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IL-6 缺乏可减轻小鼠饮食诱导的非酒精性脂肪性肝炎。

IL-6 deficiency attenuates murine diet-induced non-alcoholic steatohepatitis.

机构信息

INSERM, U858, Toulouse, France.

出版信息

PLoS One. 2009 Nov 20;4(11):e7929. doi: 10.1371/journal.pone.0007929.

DOI:10.1371/journal.pone.0007929
PMID:19936233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2775411/
Abstract

BACKGROUND

The role of inflammation in the pathogenesis of non-alcoholic steatohepatitis (NASH), a common cause of liver disease, is still poorly understood. This study aimed at assessing the involvement of a major inflammatory cytokine, IL-6, in NASH.

MATERIALS AND METHODS

Steatohepatitis was induced by feeding wild-type or IL-6(-/-) mice for 5 weeks with a methionine and choline-deficient (MCD) diet.

RESULTS

Whereas MCD diet-induced weight loss and decreases in serum glucose, cholesterol and triglyceride levels were similar in both genotypes, serum alanine aminotransferase was less elevated in IL-6(-/-) mice than in wild-type animals. Despite having a comparable liver steatosis score, IL-6-deficient mice exhibited less lobular inflammation than their wild-type littermates. Liver gene expression of TGF-beta and MCP-1 was also strongly attenuated in mutant mice; a more modest reduction was observed for PPAR-gamma and F4/80 transcripts as well as proteins. Chromatographic analysis of liver lipids demonstrated that MCD diet induced in normal and mutant mice a similar decrease in the ratio of phosphatidylcholine to phosphatidylethanolamine. However, the diet-induced increase in the levels of sphingomyelin and ceramide was less important in IL-6(-/-) mice.

CONCLUSION

Altogether, these results indicate that IL-6 deficiency does not block the development of NASH; yet, IL-6 plays a critical role in the accompanying liver inflammation.

摘要

背景

炎症在非酒精性脂肪性肝炎（NASH）发病机制中的作用仍知之甚少，NASH 是一种常见的肝病病因。本研究旨在评估主要炎症细胞因子 IL-6 在 NASH 中的作用。

材料和方法

采用蛋氨酸和胆碱缺乏（MCD）饮食喂养野生型或 IL-6（-/-）小鼠 5 周，诱导脂肪性肝炎。

结果

尽管 MCD 饮食诱导的体重减轻和血清葡萄糖、胆固醇和甘油三酯水平下降在两种基因型中相似，但 IL-6（-/-）小鼠的血清丙氨酸氨基转移酶升高幅度低于野生型动物。尽管肝脂肪变性评分相似，但 IL-6 缺陷小鼠的肝小叶炎症程度低于其野生型同窝仔鼠。突变小鼠肝脏 TGF-β和 MCP-1 的基因表达也明显减弱；PPAR-γ和 F4/80 转录物以及蛋白的减少程度较小。对肝脂质的色谱分析表明，MCD 饮食在正常和突变小鼠中诱导了类似的磷脂酰胆碱与磷脂酰乙醇胺比例降低。然而，在 IL-6（-/-）小鼠中，饮食诱导的鞘磷脂和神经酰胺水平升高幅度较小。

结论

总之，这些结果表明 IL-6 缺乏并不阻止 NASH 的发生；然而，IL-6 在伴随的肝脏炎症中起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/68f6d9b85270/pone.0007929.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/6c901a37cffc/pone.0007929.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/a1aa018651f3/pone.0007929.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/27b5f6219fe7/pone.0007929.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/68f6d9b85270/pone.0007929.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/6c901a37cffc/pone.0007929.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/9a6e8db16036/pone.0007929.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/26325d9d669a/pone.0007929.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/eca3d8eebf3c/pone.0007929.g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/27b5f6219fe7/pone.0007929.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6af/2775411/68f6d9b85270/pone.0007929.g007.jpg

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