Protaetia brevitarsis Extract Attenuates RANKL-Induced Osteoclastogenesis by Inhibiting the JNK/NF-?B/PLC?2 Signaling Pathway

被引:3
作者
Jang, Hye-Yeon [1 ]
Kim, Jeong-Mi [2 ]
Kim, Jong-Suk [2 ,3 ]
Kim, Byeong-Soo [4 ]
Lee, Young-Rae [5 ]
Bae, Jun Sang [6 ]
机构
[1] Korea Res Inst Chem Technol KRICT, Infect Dis Therapeut Res Ctr, Daejeon 34114, South Korea
[2] Jeonbuk Natl Univ, Med Sch, Dept Biochem, 20 Geonji Ro, Jeonju 54907, South Korea
[3] Jeonbuk Natl Univ, BK21FOUR Century Med Sci Creat Human Resource Dev, 567 Baekje Daero, Jeonju 54896, South Korea
[4] Kongju Natl Univ, Dept Compan & Lab Anim Sci, Yesan 32439, South Korea
[5] Wonkwang Univ, Inst Biomat Implant, Sch Dent, Dept Oral Biochem, 460, Iksan 54538, South Korea
[6] Wonkwang Univ, Coll Korean Med, Dept Pathol, 460, Iksan 54538, South Korea
关键词
Protaetia brevitarsis; edible insect; osteoclast differentiation; JNK; NF-& kappa; B; PLC & gamma; 2; NF-KAPPA-B; RECEPTOR ACTIVATOR; NUCLEAR-FACTOR; FATTY-ACIDS; BONE-RESORPTION; UP-REGULATION; C-FOS; DIFFERENTIATION; EXPRESSION; LIGAND;
D O I
10.3390/nu15143193
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Protaetia brevitarsis (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-?B/PLC?2 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.
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页数:16
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