Protocatechuic Acid Attenuates Osteoclastogenesis by Downregulating JNK/c‐Fos/NFATc1 Signaling and Prevents Inflammatory Bone Loss in Mice

• DOI: 10.1002/ptr.5565
• Publication Date: 2016-01-21T03:59:05Z
• Authors: Sun‐Hyang Park; Ju‐Young Kim; Yoon‐Hee Cheon; Jong Min Baek; Sung‐Jun Ahn; Kwon‐Ha Yoon; Myeung Su Lee; Jaemin Oh
• Keywords: Protocatechuic acid; Bone remodeling; RANK Ligand

Protocatechuic acid (PCA) plays a critical role in nutritional metabolism; it is major metabolite of anthocyanins, which are flavonoids with range health benefits. PCA has variety biological activities including anti‐oxidant, antiinflammatory, anti‐apoptosis, and anti‐microbial activities. However, the pharmacological effect PCA, especially on osteoclastogenesis, remains unknown. We examined receptor activator NF‐κB ligand (RANKL)‐induced osteoclast differentiation bone resorption. dose‐dependently inhibited RANKL‐induced mouse marrow macrophages (BMMs) suppressed bone‐resorbing activity mature osteoclasts. At molecular level, phosphorylation JNK among MAPKs only, without significantly affecting early signaling pathway. also RANKL‐stimulated expression c‐Fos nuclear factor activated T cells c1 (NFATc1) at mRNA protein levels, altering expression. Additionally, down‐regulated downstream osteoclastogenesis‐related genes β3‐integrin , DC‐STAMP OC‐STAMP Atp6v0d2 CTR CtsK . Mice treated efficiently recovered from lipopolysaccharide‐induced loss vivo Thus, inhibits function by suppressing signaling, stability, osteoclastic marker genes. These results suggest that could be useful treatment inflammatory disorders. Copyright © 2016 John Wiley & Sons, Ltd.