ArticleDigestive diseases and sciences2024
Interleukin-22 Alleviates Caerulein-Induced Acute Pancreatitis by Activating AKT/mTOR Pathway.
Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- S-adenosylhomocysteine hydrolase-like protein 1 deficiency resulted in stronger inflammation reaction in acute pancreatitis.Journal of gastroenterology · 2026Article
- IL-22Rα1 restrains pancreatic injury independently of its C-terminal STAT3-amplifying domain.Journal of cell communication and signaling · 2026Article
- rIL-22 Alleviates Severe Acute Pancreatitis and Secondary Multiple Organ Injury Induced by Caerulein in Mice.Inflammation · 2026Article
- Diagnostic and Prognostic Value of miR-574-3p in Acute Pancreatitis: Insights from Bioinformatics and in vitro Studies.Journal of inflammation research · 2026Article
- Serum Hsa-miR-4695-5p Serves as a Novel Diagnostic Biomarker for Acute Severe Pancreatitis and Exacerbates Pathological Injury by Targeting SESN2.Digestive diseases and sciences · 2025Article
- Targeting the programmed cell death signaling mechanism with natural products for the treatment of acute pancreatitis: a review.Frontiers in pharmacology · 2025Review
- Investigating the Role of Salidroside in Alleviating Acute Pancreatitis by Inhibiting the RIPK1/RIPK3/MLKL Pathway-Mediated Necroptosis in Pancreatic Acinar Cells in Rats.Journal of inflammation research · 2025Article
- The role of autophagy in pancreatic diseases.Frontiers in pharmacology · 2024Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundAcute 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.
objectiveThis study aims to assess the potential protective effect of Interleukin -22 on caerulein-induced acute pancreatitis and to explore its mechanism.
methodsBlood 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.
resultsInterleukin -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.
conclusionThis 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.