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提取物通过抑制 JNK/NF-κB/PLCγ2 信号通路来抑制 RANKL 诱导的破骨细胞生成。

Extract Attenuates RANKL-Induced Osteoclastogenesis by Inhibiting the JNK/NF-κB/PLCγ2 Signaling Pathway.

机构信息

Infectious Diseases Therapeutic Research Center, Korea Research Institute of Chemical Technology (KRICT), Daejeon 34114, Republic of Korea.

Department of Biochemistry, Jeonbuk National University Medical School, 20 Geonji-ro, Deokjin, Jeonju 54907, Republic of Korea.

出版信息

Nutrients. 2023 Jul 19;15(14):3193. doi: 10.3390/nu15143193.

DOI:10.3390/nu15143193
PMID:37513611
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10383183/
Abstract

(PB)-derived bioactive substances have been used as food and medicine in many Asian countries because of their antioxidant, antidiabetic, anti-cancer, and hepatoprotective properties. However, the effect of PB extracts (PBE) on osteoclast differentiation is unclear. In this study, we investigated the effect of PBE on RANKL-induced osteoclastogenesis in mouse bone marrow-derived macrophages (BMMs). To investigate the cytotoxicity of PBE, the viability of BMMs was confirmed via MTT assay. Tartrate-resistant acid phosphatase (TRAP) staining and pit assays were performed to confirm the inhibitory effect of PBE on osteoclast differentiation and bone resorption. The expression levels of osteoclast differentiation-related genes and proteins were evaluated using quantitative real-time PCR and Western blotting. PBE attenuated osteoclastogenesis in BMMs in TRAP and pit assays without cytotoxicity. The expression levels of osteoclast marker genes and proteins induced by RANKL were decreased after PBE treatment. PBE suppressed osteoclastogenesis by inhibiting the RANKL-induced activated JNK/NF-κB/PLCγ2 signaling pathway and the expression of NFATc1 and c-Fos. Collectively, these results suggest that PBE could be a potential therapeutic strategy or functional product for osteoclast-related bone disease.

摘要

(PB)来源的生物活性物质因其抗氧化、抗糖尿病、抗癌和保肝特性,已在许多亚洲国家被用作食品和药物。然而,PB 提取物(PBE)对破骨细胞分化的影响尚不清楚。在这项研究中,我们研究了 PBE 对 RANKL 诱导的小鼠骨髓来源巨噬细胞(BMM)中破骨细胞分化的影响。为了研究 PBE 的细胞毒性,通过 MTT 测定法确认了 BMM 的活力。通过抗酒石酸酸性磷酸酶(TRAP)染色和陷窝试验证实了 PBE 对破骨细胞分化和骨吸收的抑制作用。通过定量实时 PCR 和 Western blot 评估破骨细胞分化相关基因和蛋白的表达水平。PBE 在无细胞毒性的情况下,在 TRAP 和陷窝试验中减弱了 BMM 中的破骨细胞生成。PBE 处理后,RANKL 诱导的破骨细胞标记基因和蛋白的表达水平降低。PBE 通过抑制 RANKL 诱导的 JNK/NF-κB/PLCγ2 信号通路和 NFATc1 和 c-Fos 的表达来抑制破骨细胞生成。总之,这些结果表明,PBE 可能是一种治疗与破骨细胞相关的骨疾病的潜在治疗策略或功能性产品。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/2491b237d45e/nutrients-15-03193-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/594b5031ef92/nutrients-15-03193-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/c0964618a048/nutrients-15-03193-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/c0f8a267b622/nutrients-15-03193-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/502f00b480bf/nutrients-15-03193-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/0c1af4de5bc4/nutrients-15-03193-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/dc3ac58645aa/nutrients-15-03193-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/2491b237d45e/nutrients-15-03193-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/594b5031ef92/nutrients-15-03193-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/c0964618a048/nutrients-15-03193-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/c0f8a267b622/nutrients-15-03193-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/502f00b480bf/nutrients-15-03193-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/0c1af4de5bc4/nutrients-15-03193-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/dc3ac58645aa/nutrients-15-03193-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0352/10383183/2491b237d45e/nutrients-15-03193-g007.jpg

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