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本文引用的文献

1
Combination therapy of rosiglitazone, a peroxisome proliferator-activated receptor-gamma ligand, and NMDA receptor antagonist (MK-801) on experimental embolic stroke in rats.罗格列酮（一种过氧化物酶体增殖物激活受体γ配体）与NMDA受体拮抗剂（MK-801）联合治疗对大鼠实验性栓塞性中风的影响。
Basic Clin Pharmacol Toxicol. 2007 Nov;101(5):309-14. doi: 10.1111/j.1742-7843.2007.00127.x.
2
Design of selective nuclear receptor modulators: RAR and RXR as a case study.选择性核受体调节剂的设计：以视黄酸受体（RAR）和视黄酸X受体（RXR）为例
Nat Rev Drug Discov. 2007 Oct;6(10):811-20. doi: 10.1038/nrd2398.
3
Evolution of peroxisome proliferator-activated receptor agonists.过氧化物酶体增殖物激活受体激动剂的演变
Ann Pharmacother. 2007 Jun;41(6):973-83. doi: 10.1345/aph.1K013. Epub 2007 May 22.
4
Caffeic acid phenethyl ester reduces neurovascular inflammation and protects rat brain following transient focal cerebral ischemia.咖啡酸苯乙酯可减轻短暂性局灶性脑缺血后大鼠的神经血管炎症并保护其大脑。
J Neurochem. 2007 Jul;102(2):365-77. doi: 10.1111/j.1471-4159.2007.04526.x. Epub 2007 Apr 16.
5
The PPAR gamma agonist Pioglitazone improves anatomical and locomotor recovery after rodent spinal cord injury.过氧化物酶体增殖物激活受体γ激动剂吡格列酮可改善啮齿动物脊髓损伤后的解剖学和运动功能恢复。
Exp Neurol. 2007 Jun;205(2):396-406. doi: 10.1016/j.expneurol.2007.02.009. Epub 2007 Feb 27.
6
PPAR-gamma: therapeutic target for ischemic stroke.过氧化物酶体增殖物激活受体γ：缺血性中风的治疗靶点
Trends Pharmacol Sci. 2007 May;28(5):244-9. doi: 10.1016/j.tips.2007.03.004. Epub 2007 Apr 9.
7
Peroxisome proliferator-activated receptor-gamma agonists induce neuroprotection following transient focal ischemia in normotensive, normoglycemic as well as hypertensive and type-2 diabetic rodents.在正常血压、正常血糖以及高血压和2型糖尿病啮齿动物中，过氧化物酶体增殖物激活受体γ激动剂在短暂局灶性缺血后可诱导神经保护作用。
J Neurochem. 2007 Apr;101(1):41-56. doi: 10.1111/j.1471-4159.2006.04376.x.
8
Neuroprotective effect of curcumin on focal cerebral ischemic rats by preventing blood-brain barrier damage.姜黄素通过预防血脑屏障损伤对局灶性脑缺血大鼠的神经保护作用。
Eur J Pharmacol. 2007 Apr 30;561(1-3):54-62. doi: 10.1016/j.ejphar.2006.12.028. Epub 2007 Jan 19.
9
Brazilein protects the brain against focal cerebral ischemia reperfusion injury correlating to inflammatory response suppression.巴西苏木精通过抑制炎症反应保护大脑免受局灶性脑缺血再灌注损伤。
Eur J Pharmacol. 2007 Mar 8;558(1-3):88-95. doi: 10.1016/j.ejphar.2006.11.059. Epub 2006 Dec 6.
10
Thiazolidinedione class of peroxisome proliferator-activated receptor gamma agonists prevents neuronal damage, motor dysfunction, myelin loss, neuropathic pain, and inflammation after spinal cord injury in adult rats.噻唑烷二酮类过氧化物酶体增殖物激活受体γ激动剂可预防成年大鼠脊髓损伤后的神经元损伤、运动功能障碍、髓鞘损失、神经性疼痛和炎症。
J Pharmacol Exp Ther. 2007 Mar;320(3):1002-12. doi: 10.1124/jpet.106.113472. Epub 2006 Dec 13.

过氧化物酶体增殖物激活受体γ 在脑卒中的治疗潜能。

Therapeutic Potential of PPARγ Activation in Stroke.

机构信息

Department of Neurological Surgery and the Neuroscience Training Program, University of Wisconsin-Madison, Madison, WI 53792, USA.

出版信息

PPAR Res. 2008;2008:461981. doi: 10.1155/2008/461981. Epub 2008 Apr 13.

DOI:10.1155/2008/461981
PMID:21909480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2293414/
Abstract

Stroke (focal cerebral ischemia) is a leading cause of death and disability among adult population. Many pathological events including inflammation and oxidative stress during the acute period contributes to the secondary neuronal death leading the neurological dysfunction after stroke. Transcriptional regulation of genes that promote these pathophysiological mechanisms can be an effective strategy to minimize the poststroke neuronal death. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors known to be upstream to many inflammatory and antioxidant genes. The goal of this review is to discuss the therapeutic potential and putative mechanisms of neuroprotection following PPAR activation after stroke.

摘要

中风（局部脑缺血）是成年人群死亡和残疾的主要原因。在急性期间，包括炎症和氧化应激在内的许多病理事件导致中风后神经功能障碍的继发性神经元死亡。促进这些病理生理机制的基因的转录调控可能是最小化中风后神经元死亡的有效策略。过氧化物酶体增殖物激活受体（PPARs）是配体激活的转录因子，已知是许多炎症和抗氧化基因的上游。本综述的目的是讨论中风后 PPAR 激活的神经保护治疗潜力和潜在机制。