培马颤酯预处理通过调控JAK2/STAT3β/PPARα通路减轻肝缺血-再灌注损伤中的细胞凋亡和自噬。

IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL PPAR Research Pub Date : 2021-03-11 eCollection Date: 2021-01-01 DOI:10.1155/2021/6632137
Ziqi Cheng, Chuanyong Guo
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引用次数: 8

摘要

肝缺血再灌注损伤(HIRI)是肝移植和肝外科手术中的常见现象。本文旨在通过JAK2/STAT3β/PPARα阐明保心颤在HIRI中的作用。实验中,我们将Balb/c分为正常对照(NC)、Sham、PEM (1.0 mg/kg)、IRI、IRI + PEM (0.1 mg/kg)、IRI + PEM (0.5 mg/kg)和IRI + PEM (1.0 mg/kg) 7组。采用生化测定、组织病理学评价、免疫组织化学、RT-PCR、qRT-PCR、ELISA分析等方法,测定凋亡因子、自噬因子再灌注后2 h、8 h、24 h三个时间点肝脏血清AST、ALT、IL-1β、TNF-α水平及组织中JAK2/STAT3/PPARα含量。我们的实验结果表明,培马颤可有效降低肝脏IR损伤水平。此外,pemafbrate具有抗炎、抗凋亡和抗自噬作用,这些作用是通过JAK2/STAT3β/PPARα途径介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Pemafibrate Pretreatment Attenuates Apoptosis and Autophagy during Hepatic Ischemia-Reperfusion Injury by Modulating JAK2/STAT3β/PPARα Pathway.

Hepatic ischemia-reperfusion injury (HIRI) is a common phenomenon in liver transplantation and liver surgery. This article is aimed at clarifying the role of pemafibrate in HIRI through JAK2/STAT3β/PPARα. In the experiment, we divided Balb/c into seven groups, namely, normal control (NC), Sham, PEM (1.0 mg/kg), IRI, IRI + PEM (0.1 mg/kg), IRI + PEM (0.5 mg/kg), and IRI + PEM (1.0 mg/kg). We used biochemical assay, histopathological evaluation, immunohistochemistry, RT-PCR and qRT-PCR, ELISA analysis, and other methods to determine the level of serum AST, ALT, IL-1β, and TNF-α in the liver at three time points (2 h, 8 h, and 24 h) after reperfusion of apoptosis factor, autophagy factor, and the JAK2/STAT3/PPARα content in tissues. Our experiment results showed that the pemafibrate can effectively reduce the level of hepatic IR injury. In addition, pemafibrate has anti-inflammatory, antiapoptotic, and antiautophagy effects, which are mediated by the JAK2/STAT3β/PPARα pathway.

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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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