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

Author:

Jang Hye-Yeon1,Kim Jeong-Mi2,Kim Jong-Suk23,Kim Byeong-Soo4,Lee Young-Rae5,Bae Jun Sang6ORCID

Affiliation:

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

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

3. BK21FOUR 21st Century Medical Science Creative Human Resource Development Center, Jeonbuk National University, 567 Baekje-daero, Deokjin, Jeonju 54896, Republic of Korea

4. Department of Companion and Laboratory Animal Science, Kongju National University, Yesan 32439, Republic of Korea

5. Department of Oral Biochemistry, Institute of Biomaterials-Implant, School of Dentistry, Wonkwang University, 460, Iksan 54538, Republic of Korea

6. Department of Pathology, College of Korean Medicine, Wonkwang University, 460, Iksan 54538, Republic of Korea

Abstract

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-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.

Funder

Wonkwang University

Publisher

MDPI AG

Subject

Food Science,Nutrition and Dietetics

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Role and Regulation of Transcription Factors in Osteoclastogenesis;International Journal of Molecular Sciences;2023-11-10

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