15d-prostaglandin J2 protects brain from ischemia-reperfusion injury

Teng Nan Lin, Wai Mui Cheung, Jui Sheng Wu, Jean Ju Chen, Heng Lin, Jin Jer Chen, Jun Yang Liou, Song Kun Shyue, Kenneth K. Wu

研究成果: 雜誌貢獻文章同行評審

119 引文 斯高帕斯(Scopus)


Objective - Brain expresses abundant lipocalin-type prostaglandin (PG) D2 (PGD2) synthase but the role of PGD2 and its metabolite, 15-deoxy-Δ12,14 PGJ2 (15d-PGJ 2) in brain protection is unclear. The aim of this study is to assess the effect of 15d-PGJ2 on neuroprotection. Methods and Results - Adenoviral transfer of cyclooxygenase-1 (Adv-COX-1) was used to amplify the production of 15d-PGJ2 in ischemic cortex in a rat focal infarction model. Cortical 15d-PGJ2 in Adv-COX-1-treated rats was increased by 3-fold over control, which was correlated with reduced infarct volume and activated caspase 3, and increased peroxisome proliferator activated receptor-γ (PPARγ) and heme oxygenase-1 (HO-1). Intraventricular infusion of 15d-PGJ2 resulted in reduction of infarct volume, which was abrogated by a PPARγ inhibitor. Rosiglitazone infusion had a similar effect. 15d-PGJ2 and rosiglitazone at low concentrations suppressed H2O2-induced rat or human neuronal apoptosis and necrosis and induced PPARγ and HO-1 expression. The anti-apoptotic effect was abrogated by PPARγ inhibition. Conclusion - 15d-PGJ2 suppressed ischemic brain infarction and neuronal apoptosis and necrosis in a PPARγ dependent manner. 15d-PGJ2 may play a role in controlling acute brain damage induced by ischemia-reperfusion.

頁(從 - 到)481-487
期刊Arteriosclerosis, Thrombosis, and Vascular Biology
出版狀態已發佈 - 3月 2006

ASJC Scopus subject areas

  • 心臟病學與心血管醫學


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