Title:Restoration of Intestinal Mucosa in Euphorbia kansui-treated Severe Acute Pancreatitis Rats based on HMGB1/MFG-E8 Expression
Volume: 22
Issue: 12
Author(s): Chengjiang Qiu, Kairui Liu, Xuguang Li, Weirun Chen, Sheng Zhang and Youxing Huang*
Affiliation:
- Department of Abdominal Surgery, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510000, Guangdong Province,China
Keywords:
Severe acute pancreatitis, Euphorbia kansui, traditional Chinese medicine, intestinal barrier dysfunction, HMGB1,
MFG-E8.
Abstract:
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 are 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 72h 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 the intestinal barrier function and modulating
the HMGB1/MFG-E8 signaling axis.
