Published online Aug 7, 2022. doi: 10.3748/wjg.v28.i29.3825
Peer-review started: September 18, 2021
First decision: December 4, 2021
Revised: December 15, 2021
Accepted: July 8, 2022
Article in press: July 8, 2022
Published online: August 7, 2022
Severe acute pancreatitis (SAP) is a severe acute abdominal disease characterized by high morbidity and mortality. A considerable amount of literature has demonstrated that intestinal barrier dysfunction is a significant contributory factor to SAP development. Qingyi decoction (QYD) has been used to treat acute pancreatitis in China for many years.
The protective functions of QYD against intestinal mucosa injuries caused by SAP will provide new therapeutic information on SAP.
To research the function and mechanism of QYD in treating intestinal mucosa injuries caused by SAP.
A rat model of SAP was created. Hematoxylin and eosin staining of pancreatic and intestinal tissue was performed. Enzyme-linked immunosorbent assay was used to estimate the concentrations of tumor necrosis factor (TNF-α), interleukin (IL)-6, D-lactic acid, and diamine oxidase (DAO). Terminal deoxynucleotidyl transferase dUTP nick-end labeling was carried out to assess intestinal epithelial cell (IEC) apoptosis. Quantitative real-time polymerase chain reaction, western blotting, and immunofluorescence were used to determine the expression of calcineurin (CaN) and nuclear factor of activated T-cells (NFATc3). MTT and confocal laser scanning microscope were used to detect cell viability and intracellular calcium levels in vitro studies.
In this study, the severity of SAP in the QYD group was attenuated. In addition, the levels of IEC apoptosis declined in the QYD group. QYD significantly restrained CaN and NFATc3 gene expression in the intestine. Further study indicated that QYD serum significantly decreased the lipopolysaccharide-induced elevation in intracellular free Ca2+ levels and cell death.
This research demonstrated that the CaN/NFATc3 pathway might play a key role in IEC injury caused by SAP and that QYD can exert protective effects, at least partially, by restraining IEC apoptosis via the CaN/NFATc3 pathway.
This study provides insight into the function and mechanism of QYD in the treatment of intestinal mucosa injuries caused by SAP in vivo and in vitro experiments, thereby providing theoretical support for the clinical application of QYD.