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<p>This study was to investigate the therapeutic effect of Panax notoginseng-Bletilla striata (PN-BS) in reflux esophagitis (RE) and its molecular mechanism. Using the ‘4.2&#xa0;mm pyloric clamp + 2/3 fundoplication’ method, a rat model of RE was developed. RE cell model was established by exposing HET-1&#xa0;A (esophageal epithelial cells) to bile salt. Esophageal mucosal injury was observed by HE staining, and epithelial barrier dysfunction was assessed using Toluidine blue staining. HET-1&#xa0;A cell viability was measured by CCK-8. Inflammatory factors in tissues and cells were detected by enzyme-linked immunosorbent assay. Claudin-4, Claudin-5, NLRP3, cleaved-caspase-1, p-p38 MAPK, and p38 MAPK protein levels were detected by Western blot. PN-BS attenuated esophageal mucosal injury and inflammation and improved esophageal barrier dysfunction in RE rats. Panax notoginseng saponins (PNS, the main active ingredient of PN) and Bletilla striata polysaccharides (BSP, the main active ingredient of BS) attenuated acid and bile salt-induced esophageal barrier dysfunction. PNS and BSP inhibited NLRP3 inflammasomes and p38 MAPK pathway activation. An inhibitor of NLRP3 inflammasomes (MCC950) or an inhibitor of the p38 MAPK pathway (SB203580) further enhanced the ameliorative effects of PNS and BSP. PN-BS reduces esophageal barrier dysfunction by inhibiting the activation of NLRP3 inflammasomes and p38 MAPK pathway, thereby improving RE.</p>

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Panax notoginseng-Bletilla striata ameliorates reflux esophagitis by modulating NLRP3 inflammasomes and p38 MAPK pathway

  • 期刊论文

  • 发表日期：

    2025年11月19日

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  • Xin Yang,
  • TingTing Wu,
  • HuiPing Zhu,
  • HengYue Ding,
  • Xuan Chen,
  • QianFei Xu,
  • HongWen Sun,
  • GuoQiang Liang

摘要

This study was to investigate the therapeutic effect of Panax notoginseng-Bletilla striata (PN-BS) in reflux esophagitis (RE) and its molecular mechanism. Using the ‘4.2 mm pyloric clamp + 2/3 fundoplication’ method, a rat model of RE was developed. RE cell model was established by exposing HET-1 A (esophageal epithelial cells) to bile salt. Esophageal mucosal injury was observed by HE staining, and epithelial barrier dysfunction was assessed using Toluidine blue staining. HET-1 A cell viability was measured by CCK-8. Inflammatory factors in tissues and cells were detected by enzyme-linked immunosorbent assay. Claudin-4, Claudin-5, NLRP3, cleaved-caspase-1, p-p38 MAPK, and p38 MAPK protein levels were detected by Western blot. PN-BS attenuated esophageal mucosal injury and inflammation and improved esophageal barrier dysfunction in RE rats. Panax notoginseng saponins (PNS, the main active ingredient of PN) and Bletilla striata polysaccharides (BSP, the main active ingredient of BS) attenuated acid and bile salt-induced esophageal barrier dysfunction. PNS and BSP inhibited NLRP3 inflammasomes and p38 MAPK pathway activation. An inhibitor of NLRP3 inflammasomes (MCC950) or an inhibitor of the p38 MAPK pathway (SB203580) further enhanced the ameliorative effects of PNS and BSP. PN-BS reduces esophageal barrier dysfunction by inhibiting the activation of NLRP3 inflammasomes and p38 MAPK pathway, thereby improving RE.