFATc1) and c-Fos. IPA significantly suppressed RANKL-activated extracellular signal-regulated kinase (ERK), and NF-κB in RAW 264.7 cells. Our data indicated that the ERK and NF-κB pathways were associated with the osteoclastogenesis inhibitory activity of IPA. Next, we demonstrated the effect of IPA on osteoblastogenesis in MG-63 cells. IPA significantly promoted alkaline phosphatase (ALP) activity in MG-63 cells, along with the osteoblast differentiation-related markers bone morphogenetic protein 2 (BMP2), type 1 collage (COL1), p-Smad1/5/8, and Runx2, by activating the MAPK signaling pathways. Taken together, the study indicated that IPA could be effective in treating bone diseases, such as osteoporosis.

摘要

破骨细胞和成骨细胞之间的平衡对于骨重塑过程至关重要。本研究旨在探讨从分离得到的异补骨脂查尔酮 A（IPA）对体外破骨细胞和成骨细胞功能的影响。首先，我们证明了 IPA 对核因子κB 受体激活剂配体（RANKL）诱导的 RAW 264.7 细胞中破骨细胞发生的影响。IPA 抑制 RANKL 诱导的 RAW 264.7 细胞中抗酒石酸酸性磷酸酶（TRAP）活性和破骨细胞分化。此外，它抑制了 RANKL 诱导的破骨细胞相关因子，如 TRAP、基质金属蛋白酶-9（MMP-9）和降钙素受体（CTR），以及转录因子，如活化 T 细胞核因子 1（NFATc1）和 c-Fos。IPA 显著抑制了 RANKL 激活的 RAW 264.7 细胞中的细胞外信号调节激酶（ERK）和核因子-κB（NF-κB）。我们的数据表明，ERK 和 NF-κB 途径与 IPA 抑制破骨细胞发生的活性有关。接下来，我们证明了 IPA 对 MG-63 细胞中成骨细胞发生的影响。IPA 显著促进了 MG-63 细胞中的碱性磷酸酶（ALP）活性，同时通过激活丝裂原活化蛋白激酶（MAPK）信号通路，促进了骨形态发生蛋白 2（BMP2）、I 型胶原（COL1）、p-Smad1/5/8 和 Runx2 等成骨细胞分化相关标志物的表达。总之，该研究表明 IPA 可有效治疗骨质疏松症等骨骼疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/db5374dfa159/marinedrugs-21-00377-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/73de56093487/marinedrugs-21-00377-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/db56cb789a4a/marinedrugs-21-00377-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/5ed1e5835138/marinedrugs-21-00377-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/d6804de17b07/marinedrugs-21-00377-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/a2c15d477da3/marinedrugs-21-00377-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/70cc5bd3e777/marinedrugs-21-00377-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/3baaa9590593/marinedrugs-21-00377-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/98260c20ca33/marinedrugs-21-00377-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/db5374dfa159/marinedrugs-21-00377-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/73de56093487/marinedrugs-21-00377-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/db56cb789a4a/marinedrugs-21-00377-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/5ed1e5835138/marinedrugs-21-00377-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/d6804de17b07/marinedrugs-21-00377-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/a2c15d477da3/marinedrugs-21-00377-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/70cc5bd3e777/marinedrugs-21-00377-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/3baaa9590593/marinedrugs-21-00377-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/98260c20ca33/marinedrugs-21-00377-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f7f/10381815/db5374dfa159/marinedrugs-21-00377-g009.jpg

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