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.

中文翻译：

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Interleukin-22 通过激活 AKT/mTOR 通路减轻雨蛙素诱发的急性胰腺炎

背景

急性胰腺炎（AP）是最常见的急腹症之一；由于缺乏特异性治疗手段，急性胰腺炎特别是重症急性胰腺炎（SAP）的治疗十分困难且具有挑战性。我们将观察急性胰腺炎动物模型中白细胞介素-22水平的变化，探讨白细胞介素-22在急性胰腺炎中的作用机制。

客观的

本研究旨在评估白细胞介素-22对雨蛙素诱发的急性胰腺炎的潜在保护作用并探讨其机制。

方法

在患有急性胰腺炎的小鼠中评估了淀粉酶、脂肪酶和白细胞介素-22的血液水平。在雨蛙素诱导的急性胰腺炎动物模型和细胞模型中，采用PCR法测定P62和Beclin-1的mRNA水平，以及P62、LC3-II、mTOR、AKT、p-mTOR和p-AKT的蛋白表达量。通过蛋白质印迹分析进行评估。

结果

白介素 -22 给药可降低急性胰腺炎小鼠模型的血液淀粉酶和脂肪酶水平并减轻组织损伤。白细胞介素-22抑制P62和Beclin-1的相对mRNA水平，白细胞介素-22组表现出LC3-II和P62蛋白表达降低以及AKT/mTOR通路磷酸化。此外，我们在急性胰腺炎细胞模型中获得了类似的结果。

结论

这项研究表明，白细胞介素 -22 给药可以减轻雨蛙素诱发的急性胰腺炎的胰腺损伤。这种效应可能是由于 AKT/mTOR 通路的激活导致自噬受到抑制。因此，白细胞介素 -22 显示出作为治疗的潜力。