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过氧化物酶体增殖物激活受体-β/δ的激活可减轻大鼠心肌缺血/再灌注损伤。

Activation of peroxisome proliferator-activated receptor-beta/delta attenuates myocardial ischemia/reperfusion injury in the rat.

机构信息

Center for Translational Medicine & Therapeutics, Queen Mary University of London, William Harvey Research Institute, London, United Kingdom.

出版信息

Shock. 2010 Aug;34(2):117-24. doi: 10.1097/SHK.0b013e3181cd86d6.

Abstract

Peroxisome proliferator-activated receptor-beta/delta (PPAR-beta/delta) is a transcription factor that belongs to the PPAR nuclear hormone receptor family. There is little information about the effects of the immediate administration of specific ligands of PPAR-beta/delta (e.g., GW0742) in animal models of myocardial I/R injury. Using a rat model of regional myocardial I/R in vivo, we have investigated the effects of immediate administration of GW0742 on myocardial infarct size. Male Wistar rats were subjected to 25 min of regional ischemia followed by 2 h of reperfusion and treated with GW0742 (3, 30, or 300microg/kg i.v. given at 30 min before ischemia and again at the start of reperfusion). Higher doses (30 or 300 microg/kg i.v.) of GW0742 caused a reduction in infarct size, whereas the lowest dose used was not effective. The degree of cardioprotection was similar when GW0742 (30 microg/kg i.v.) was given on reperfusion alone. The reduction in infarct size afforded by GW0742 was not reduced by the competitive irreversible PPAR-alpha antagonist GW6471 (1 mg/kg i.v., 15 min before ischemia). GW0742 (30 microg/kg i.v.) reduced the I/R-induced (a) decrease in the phosphorylation of Akt and glycogen synthase kinase-3beta, (b) nuclear translocation of the p65 subunit of nuclear factor-kappaB (activation of nuclear factor-kappaB), and (c) increase in the expression of iNOS and cyclooxygenase-2. Thus, immediate administration of the PPAR-beta/delta ligand GW0742 during reperfusion reduces myocardial infarct size in the rat by a mechanism that may involve inhibition of the activity of glycogen synthase kinase-3beta secondary to activation of the Akt pathway.

摘要

过氧化物酶体增殖物激活受体-β/δ(PPAR-β/δ)是一种转录因子,属于过氧化物酶体增殖物激活受体核激素受体家族。关于即刻给予 PPAR-β/δ(例如 GW0742)的特定配体对心肌 I/R 损伤动物模型的影响,信息很少。本研究在体内大鼠局部心肌 I/R 模型中,研究了即刻给予 GW0742 对心肌梗死面积的影响。雄性 Wistar 大鼠接受 25 分钟的区域缺血,然后再进行 2 小时的再灌注,并给予 GW0742(3、30 或 300μg/kg 静脉注射,在缺血前 30 分钟给予,再灌注开始时再次给予)。更高剂量(30 或 300μg/kg 静脉注射)的 GW0742 可减少梗死面积,而使用的最低剂量则无效。当仅在再灌注时给予 GW0742(30μg/kg 静脉注射)时,心脏保护程度相似。GW0742 赋予的梗死面积减少不会因竞争性不可逆的 PPAR-α拮抗剂 GW6471(缺血前 15 分钟给予 1mg/kg 静脉注射)而减少。GW0742(30μg/kg 静脉注射)可减少 I/R 诱导的(a)Akt 和糖原合成酶激酶-3β的磷酸化减少,(b)核因子-κB 的 p65 亚基的核易位(核因子-κB 的激活),和(c)iNOS 和环氧化酶-2 的表达增加。因此,在再灌注期间即刻给予 PPAR-β/δ 配体 GW0742 可通过可能涉及 Akt 途径激活继发于糖原合成酶激酶-3β活性抑制的机制来减少大鼠的心肌梗死面积。

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