一氧化氮通过PPARγ/eNOS信号通路介导II型糖尿病炎症

IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL PPAR Research Pub Date : 2020-11-26 eCollection Date: 2020-01-01 DOI:10.1155/2020/8889612
Hua Guo, Qinglan Zhang, Haipo Yuan, Lin Zhou, Fang-Fang Li, Sheng-Ming Wang, Gang Shi, Maojuan Wang
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引用次数: 11

摘要

炎症参与了2型糖尿病(T2DM)的发病过程,其具体机制尚不清楚。一氧化氮(NO)是一种关键的炎症调节剂,其作用是T2DM的炎症,但很少报道。因此,我们的研究旨在探讨NO对T2DM炎症的影响及其机制。采用一氧化氮分析仪分析T2DM患者和配对健康成人血浆样品中的NO水平,测定NO供体或NO清除剂处理胰岛素诱导HepG2细胞中炎症因子(c反应蛋白、肝球蛋白、IL-1β、TNF-α、IL-6)的表达,并采用RT-PCR和western blot检测si-PPARγ转染胰岛素诱导HepG2细胞中PPARγ、eNOS、c反应蛋白、肝球蛋白、IL-1β、TNF-α和IL-6的水平。结果表明,过量NO可增加T2DM患者炎症标志物水平,这是由PPARγ/eNOS通路激活的。这些发现将加强对NO在T2DM中的认识,并为T2DM的治疗提供新的靶点。
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Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway.

Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1β, TNF-α, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPARγ, eNOS, C-reactive protein, heptoglobin, IL-1β, TNF-α, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPARγ. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPARγ/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM.

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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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