首页> 外文期刊>Journal of immunology research. >Blocking the Hepatic Branch of the Vagus Aggravates Hepatic Ischemia-Reperfusion Injury via Inhibiting the Expression of IL-22 in the Liver
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Blocking the Hepatic Branch of the Vagus Aggravates Hepatic Ischemia-Reperfusion Injury via Inhibiting the Expression of IL-22 in the Liver

机译:阻断迷水的肝脏分支通过抑制肝脏中IL-22的表达来加剧肝缺血再灌注损伤

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Liver ischemia-reperfusion injury (IRI) is an inevitable process during liver transplantation, hemorrhagic shock, resection, and other liver surgeries. It is an important cause of postoperative liver dysfunction and increased medical costs. The protective effects of the vagus nerve on hepatic IRI have been reported, but the underlying mechanism has not been fully understood. We established a hepatic vagotomy (Hv) mouse model to study the effect of the vagus on liver IRI and to explore the underlying mechanism. Liver IRI was more serious in mice with Hv, which showed higher serum ALT and AST activities and histopathological changes. Further experiments confirmed that Hv significantly downregulated the expression of IL-22 protein and mRNA in the liver, blocking the activation of the STAT3 pathway. The STAT3 pathway in the livers of Hv mice was significantly activated, and liver injury was clearly alleviated after treatment with exogenous IL-22 recombinant protein. In conclusion, Hv can aggravate hepatic IRI, and its mechanism may be related to inhibition of IL-22 expression and downregulation of the STAT3 pathway in the liver.
机译:肝脏缺血再灌注损伤(IRI)是肝移植,出血休克,切除和其他肝脏手术中的必然过程。这是术后肝功能障碍和增加医疗费用的重要原因。据报道,迷走神经对肝IRI对肝脏IRI的保护作用,但潜在的机制尚未得到完全理解。我们建立了一种肝脏阴道术(HV)小鼠模型,以研究迷走神经对肝脏IRI的影响,并探索潜在机制。肝脏IRI在具有HV的小鼠中更严重,显示出更高的血清ALT和AST活动和组织病理学变化。进一步的实验证实,HV显着下调了IL-22蛋白和mRNA在肝脏中的表达,阻断了STAT3途径的激活。 HV小鼠肝脏中的STAT3途径显着激活,用外源IL-22重组蛋白处理后清楚地缓解了肝损伤。总之,HV可以加剧肝IRI,其机制可能与肝脏中IL-22表达的抑制和下调有关。

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