Shayan Chen , Zhihuang Wu , Wendie Yu , Di Zou , Jiongtang Lu
{"title":"Qingyi decoction modulates fibrotic pathways in severe acute pancreatitis: A histological and molecular study","authors":"Shayan Chen , Zhihuang Wu , Wendie Yu , Di Zou , Jiongtang Lu","doi":"10.1016/j.prmcm.2025.100684","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Qingyi Decoction (QYD), a traditional Chinese medicine (TCM) formulation derived from Dachaihu Decoction, is used to treat severe acute pancreatitis (SAP). While QYD's components, <em>rhubarb</em> and <em>bupleurum</em>, possess known anti-fibrotic properties, their mechanisms in SAP remain unclear. This study investigated QYD's anti-fibrotic effects and underlying mechanisms in a lipopolysaccharide (LPS)- and cerulein-induced mouse model of SAP.</div></div><div><h3>Methods</h3><div>SAP was induced in mice by intraperitoneal injection of cerulein and LPS. The QYD+SAP group received oral administration of QYD at twice the clinical dosage. Following modeling and QYD treatment, pancreatic tissues were harvested for examination of fibrotic parameters using histological methods. Additionally, the anti-fibrogenic effects of QYD on pancreatic tissue were investigated using Western blotting and laser scanning confocal microscopy.</div></div><div><h3>Results</h3><div>In SAP mice, histological examination of pancreatic tissues revealed significant tissue damage. However, QYD treatment ameliorated the histological severity of SAP. Furthermore, QYD decreased the expression of pancreatic fibrosis and PSC activation markers, including α-SMA, collagen, and fibronectin, while enhancing pancreatic acinar cell survival and restoring exocrine pancreatic function. Mechanistically, QYD treatment inhibited the activation of JNK, ERK, and p38 MAPK pathways, as well as prevented IκBα degradation in pancreatic tissues.</div></div><div><h3>Conclusion</h3><div>This study demonstrates the presence of mild pancreatic fibrosis in SAP and reveals QYD's anti-fibrotic effects through the inhibition of JNK, ERK, and p38 MAPK signaling pathways and the prevention of IκBα degradation.</div></div>","PeriodicalId":101013,"journal":{"name":"Pharmacological Research - Modern Chinese Medicine","volume":"17 ","pages":"Article 100684"},"PeriodicalIF":0.0000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pharmacological Research - Modern Chinese Medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667142525001113","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Qingyi Decoction (QYD), a traditional Chinese medicine (TCM) formulation derived from Dachaihu Decoction, is used to treat severe acute pancreatitis (SAP). While QYD's components, rhubarb and bupleurum, possess known anti-fibrotic properties, their mechanisms in SAP remain unclear. This study investigated QYD's anti-fibrotic effects and underlying mechanisms in a lipopolysaccharide (LPS)- and cerulein-induced mouse model of SAP.
Methods
SAP was induced in mice by intraperitoneal injection of cerulein and LPS. The QYD+SAP group received oral administration of QYD at twice the clinical dosage. Following modeling and QYD treatment, pancreatic tissues were harvested for examination of fibrotic parameters using histological methods. Additionally, the anti-fibrogenic effects of QYD on pancreatic tissue were investigated using Western blotting and laser scanning confocal microscopy.
Results
In SAP mice, histological examination of pancreatic tissues revealed significant tissue damage. However, QYD treatment ameliorated the histological severity of SAP. Furthermore, QYD decreased the expression of pancreatic fibrosis and PSC activation markers, including α-SMA, collagen, and fibronectin, while enhancing pancreatic acinar cell survival and restoring exocrine pancreatic function. Mechanistically, QYD treatment inhibited the activation of JNK, ERK, and p38 MAPK pathways, as well as prevented IκBα degradation in pancreatic tissues.
Conclusion
This study demonstrates the presence of mild pancreatic fibrosis in SAP and reveals QYD's anti-fibrotic effects through the inhibition of JNK, ERK, and p38 MAPK signaling pathways and the prevention of IκBα degradation.