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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Interleukin-22 treatment ameliorates alcoholic liver injury in a murine model of chronic-binge ethanol feeding: role of signal transducer and activator of transcription 3.
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Interleukin-22 treatment ameliorates alcoholic liver injury in a murine model of chronic-binge ethanol feeding: role of signal transducer and activator of transcription 3.

机译：白介素22的治疗改善了慢性酒精喂养小鼠模型中的酒精性肝损伤：信号转导和转录激活因子的作用3。

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Interleukin-22 (IL-22), a recently identified member of the IL-10 family of cytokines that is produced by Th17 and natural killer cells, plays an important role in controlling bacterial infection, homeostasis, and tissue repair. Here, we tested the effect of IL-22 on alcohol-induced liver injury in a murine model of chronic-binge ethanol feeding. Feeding male C57BL/6 mice with a Lieber-DeCarli diet containing 5% ethanol for 10 days, followed by a single dose of ethanol (5 g/kg body weight) by gavage, induces significant fatty liver and liver injury with peak serum levels of approximately 250 IU/L alanine aminotransferase and 420 IU/L aspartate aminotransferase 9 hours after gavage. Moreover, chronic-binge ethanol administration increases expression of hepatic and serum inflammatory cytokines and hepatic oxidative stress. Using this model, we demonstrate that treatment with IL-22 recombinant protein activates hepatic signal transducer and activator of transcription 3 (STAT3) and ameliorates alcoholic fatty liver, liver injury, and hepatic oxidative stress. Administration with IL-22 adenovirus also prevents alcohol-induced steatosis and liver injury. Deletion of STAT3 in hepatocytes abolishes the hepatoprotection provided by IL-22 in alcoholic liver injury. In addition, IL-22 treatment down-regulates the hepatic expression of fatty acid transport protein, but up-regulates several antioxidant, antiapoptotic, and antimicrobial genes. Finally, expression of IL-22 receptor 1 is up-regulated whereas IL-22 is undetectable in the livers from mice with chronic-binge ethanol feeding or patients with alcoholic hepatitis. CONCLUSION: Chronic-binge ethanol feeding may be a useful model to study the early stages of alcoholic liver injury. IL-22 treatment could be a potential therapeutic option to ameliorate alcoholic liver disease, due to its antioxidant, antiapoptotic, antisteatotic, proliferative, and antimicrobial effects with the added benefit of potentially few side effects.
机译：白细胞介素-22（IL-22）是由Th17和自然杀伤细胞产生的IL-10细胞因子家族中最近被确定的成员，在控制细菌感染，体内平衡和组织修复中起着重要作用。在这里，我们在慢性酒精摄入的小鼠模型中测试了IL-22对酒精诱导的肝损伤的影响。用含5％乙醇的Lieber-DeCarli饮食给雄性C57BL / 6小鼠喂养10天，然后通过强饲法单剂量使用乙醇（5 g / kg体重），可引起明显的脂肪肝和肝损伤，血清峰值为灌胃后9小时大约需要250 IU / L丙氨酸转氨酶和420 IU / L天冬氨酸转氨酶。此外，长期使用酒精可以增加肝脏和血清炎性细胞因子的表达以及肝脏氧化应激。使用此模型，我们证明用IL-22重组蛋白进行治疗可激活肝信号转导子和转录激活子3（STAT3），并改善酒精性脂肪肝，肝损伤和肝氧化应激。 IL-22腺病毒的给药还可以防止酒精引起的脂肪变性和肝损伤。肝细胞中STAT3的缺失消除了IL-22对酒精性肝损伤的保护作用。另外，IL-22处理下调脂肪酸转运蛋白的肝表达，但上调一些抗氧化剂，抗凋亡和抗菌基因。最终，IL-22受体1的表达上调，而长期饲喂乙醇的小鼠肝脏或酒精性肝炎患者的肝脏中IL-22则检测不到。结论：长期饮酒可能是研究酒精性肝损伤早期的有用模型。由于IL-22具有抗氧化，抗凋亡，抗硬脂化，增生和抗菌作用，且可能具有很少的副作用，因此IL-22治疗可能是改善酒精性肝病的潜在治疗选择。

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