@Article{biocell.2025.067011,
AUTHOR = {Ya-Yi Chen, Tzu-Ting Chen, Ya-Hsuan Chao, Wen-Ho Chuo, Chieh-Shan Wu, Ruo-Han Tseng, Chieh-Chen Huang},
TITLE = {Hibifolin Modulates the Activation of Mouse Bone Marrow-Derived Dendritic Cells and Attenuates Contact Dermatitis Induced by 2,4-Dinitro-1-Fluorobenzene},
JOURNAL = {BIOCELL},
VOLUME = {49},
YEAR = {2025},
NUMBER = {9},
PAGES = {1733--1748},
URL = {http://www.techscience.com/biocell/v49n9/63867},
ISSN = {1667-5746},
ABSTRACT = { <b>Objectives:</b> Professional antigen-presenting cells known as dendritic cells (DCs) assist as a connection between the innate and adaptive components of the immune response. DCs are attractive targets for immunomodulatory drugs because of their crucial function in triggering immunity. This study set out to examine, for the first time, how hibifolin affected mouse bone-marrow derived (BMDCs) dendritic cells, triggered by lipopolysaccharide (LPS) <i>in vitro</i>. Additionally, a mouse model of contact hypersensitivity (CHS) was used to assess its possible therapeutic effects <i>in vivo</i>. <b>Methods:</b> LPS was administered to BMDCs with or without hibifolin. Major Histocompatibility Complex (MHC) class II, cytokine production, and co-stimulatory molecule (CD80, CD86) expression levels were assessed. To evaluate the functional effects on T-cell activation, mixed lymphocyte responses using OVA specific T-cells were conducted. <i>In vivo</i>, immunoregulatory potential of hibifolin was examined using a CHS mouse model sensitized with 2,4-dinitrofluorobenzene (DNFB). <b>Results:</b> Hibifolin significantly reduced the expression of the proinflammatory cytokines TNF-α and IL-6, as well as the costimulatory molecules CD80, CD86, and MHC II induced by LPS, by about 40–50%. These effects were associated with reduced NF-κB and p38-MAPK pathway activity. JNK and ERK phosphorylation levels did not alter significantly. <i>In vitro</i>, BMDCs treated with hibifolin showed a 40%–45% down-regulated capacity to stimulate T-cell propagation and IFN-γ release. Oral hibifolin treatment <i>in vivo</i> modestly decreased DNFB-induced CHS responses by 30%–40%. <b>Conclusion:</b> Overall, our results offer new insights that by inhibiting NF-κB and p38-MAPK signaling, hibifolin decreases the expression of costimulatory molecules and cytokines, thereby limiting BMDC activation, suppressing T-cell responses, and exerting immunomodulatory effects in the CHS mouse model.},
DOI = {10.32604/biocell.2025.067011}
}