Anti‑osteoclastogenic effects of Coriandrum sativumL. via the NF‑κB and ERK‑mediated NFATc1 signaling pathways.

Abstract

Coriandrum sativumL. (CSL) is an aromatic plant that belongs to the Apiaceae family. The present study aimed to determine the effects of the ethanol extract of the aerial part of CSL on osteoclast formation invitro and invivo, and the underlying molecular mechanism of its anti‑osteoclastogenic effect. The levels of osteoclast formation and bone resorption were evaluated by tartrate‑resistant acid phosphatase staining and bone resorption pit assays. The expression levels of osteoclast‑related molecules were analyzed by reverse transcription‑quantitative PCR and western blotting. The ethanol extract of CSL suppressed osteoclast formation in a mouse co‑culture system. In osteoblasts, CSL exerted a minor effect on the mRNA ratio of receptor activator of nuclear factor‑κB (NF‑κB) ligand (RANKL) to osteoprotegerin, suggesting a direct effect of CSL on osteoclast precursors. Notably, CSL inhibited RANKL‑induced osteoclast differentiation and bone resorption activity in bone marrow‑derived macrophage cultures. Mechanistically, CSL abolished RANKL‑induced NF‑κB and extracellular signal‑regulated kinase (ERK) MAPK activation, which effectively impaired the induction of c‑Fos and nuclear factor of activated Tcells (NFATc1). Finally, the ethanol extract of CSL prevented osteoclast formation in a lipopolysaccharide‑induced calvarial bone loss model invivo. The findings of the present study suggested that CSL may suppress osteoclast differentiation and function by downregulating the NF‑κB and ERK/c‑Fos/NFATc1 signaling pathways. Thus, CSL could be explored as a potential candidate for the prevention and treatment of osteolytic diseases.