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首页> 外文期刊>Behavioural Brain Research: An International Journal >GW1929: a nonthiazolidinedione PPARγ agonist, ameliorates neurological damage in global cerebral ischemic-reperfusion injury through reduction in inflammation and DNA fragmentation.
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GW1929: a nonthiazolidinedione PPARγ agonist, ameliorates neurological damage in global cerebral ischemic-reperfusion injury through reduction in inflammation and DNA fragmentation.

机译：GW1929：一种非噻唑烷二酮PPARγ激动剂，可通过减少炎症和DNA片段化减轻全球脑缺血再灌注损伤中的神经系统损害。

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摘要

Transient global cerebral ischemia results in acute neurodegeneration in selective brain areas. Global cerebral ischemic-reperfusion (IR) injury induced selective hippocampal damage results into various neurobehavioral deficits including spatial memory and learning deficiencies. In this study, we have investigated the protective effects of a nonthiazolidinedione PPARγ agonist, N-(2-benzoylphenyl)-O-[2-(methyl-2-pyridinylamino)ethyl]-l-tyrosine (GW1929), against global cerebral IR injury induced neurobehavioral deficits and brain damage in gerbils. Bilateral carotid artery occlusion induced global cerebral ischemia in gerbils resulted in neurological deficits, hyperlocomotion, reduced response latency in passive avoidance test and hippocampal damage. Hippocampal neurodegeneration after cerebral IR injury was also associated with significant increase in iNOS and MMP-9 immunoreactivity along with TNFα and IL-6 levels. Massive apoptotic DNA fragmentation as evident from increased TUNEL (terminal deoxynucleotidyl transferase mediated dUTP nick end labelling)-positive cells was also observed in the CA1 hippocampal region of IR challenged gerbils. GW1929 treatment significantly ameliorated cerebral IR induced neurological symptoms, hyperlocomotion, cognitive deficits and hippocampal neuronal damage in CA1 hippocampus region in gerbils. Significant reduction in IR injury induced iNOS and MMP-9 immunoreactivity, TNFα and IL-6 levels and apoptotic DNA fragmentation was also observed with GW1929 treatment. Pioglitazone, thiazolidinedione PPARγ agonist also exhibited similar effects on inflammatory parameters after global cerebral IR injury. In summary, this study demonstrates neuroprotective effects of GW1929 in global cerebral IR injury induced neurobehavioral deficits and brain pathology which may be attributed to reduced inflammation and apoptotic DNA fragmentation, suggesting therapeutic potential of PPARγ agonists in cerebral IR injury.
机译：短暂性全脑缺血导致选择性脑区域发生急性神经变性。全球性脑缺血再灌注（IR）损伤引起的选择性海马损伤导致各种神经行为缺陷，包括空间记忆和学习缺陷。在这项研究中，我们研究了非噻唑烷二酮PPARγ激动剂N-（2-苯甲酰基苯基）-O- [2-（甲基-2-吡啶基氨基）乙基] -1-酪氨酸（GW1929）对全脑IR的保护作用损伤引起沙鼠的神经行为缺陷和脑损伤。双边颈动脉阻塞导致沙鼠的整体脑缺血，导致神经功能缺损，运动过度，被动回避测试中的反应潜伏期缩短和海马损伤。脑IR损伤后的海马神经变性也与iNOS和MMP-9免疫反应性以及TNFα和IL-6水平的显着升高有关。从IR攻击的沙鼠的CA1海马区中也观察到大量凋亡DNA片段化，这从增加的TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）阳性细胞可见。 GW1929治疗显着改善沙土鼠CA1海马区的脑IR诱发的神经系统症状，运动过度，认知缺陷和海马神经元损伤。用GW1929处理还观察到IR损伤诱导的iNOS和MMP-9免疫反应性，TNFα和IL-6水平以及凋亡DNA片段的显着降低。吡格列酮，噻唑烷二酮PPARγ激动剂对全脑IR损伤后的炎症参数也表现出相似的作用。总而言之，这项研究证明了GW1929在全脑IR损伤引起的神经行为缺陷和脑病理学中的神经保护作用，这可能归因于炎症反应和凋亡DNA片段减少，提示PPARγ激动剂在脑IR损伤中具有治疗潜力。

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