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Interleukin-22 Alleviates Caerulein-Induced Acute Pancreatitis by Activating AKT/mTOR Pathway.
- Source :
- Digestive Diseases & Sciences; May2024, Vol. 69 Issue 5, p1691-1700, 10p
- Publication Year :
- 2024
-
Abstract
- Background: Acute pancreatitis (AP) is one of the most common acute abdominal disorders; due to the lack of specific treatment, the treatment of acute pancreatitis, especially serious acute pancreatitis (SAP), is difficult and challenging. We will observe the changes of Interleukin -22 levels in acute pancreatitis animal models, and explore the mechanism of Interleukin -22 in acute pancreatitis. Objective: This study aims to assess the potential protective effect of Interleukin -22 on caerulein-induced acute pancreatitis and to explore its mechanism. Methods: Blood levels of amylase and lipase and Interleukin -22 were assessed in mice with acute pancreatitis. In animal model and cell model of caerulein-induced acute pancreatitis, the mRNA levels of P62 and Beclin-1 were determined using PCR, and the protein expression of P62, LC3-II, mTOR, AKT, p-mTOR, and p-AKT were evaluated through Western blot analysis. Results: Interleukin -22 administration reduced blood amylase and lipase levels and mitigated tissue damage in acute pancreatitis mice model. Interleukin -22 inhibited the relative mRNA levels of P62 and Beclin-1, and the Interleukin -22 group showed a decreased protein expression of LC3-II and P62 and the phosphorylation of the AKT/mTOR pathway. Furthermore, we obtained similar results in the cell model of acute pancreatitis. Conclusion: This study suggests that Interleukin -22 administration could alleviate pancreatic damage in caerulein-induced acute pancreatitis. This effect may result from the activation of the AKT/mTOR pathway, leading to the inhibition of autophagy. Consequently, Interleukin -22 shows potential as a treatment. [ABSTRACT FROM AUTHOR]
- Subjects :
- INTERLEUKIN-22
PANCREATITIS
WESTERN immunoblotting
Subjects
Details
- Language :
- English
- ISSN :
- 01632116
- Volume :
- 69
- Issue :
- 5
- Database :
- Complementary Index
- Journal :
- Digestive Diseases & Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 177775662
- Full Text :
- https://doi.org/10.1007/s10620-024-08360-6