Scholarlink

<p>Pharyngeal inflammation is a common upper respiratory tract disease characterized by increased inflammatory responses and mucin accumulation. Gentiopicroside (GPS), a natural compound with anti-inflammatory activity, has not been previously studied for its inhibitory effects on pharyngeal inflammation and its underlying mechanisms. This study aimed to investigate whether GPS inhibits pharyngeal inflammation in rats induced by Staphylococcus aureus (<i>S. aureus</i>) components and to elucidate the underlying mechanisms. In vivo, pharyngeal inflammation was induced in rats using <i>S. aureus</i> components, and GPS was administered to assess its effects on pharyngeal histopathological damage, mucosa injury, immune cell balance, secretory immunoglobulin A (SIgA) levels, cytokine production, and the expressions of E-cadherin, mucin5AC (MUC5AC), and cyclooxygenase-2 (COX-2). In vitro, human lung mucoepidermoid carcinoma cells (NCI-H292) were stimulated with lipoteichoic acid (LTA) to mimic <i>S. aureus</i> component-induced inflammatory stimulation. The effects of GPS on LTA-induced cytokine IL-1β and IL-6, COX-2, prostaglandin E2 (PGE2), MUC5AC, and E-cadherin expressions were evaluated. SiRNA against COX-2 was transfected, and a limited in vitro biochemical observation of GPS with recombinant MUC5AC was performed. GPS alleviated rat pharyngeal inflammation by improving pharyngeal histopathology, reducing mucosa injury, balancing immune cells, enhancing SIgA, and downregulating cytokines. It also inhibited the reduction of E-cadherin and the upregulation of MUC5AC and COX-2 in the rat pharynx and trachea. In NCI-H292 cells, GPS blocked LTA-induced increases in IL-1β, IL-6, COX-2, PGE2, and MUC5AC, as well as LTA-reduced E-cadherin. Transfection with siRNA against COX-2 further blocked LTA-induced MUC5AC expression, and GPS lost its inhibitory effect on MUC5AC expression, indicating that COX-2 was involved. Additionally, GPS showed a limited in vitro biochemical observation on recombinant MUC5AC, with uncertain physiological relevance. GPS alleviates S. aureus component-induced pharyngeal inflammatory damage in rats, with concomitant reductions in COX-2/PGE2 signaling activity and MUC5AC overexpression. These correlative observations provide a preliminary experimental basis for the potential application of GPS in ameliorating bacterial component-associated pharyngeal inflammation.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Gentiopicroside attenuates pharyngeal inflammation in rats by inhibiting MUC5AC production associated with the COX-2/PGE2 signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月10日

查看全文
  • Wei Zhao,
  • Jiabin Guo,
  • Ying Yang,
  • Na Sun,
  • Xingdi Xu,
  • Jinjun Zhang,
  • Xiuping Liu,
  • Han Zhang,
  • Lin Miao

摘要

Pharyngeal inflammation is a common upper respiratory tract disease characterized by increased inflammatory responses and mucin accumulation. Gentiopicroside (GPS), a natural compound with anti-inflammatory activity, has not been previously studied for its inhibitory effects on pharyngeal inflammation and its underlying mechanisms. This study aimed to investigate whether GPS inhibits pharyngeal inflammation in rats induced by Staphylococcus aureus (S. aureus) components and to elucidate the underlying mechanisms. In vivo, pharyngeal inflammation was induced in rats using S. aureus components, and GPS was administered to assess its effects on pharyngeal histopathological damage, mucosa injury, immune cell balance, secretory immunoglobulin A (SIgA) levels, cytokine production, and the expressions of E-cadherin, mucin5AC (MUC5AC), and cyclooxygenase-2 (COX-2). In vitro, human lung mucoepidermoid carcinoma cells (NCI-H292) were stimulated with lipoteichoic acid (LTA) to mimic S. aureus component-induced inflammatory stimulation. The effects of GPS on LTA-induced cytokine IL-1β and IL-6, COX-2, prostaglandin E2 (PGE2), MUC5AC, and E-cadherin expressions were evaluated. SiRNA against COX-2 was transfected, and a limited in vitro biochemical observation of GPS with recombinant MUC5AC was performed. GPS alleviated rat pharyngeal inflammation by improving pharyngeal histopathology, reducing mucosa injury, balancing immune cells, enhancing SIgA, and downregulating cytokines. It also inhibited the reduction of E-cadherin and the upregulation of MUC5AC and COX-2 in the rat pharynx and trachea. In NCI-H292 cells, GPS blocked LTA-induced increases in IL-1β, IL-6, COX-2, PGE2, and MUC5AC, as well as LTA-reduced E-cadherin. Transfection with siRNA against COX-2 further blocked LTA-induced MUC5AC expression, and GPS lost its inhibitory effect on MUC5AC expression, indicating that COX-2 was involved. Additionally, GPS showed a limited in vitro biochemical observation on recombinant MUC5AC, with uncertain physiological relevance. GPS alleviates S. aureus component-induced pharyngeal inflammatory damage in rats, with concomitant reductions in COX-2/PGE2 signaling activity and MUC5AC overexpression. These correlative observations provide a preliminary experimental basis for the potential application of GPS in ameliorating bacterial component-associated pharyngeal inflammation.