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Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ): Molecular Effects and Its Importance as a Novel Therapeutic Target for Cerebral Ischemic Injury
Neurochemical Research ( IF 4.4 ) Pub Date : 2021-07-20 , DOI: 10.1007/s11064-021-03402-1
Ashi Mannan 1 , Nikhil Garg 1 , Thakur Gurjeet Singh 1 , Harmeet Kaur Kang 2
Affiliation  

Cerebral ischemic injury is a leading cause of death and long-term disability throughout the world. Peroxisome proliferator-activated receptor gamma (PPAR-ɣ) is a ligand-activated nuclear transcription factor that is a member of the PPAR family. PPAR-ɣ has been shown in several in vitro and in vivo models to prevent post-ischemic inflammation and neuronal damage by negatively controlling the expression of genes modulated by cerebral ischemic injury, indicating a neuroprotective effect during cerebral ischemic injury. A extensive literature review of PubMed, Medline, Bentham, Scopus, and EMBASE (Elsevier) databases was carried out to understand the nature of the extensive work done on the mechanistic role of Peroxisome proliferator activated receptor gamma and its modulation in Cerebral ischemic injury. PPAR-ɣ can interact with specific DNA response elements to control gene transcription and expression when triggered by its ligand. It regulates lipid metabolism, improves insulin sensitivity, modulates antitumor mechanisms, reduces oxidative stress, and inhibits inflammation. This review article provides insights on the current state of research into the neuroprotective effects of PPAR-ɣ in cerebral ischemic injury, as well as the cellular and molecular mechanisms by which these effects are modulated, such as inhibition of inflammation, reduction of oxidative stress, suppression of pro-apoptotic production, modulation of transcription factors, and restoration of injured tissue through neurogenesis and angiogenesis.



中文翻译:

过氧化物酶体增殖物激活受体-γ (PPAR-ɣ):分子效应及其作为脑缺血性损伤新治疗靶点的重要性

脑缺血性损伤是全世界死亡和长期残疾的主要原因。过氧化物酶体增殖物激活受体 γ (PPAR-ɣ) 是一种配体激活的核转录因子,是 PPAR 家族的成员。PPAR-ɣ 已在多个体外和体内模型中显示,通过负控制受脑缺血损伤调节的基因的表达来预防缺血后炎症和神经元损伤,表明在脑缺血损伤期间具有神经保护作用。对 PubMed、Medline、Bentham、Scopus 和 EMBASE (Elsevier) 数据库进行了广泛的文献回顾,以了解对过氧化物酶体增殖物激活受体 γ 的机制作用及其在脑缺血性损伤中的调节所做的广泛工作的性质。PPAR-ɣ在其配体触发时可以与特定的DNA反应元件相互作用以控制基因的转录和表达。它调节脂质代谢,提高胰岛素敏感性,调节抗肿瘤机制,减少氧化应激,抑制炎症。这篇综述文章提供了关于 PPAR-ɣ 在脑缺血性损伤中的神经保护作用的研究现状,以及调节这些作用的细胞和分子机制,例如抑制炎症、减少氧化应激、抑制促凋亡产生,调节转录因子,并通过神经发生和血管生成恢复受损组织。提高胰岛素敏感性,调节抗肿瘤机制,减少氧化应激,抑制炎症。这篇综述文章提供了关于 PPAR-ɣ 在脑缺血性损伤中的神经保护作用的研究现状,以及调节这些作用的细胞和分子机制,例如抑制炎症、减少氧化应激、抑制促凋亡产生,调节转录因子,并通过神经发生和血管生成恢复受损组织。提高胰岛素敏感性,调节抗肿瘤机制,减少氧化应激,抑制炎症。这篇综述文章提供了关于 PPAR-ɣ 在脑缺血性损伤中的神经保护作用的研究现状,以及调节这些作用的细胞和分子机制,例如抑制炎症、减少氧化应激、抑制促凋亡产生,调节转录因子,并通过神经发生和血管生成恢复受损组织。

更新日期:2021-07-20
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