Background

Myricetin, a flavonoid, has anti-inflammation effects and can improve pancreatic β cells dysfunction. However, the role of myricetin in severe acute pancreatitis (SAP) and the precise mechanism remain unclear.

Objectives

This study aimed to investigate how myricetin affects pancreatic damage induced by SAP.

Results

Myricetin substantially reduced the expression of lipase and amylase, and ameliorated pancreatic damage induced by SAP. Moreover, myricetin inhibited the release of several inflammatory relevant cytokines including tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-10, alleviated apoptosis of pancreatic alveolar cells, and ameliorated microcirculatory dysfunction in SAP rats. Furthermore, myricetin inhibited the acetylation of forkhead box protein O1(FOXO1) and the phosphorylation of NF-kB.

Conclusion

Myricetin improves SAP-induced pancreatic injury through suppressing microcirculation dysfunction, overactive inflammatory response, and cell apoptosis. In addition, myricetin deregulates acetylated FOXO1 and phosphorylated nuclear factor kappa B (NF-kB), which may be the potential mechanism for SAP alleviation.

中文翻译：

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杨梅素通过 FOXO1 和 NF-κB 通路减轻重症急性胰腺炎大鼠胰腺微循环和炎症

背景

杨梅素是一种黄酮类化合物，具有抗炎作用，并能改善胰腺β细胞功能障碍。然而，杨梅素在重症急性胰腺炎（SAP）中的作用及其确切机制仍不清楚。

目标

本研究旨在探讨杨梅素如何影响 SAP 引起的胰腺损伤。

结果

杨梅素显着降低脂肪酶和淀粉酶的表达，并改善 SAP 引起的胰腺损伤。此外，杨梅素还能抑制多种炎症相关细胞因子的释放，包括肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-1β、IL-6和IL-10，减轻胰腺肺泡细胞的凋亡，改善微循环功能障碍。 SAP 大鼠。此外，杨梅素还抑制叉头盒蛋白O1（FOXO1）的乙酰化和NF-kB的磷酸化。

结论

杨梅素通过抑制微循环功能障碍、过度活跃的炎症反应和细胞凋亡来改善 SAP 引起的胰腺损伤。此外，杨梅素可解除乙酰化 FOXO1 和磷酸化核因子 kappa B (NF-kB) 的调节，这可能是缓解 SAP 的潜在机制。