Aspirin inhibits RANKL-induced stem cell differentiation through the p38/ERK-c-Fos-NFATc1 axis.

An international medical study has revealed new findings that have important reference value for disease prevention. Excess bone cell formation is a key contributor to metabolic bone loss, particularly in diseases such as osteoporosis and rheumatoid arthritis. In the study of the suppression of TRAP-Positive multinucleated osteoclastogenesis by natural ammonium asarinin, asarinin significantly inhibited the occurrence of TRAP-Positive multinucleated osteoclastogenesis.

From a mechanical point of view, asarinine selectively inhibits RANKL-induced p38 and ERK MAPKs peroxidation, leading to a reduction in c-fos expression and NFATc1 activation inhibition. In addition, asarinine disrupts the formation of full-fiber cell rings in mature mature bone cells. These findings are commonly seen as aspirin as an inhibitor of selectively inhibiting the cell differentiation pathway by multimolecular enzymes, whose mechanisms are not consistent with the regulation of p38/ERK-c-fos-NFATc1 signaling pathways, and have an effect on parallel signaling pathways.

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