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<p>Rosmarinic acid (RA) is a naturally occurring polyphenol found in various plant species, with diverse therapeutic applications. The receptor activator of nuclear factor kappa-B ligand (RANKL) plays a crucial role in inflammation, contributing to the production of inflammatory cytokines through the activation of phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinases (MAPKs) signaling pathways in mast cells. In this study, we investigated the potential of RA to suppress RANKL-induced inflammatory response signaling pathways in the human mast cell line, HMC-1 cells. The results demonstrated that RA effectively inhibits the activation of PI3K/AKT and MAPKs, including extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase in activated HMC-1 cells. The suppression of these pathways by RA led to reduced caspase-1 and nuclear factor-κB activation. Furthermore, RA decreased the secretion and mRNA expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and thymic stromal lymphopoietin, without affecting cytotoxicity. Our findings suggest that RA exerts a regulatory effect on RANKL-induced inflammatory reactions, potentially indicating its therapeutic role in treating RANKL-mediated inflammatory diseases.</p>

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Rosmarinic Acid Alleviates Inflammation in Mast Cells Induced by RANKL by Inhibiting the PI3K/MAPK Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年2月9日

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  • Ho-Geun Kang,
  • Hee-Yun Kim,
  • Kyung-Min Jeong,
  • Yu-Jin Choi,
  • Hyun-Ja Jeong

摘要

Rosmarinic acid (RA) is a naturally occurring polyphenol found in various plant species, with diverse therapeutic applications. The receptor activator of nuclear factor kappa-B ligand (RANKL) plays a crucial role in inflammation, contributing to the production of inflammatory cytokines through the activation of phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT) and mitogen-activated protein kinases (MAPKs) signaling pathways in mast cells. In this study, we investigated the potential of RA to suppress RANKL-induced inflammatory response signaling pathways in the human mast cell line, HMC-1 cells. The results demonstrated that RA effectively inhibits the activation of PI3K/AKT and MAPKs, including extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase in activated HMC-1 cells. The suppression of these pathways by RA led to reduced caspase-1 and nuclear factor-κB activation. Furthermore, RA decreased the secretion and mRNA expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and thymic stromal lymphopoietin, without affecting cytotoxicity. Our findings suggest that RA exerts a regulatory effect on RANKL-induced inflammatory reactions, potentially indicating its therapeutic role in treating RANKL-mediated inflammatory diseases.