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微粒体前列腺素 E 合酶-1(mPGES-1)与过氧化物酶体增殖物激活受体 γ(PPARγ)在炎症发生中的功能联系。

The functional link between microsomal prostaglandin E synthase-1 (mPGES-1) and peroxisome proliferator-activated receptor γ (PPARγ) in the onset of inflammation.

机构信息

ImmunoPharmaLab, Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Via Domenico Montesano 49, 80131, Naples, Italy.

ImmunoPharmaLab, Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Via Domenico Montesano 49, 80131, Naples, Italy.

出版信息

Pharmacol Res. 2020 Jul;157:104807. doi: 10.1016/j.phrs.2020.104807. Epub 2020 Apr 22.

DOI:10.1016/j.phrs.2020.104807
PMID:32330552
Abstract

Many years have elapsed since the discovery of anti-inflammatories as effective therapeutics for the treatment of inflammatory-related diseases, but we are still uncovering their various mechanisms of action. Recent biochemical and pharmacological studies have shown that in different tissues and cell types lipid mediators from thearachidonic acid cascade, play a crucial role in the initiation and resolution of inflammation by shifting from pro-inflammatory prostaglandin (PG)E to anti-inflammatory PGD and PGJ. Considering that until now very little is known about the biological effects evoked by microsomal prostaglandin E synthase-1 (mPGES-1) and contextually by peroxisome proliferator-activated receptor γ (PPARγ) modulation (key enzymes involved in PGE and PGD/PGJmetabolism), in this opinion paper we sought to define the coordinate functional regulation between these two enzymes at the "crossroads of phlogistic pathway" involved in the induction and resolution of inflammation.

摘要

自发现抗炎药作为治疗炎症相关疾病的有效疗法以来,已经过去了多年,但我们仍在揭示它们的各种作用机制。最近的生化和药理学研究表明,在不同的组织和细胞类型中,花生四烯酸级联的脂质介质通过从促炎前列腺素 (PG)E 转变为抗炎 PGD 和 PGJ,在炎症的发生和消退中发挥关键作用。考虑到到目前为止,人们对微粒体前列腺素 E 合酶-1 (mPGES-1) 和过氧化物酶体增殖物激活受体 γ (PPARγ) 调节(参与 PGE 和 PGD/PGJ 代谢的关键酶)引起的生物学效应知之甚少,在这篇观点文章中,我们试图定义这两种酶在参与炎症发生和消退的“炎症途径的十字路口”处的协调功能调节。

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