6-Hydroxyrubiadin Regulates TNF-α-Induced MUC5AC Gene Expression via Affecting NF-κB and MAPK Signaling Pathways in Human Airway Epithelial Cells
4 affiliations
- 1Department of Pharmacology and Department of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015 Seoul 01795 Republic of Korea
- 2Brain Korea 21 FOUR Project for Medical Science, Chungnam National University, Daejeon 35015 Seoul 01795 Republic of Korea
- 3Department of Pharmacognosy, College of Pharmacy, Chungnam National University, Daejeon 34134 Seoul 01795 Republic of Korea
- 4Smith Liberal Arts College and Department of Addiction Science, Graduate School, Sahmyook University Seoul 01795 Republic of Korea
Abstract
In this study, we aimed to investigate whether 6-hydroxyrubiadin (6-HR), a compound derived from the root of Rubia akane Nakai, exerts a regulatory effect on the gene expression of MUC5AC mucin under conditions mimicking pulmonary inflammation in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with 6-HR for 30 min, followed by stimulation with tumor necrosis factor (TNF)-α for 24 h. MUC5AC mRNA expression and glycoprotein production were measured using reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Further, we examined the effect of 6-HR on TNF-α-induced activation of the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways via immunoblot analysis. The results were as follows: (1) 6-HR significantly reduced both the production of MUC5AC glycoprotein and MUC5AC mRNA expression in NCI-H292 cells. (2) 6-HR inhibited TNF-α-induced NF-κB activation through a transforming growth factor-β-activated kinase 1 (TAK1)-dependent mechanism. (3) 6-HR also inhibited TAK1-dependent MAPK signaling pathways activated by TNF-α, resulting in the downregulation of MUC5AC mucin production in NCI-H292 cells. These findings suggest that 6-HR regulates the gene expression of MUC5AC mucin by directly acting on airway epithelial cells through modulation of the MAPK and NF-κB signaling pathways.
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BibTeX
@article{hossain20266hydroxyrubiadin,
title = {{6-Hydroxyrubiadin Regulates TNF-α-Induced MUC5AC Gene Expression via Affecting NF-κB and MAPK Signaling Pathways in Human Airway Epithelial Cells}},
author = {Rajib Hossain and MinKyun Na and Sainan Li and Hyun Jae Lee and Gang Min Hur and Choong Jae Lee},
journal = {Biomolecules \& Therapeutics},
year = {2026},
month = nov,
doi = {10.4062/biomolther.2026.187},
url = {https://doi.org/10.4062/biomolther.2026.187},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - 6-Hydroxyrubiadin Regulates TNF-α-Induced MUC5AC Gene Expression via Affecting NF-κB and MAPK Signaling Pathways in Human Airway Epithelial Cells
AU - Rajib Hossain
AU - MinKyun Na
AU - Sainan Li
AU - Hyun Jae Lee
AU - Gang Min Hur
AU - Choong Jae Lee
PY - 2026
DA - 2026/11/01
JO - Biomolecules & Therapeutics
DO - 10.4062/biomolther.2026.187
UR - https://doi.org/10.4062/biomolther.2026.187
AB - In this study, we aimed to investigate whether 6-hydroxyrubiadin (6-HR), a compound derived from the root of Rubia akane Nakai, exerts a regulatory effect on the gene expression of MUC5AC mucin under conditions mimicking pulmonary inflammation in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with 6-HR for 30 min, followed by stimulation with tumor necrosis factor (TNF)-α for 24 h. MUC5AC mRNA expression and glycoprotein production were measured using reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Further, we examined the effect of 6-HR on TNF-α-induced activation of the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways via immunoblot analysis. The results were as follows: (1) 6-HR significantly reduced both the production of MUC5AC glycoprotein and MUC5AC mRNA expression in NCI-H292 cells. (2) 6-HR inhibited TNF-α-induced NF-κB activation through a transforming growth factor-β-activated kinase 1 (TAK1)-dependent mechanism. (3) 6-HR also inhibited TAK1-dependent MAPK signaling pathways activated by TNF-α, resulting in the downregulation of MUC5AC mucin production in NCI-H292 cells. These findings suggest that 6-HR regulates the gene expression of MUC5AC mucin by directly acting on airway epithelial cells through modulation of the MAPK and NF-κB signaling pathways.
SN - 1976-9148
SN - 2005-4483
ER -