MicroRNA-21 Contributes to Acute Liver Injury in LPS-Induced Sepsis Mice by Inhibiting PPARα Expression.

IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL PPAR Research Pub Date : 2020-12-22 eCollection Date: 2020-01-01 DOI:10.1155/2020/6633022
Xianjin Du, Miao Wu, Dan Tian, Jianlin Zhou, Lu Wang, Liying Zhan
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引用次数: 5

Abstract

The severity of sepsis may be associated with excessive inflammation, thus leading to acute liver injury. MicroRNA-21 is highly expressed in the liver of a variety of inflammation-related diseases, and PPARα is also proved to participate in regulating inflammation. In the present study, the LPS-induced sepsis model was established. We found that microRNA-21 expression was upregulated in the liver of sepsis mice, and microRNA-21 inhibition significantly reduced the liver injury. The expression of liver injury markers, inflammation cytokines, and PPARα in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPARα is the target gene of microRNA-21; PPARα antagonist GW6471 could reverse the effect of antagomir-21. In conclusion, our study illustrated that microRNA-21 exacerbate acute liver injury in sepsis mice by inhibiting PPARα expression.

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MicroRNA-21通过抑制PPARα表达参与lps诱导的脓毒症小鼠急性肝损伤
脓毒症的严重程度可能与过度炎症有关,从而导致急性肝损伤。MicroRNA-21在多种炎症相关疾病的肝脏中高表达,PPARα也被证明参与调节炎症。本研究建立lps致脓毒症模型。我们发现microRNA-21在脓毒症小鼠肝脏中表达上调,抑制microRNA-21可显著减轻肝损伤。脓毒症小鼠的肝损伤标志物、炎症细胞因子和PPARα的表达高于阿塔戈米尔-21处理的脓毒症小鼠。此外,我们还发现PPARα是microRNA-21的靶基因;PPARα拮抗剂GW6471可逆转安他哥米-21的作用。总之,我们的研究表明,microRNA-21通过抑制PPARα的表达加重脓毒症小鼠的急性肝损伤。
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来源期刊
PPAR Research
PPAR Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
6.20
自引率
3.40%
发文量
17
审稿时长
12 months
期刊介绍: PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.
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