ArticleJournal of inflammation research2025
The Effects of Da-Chai-Hu Decoction Alleviating Pancreatic Exocrine Dysfunction by Inhibiting Endoplasmic Reticulum Stress of Acinar Cell in Mice with Chronic Pancreatitis.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Expression characteristics of ferroptosis-related immune genes in chronic pancreatitis and screening and validation of key genes.BMC gastroenterology · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic pancreatitis (CP) is characterized by significant pancreatic exocrine dysfunction, with limited targeting therapeutic strategies. It has been reported that DCHD can effectively alleviate pancreatic injury in chronic pancreatitis; however, its effect and mechanism on pancreatic exocrine dysfunction remain unclear. Objective: To investigate the therapeutic effects of Da-Chai-Hu Decoction (DCHD) on pancreatic exocrine dysfunction in CP and explore its underlying mechanisms. Methods: Thirty male C57BL/6 mice were divided into control, CP model, and three DCHD dose groups (11, 22, 44 g/kg). CP was induced via repeated caerulein injections (50 μg/kg), followed by 3 weeks of DCHD treatment. Histopathological analysis of pancreatic tissue (via HE staining, IHC, IF), molecular assays (Western blot, RT-PCR), and RNA-seq were performed. LC-MS/MS identified chemical components in the serum of DCHD-treated mice, and network pharmacology predicted potential targets. Mouse pancreatic acinar cells (266-6) exposed to caerulein and PI3K inhibitor LY294002 were treated with DCHD serum to validate pathways. Results: DCHD not only alleviated pancreatic fibrosis (α-SMA) and inflammation (IL-6), but also maintained the level of Amylase. RNA-seq revealed that DCHD treatment downregulated the expression of genes related to inflammation, fibrosis, apoptosis, and ERS. The bioactive compounds in DCHD serum were identified by LC-MS/MS, and further were linked to PI3K/AKT and ERS pathway through network pharmacology. In vivo validation experiment showed that the expression of PI3K/AKT pathway and ERS markers in pancreatic tissue was significantly reduced in the DCHD group compared with CP mice ( Conclusion: DCHD suppress ERS by regulating the PI3K/AKT pathway in pancreatic acinar cells and further alleviates pancreatic exocrine dysfunction. This study confirms the therapeutic potential of DCHD in pancreatic exocrine dysfunction, and offers a new therapeutic option for CP with pancreatic exocrine dysfunction.
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