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Emodin Inhibited MUC5AC Mucin Gene Expression via Affecting EGFR-MAPK-Sp1 Signaling Pathway in Human Airway Epithelial Cells

  • Rajib Hossain (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Hyun Jae Lee (Smith Liberal Arts College and Department of Addiction Science, Graduate School, Sahmyook University) ;
  • Chang-Heon Baek (Department of Orthopaedic Surgery and Institute of Health Sciences, Gyeongsang National University College of Medicine and Gyeongsang National University Hospital) ;
  • Sun-Chul Hwang (Department of Orthopaedic Surgery and Institute of Health Sciences, Gyeongsang National University College of Medicine and Gyeongsang National University Hospital) ;
  • Choong Jae Lee (Department of Pharmacology, College of Medicine, Chungnam National University)
  • Received : 2024.09.04
  • Accepted : 2024.10.02
  • Published : 2024.11.01

Abstract

The aim of this study was to evaluate emodin, a natural trihydroxyanthraquinone compound found in the roots and barks of several plants including rhubarb and buckthorn, might attenuate epidermal growth factor (EGF)-induced airway MUC5AC mucin gene expression. The human pulmonary mucoepidermoid NCI-H292 cells were pretreated with for 30 min and then stimulated with EGF for the following 24 h. The effect of emodin on EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was examined. As a result, emodin blocked the expression of MUC5AC mucin mRNA and production of mucous glycoprotein via suppressing the phosphorylation of EGF receptor (EGFR), phosphorylation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) 1 and 2 (MEK1/2), phosphorylation of p38 MAPK, phosphorylation of ERK 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These findings imply that emodin has a potential to mitigate EGF-stimulated mucin gene expression by inhibiting the EGFR-MAPK-Sp1 signaling pathway, in NCI-H292 cells.

Keywords

Acknowledgement

This work was supported by BK21 FOUR Program by Chungnam National University Research Grant, 2024.

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