Introduction

Interleukin-22 (IL-22) has been proven to exhibit a protective role in hepatic ischemia-reperfusion injury (HIRI). This study aimed to explore the change of IL-22 and IL-22 receptor 1 (IL-22R1) axis in HIRI and its role in mitochondrial apoptosis associated with STAT3 activation.

Materials and Methods

I/R mice were examined for the expression of IL-22, IL-22R1 and IL-22BP. The roles of IL-22 in hepatic histopathology and oxidative stress injuries (ALT, MDA and SOD) were determined. Oxidative stress damages of AML-12 cells were induced by H₂O₂, and were indicated by apoptosis, Ca²⁺ concentration, and mitochondrial function. The effects of IL-22 on p-STAT3^Try705 were analyzed.

Results

We found that the expression of IL-22, IL-22R1, and IL-22BP was elevated 24 h after I/R induction, while decreased 48 h after I/R induction. Furthermore, we also discovered that IL-22 rescued the morphological damages and dysfunction of hepatocytes induced by H₂O₂, which were antagonized by IL-22BP, an endogenous antagonist of IL-22. Additionally, increased levels of Ca²⁺ concentration, MDA, ROS, apoptosis and mitochondrial dysfunction were noticed in H₂O₂-treated hepatocytes. However, IL-22 ameliorated the effects of I/R or H₂O₂. The protective effects of IL-22 were reversed by AG490, a specific antagonist of STAT3.

Conclusions

In conclusion, our results indicated that IL-22 inhibited I/R-induced oxidative stress injury, Ca²⁺ overload, and mitochondrial apoptosis via STAT3 activation.

中文翻译：

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IL-22通过激活STAT3抑制线粒体凋亡减轻肝缺血再灌注损伤

介绍

白介素 22 (IL-22) 已被证明对肝缺血再灌注损伤 (HIRI) 具有保护作用。本研究旨在探讨HIRI中IL-22和IL-22受体1（IL-22R1）轴的变化及其在STAT3激活相关线粒体凋亡中的作用。

材料和方法

检查 I/R 小鼠的 IL-22、IL-22R1 和 IL-22BP 的表达。确定了 IL-22 在肝组织病理学和氧化应激损伤（ALT、MDA 和 SOD）中的作用。_{H 2} O ₂诱导AML-12细胞氧化应激损伤，并通过细胞凋亡、Ca ²⁺浓度和线粒体功能来表征。分析IL-22对p-STAT3 ^Try705的影响。

结果

我们发现IL-22、IL-22R1和IL-22BP的表达在I/R诱导后24小时升高，而在I/R诱导后48小时降低。_{此外，我们还发现IL-22可以挽救H 2} O ₂诱导的肝细胞形态损伤和功能障碍，而这些损伤和功能障碍被IL-22内源性拮抗剂IL-22BP所拮抗。此外，在H ₂ O ₂处理的肝细胞中观察到Ca ²⁺浓度、MDA、ROS、细胞凋亡和线粒体功能障碍水平升高。_{然而，IL-22 改善了 I/R 或 H 2} O ₂的影响。IL-22 的保护作用可被 STAT3 的特异性拮抗剂 AG490 逆转。

结论

总之，我们的结果表明，IL-22 通过 STAT3 激活抑制 I/R 诱导的氧化应激损伤、Ca ²⁺超载和线粒体凋亡。