Laboratory of Molecular Genetics, Institute of Basic Medical Sciences, Beijing 100850, China.
Cytokine. 2011 Nov;56(2):174-9. doi: 10.1016/j.cyto.2011.07.022. Epub 2011 Aug 16.
Interleukin-22 (IL-22), a member of the IL-10 cytokine family that is produced by activated Th22, Th1 and Th17 cells as well as natural killer cells, plays an important role in increase of innate immunity, protection from damage and enhancement of regeneration. Here, we examined the effects of IL-22 on acute liver failure model induced by d-galactosamine (GalN) and lipopolysaccharide (LPS). Administration of recombinant human IL-22 (rhIL-22) reduced the death rate markedly and prevented mice from severe hepatic injury, as evidenced by decreased serum alanine aminotransferase (ALT) and total bilirubin (T.Bil) activity as well as improved histological signs in liver. Furthermore, IL-22 treatment decreased the hepatic malondialdehyde (MDA) contents and increased the reduced glutathione levels. Serum tumor necrosis factor α (TNF-α) level and hepatic caspase-3 activity were significantly lower in mice administrated with IL-22. Moreover, IL-22 treatment significantly enhanced activation of STAT3 and up-regulated the expression of Bcl-xL, heme oxygenase-1 (HO-1) and redox factor-1 (Ref-1) in the liver injury induced by GalN/LPS. Collectively, these data indicate that IL-22 can provide critical protection against GalN/LPS-induced liver injury through anti-apoptotic, anti-oxidant and anti-inflammatory actions.
白细胞介素 22（IL-22）是白细胞介素 10 细胞因子家族的一员，由活化的 Th22、Th1 和 Th17 细胞以及自然杀伤细胞产生，在先天免疫增强、损伤保护和增强再生方面发挥重要作用。在这里，我们研究了白细胞介素 22（IL-22）对半乳糖胺（GalN）和脂多糖（LPS）诱导的急性肝衰竭模型的影响。重组人白细胞介素 22（rhIL-22）的给药显著降低死亡率，并防止小鼠发生严重的肝损伤，血清丙氨酸氨基转移酶（ALT）和总胆红素（T.Bil）活性降低以及肝组织学标志改善证明了这一点。此外，IL-22 治疗降低了肝丙二醛（MDA）含量并增加了还原型谷胱甘肽水平。给予 IL-22 的小鼠血清肿瘤坏死因子 α（TNF-α）水平和肝半胱天冬酶-3 活性显著降低。此外，IL-22 治疗显著增强了 STAT3 的激活，并上调了 GalN/LPS 诱导的肝损伤中 Bcl-xL、血红素加氧酶-1（HO-1）和还原因子-1（Ref-1）的表达。总的来说，这些数据表明 IL-22 可以通过抗凋亡、抗氧化和抗炎作用为 GalN/LPS 诱导的肝损伤提供关键保护。
