Background:
The pathogenesis of severe acute pancreatitis (SAP) is mediated substantially by dysfunctions in
the intestinal barrier. Euphorbia kansui (EK) is a medicinal plant used widely in traditional Chinese medicine to treat
inflammation; however, its efficacy and mechanism of action in SAP treatment is not yet well understood.
Objective:
To investigate the role of EK in intestinal barrier tissue repair and in the pathogenesis and development of SAP.
Methods:
The rat SAP model was established by a retrograde injection of sodium taurocholate into the pancreatic bile duct.
The SAP model group and the SAP + EK treatment groups were divided into 6 subgroups according to timing: 2, 6, 12, 24,
48, or 72 h after inducing SAP. The progression of the SAP rats and of the rats receiving the EK treatment was evaluated
using the ascites volume, serum amylase and plasma endotoxin levels, and histological grading of intestinal mucosal
damage. In addition, serum inflammatory factor contents were measured using enzyme-linked immunosorbent assay
(ELISA) tests and apoptotic cells in damaged ileum tissue were detected using TUNEL staining. Apoptosis markers and
other signaling proteins in intestinal mucosal cells were detected by immunohistochemical assays and then validated by
combining these data with quantitative polymerase chain reactions and western blotting.
Results:
Compared with the results of the SAP model rats, the results of the rats that received EK treatment demonstrated
that EK could effectively reduce the ascites volume and serum amylase and plasma endotoxin levels. EK treatment also
greatly reduced the abnormal intestinal morphological alterations in the rat SAP model and significantly downregulated the
serum contents of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. EK treatment inhibited the elevation of capapse-3,
inhibited the decrease of the Bcl-2 protein, and decreased the number of apoptotic cells in rat ileum tissue. Finally, EK
treatment abrogated the increase of HMGB1 and the suppression of MFG-E8 protein expression in the SAP + EK rat ileum
tissue.
Conclusion:
EK suppresses SAP pathogenesis by restoring intestinal barrier function and modulating the HMGB1/MFG-E8
signaling axis.
