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抑制肌醇需求酶1可减轻肠外营养相关肝病(PNALD)细胞模型中的脂肪变性。

Suppression of IRE1 Attenuated the Fatty Degeneration in Parenteral Nutrition-Related Liver Disease (PNALD) Cell Model.

作者信息

Cui Ningxun, Cui Mingling, Li Jie, Zhu Xueping, Zhu Xiaoli

机构信息

Department of Neonatology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215025, China.

Department of Intervention, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

出版信息

Gastroenterol Res Pract. 2020 Feb 3;2020:7517540. doi: 10.1155/2020/7517540. eCollection 2020.

DOI:10.1155/2020/7517540
PMID:32089676
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7023833/
Abstract

AIMS

To model the parenteral nutrition-associated liver disease (PNALD) in rat normal hepatocytes BRL and investigate the role of endoplasmic reticulum stress- (ERS-) related IRE1 signal in the process of PNALD.

METHODS

The BRL cells were treated with different concentrations of soybean oil emulsion (SO) to induce hepatocyte fatty degeneration. The PNALD cell disease model was further confirmed by analysis of Oil Red O staining and biochemical parameters. Next, the IRE1 signal in the process of PNALD. signal in the process of PNALD. signal in the process of PNALD. signal in the process of PNALD.

RESULTS

The results of Oil Red O staining indicated that the PNALD was successfully established in BRL cells and the CCK-8 data indicated which 0.6% that SO was further applied to the experiment owing to its better induction of PNALD and less toxicity to the cells. Besides, the value of biochemical parameters (TBIL, DBIL, ALT, and AST) was also elevated in the SO group compared with the NG group. After knockdown of IRE1 signal in the process of PNALD. signal in the process of PNALD.

CONCLUSION

IRE1 was induced in PNALD cell model and suppression of IRE1 resulted in reduced steatosis in this cell disease model. Taken together, our data suggested that the IRE1 pathway may be involved in the development of PNALD. signal in the process of PNALD. signal in the process of PNALD. signal in the process of PNALD.

摘要

目的

在大鼠正常肝细胞BRL中建立肠外营养相关肝病(PNALD)模型,并研究内质网应激(ERS)相关的肌醇需求酶1(IRE1)信号在PNALD发生过程中的作用。

方法

用不同浓度的大豆油乳剂(SO)处理BRL细胞以诱导肝细胞脂肪变性。通过油红O染色和生化参数分析进一步确认PNALD细胞疾病模型。接下来,研究PNALD过程中的IRE1信号。

结果

油红O染色结果表明,在BRL细胞中成功建立了PNALD模型,CCK-8数据表明,由于0.6%的SO对PNALD的诱导效果更好且对细胞毒性较小,因此进一步将其应用于实验。此外,与正常组(NG)相比,SO组的生化参数(总胆红素、直接胆红素、谷丙转氨酶和谷草转氨酶)值也升高。在PNALD过程中敲低IRE1信号后。

结论

在PNALD细胞模型中诱导了IRE1,抑制IRE1可导致该细胞疾病模型中的脂肪变性减少。综上所述,我们的数据表明IRE1通路可能参与了PNALD的发生发展。在PNALD过程中信号。在PNALD过程中信号。在PNALD过程中信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/bd4cf2e1e511/GRP2020-7517540.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/2f1e7617f479/GRP2020-7517540.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/879e0b91c103/GRP2020-7517540.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/61a8fc8b0e3c/GRP2020-7517540.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/bd4cf2e1e511/GRP2020-7517540.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/2f1e7617f479/GRP2020-7517540.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/879e0b91c103/GRP2020-7517540.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/61a8fc8b0e3c/GRP2020-7517540.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b988/7023833/bd4cf2e1e511/GRP2020-7517540.004.jpg

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