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Polyamine analogue QMA attenuated ischemic injury in MCAO rats via ERK and Akt activated Nrf2/HO-1 signaling pathway.

Juan Cen | Na Zhao | Wei-Wei Huang | Lu Liu | Yuan-Yuan Xie | Ying Gan | Chao-Jie Wang | Bian-Sheng Ji
European journal of pharmacology | 2019

Previous research showed N1-(quinolin-2-ylmethy) butane-1, 4-diamine (QMA), a polyamine analogue, was efficacious in the prevention of oxidative injury in models of cerebral ischemia. The present study manifested that pretreatment with QMA attenuated ischemic damage accompanying up regulation of Nuclear factor erythroid 2‑related factor (Nrf2), Heme oxygenase‑1 (HO‑1), p-ERK and p-Akt in cerebral cortex tissues of middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation (OGD)-treated PC12 cells. Further more, treatment with LY294002 (specific PI3K inhibitor), PD98059 (specific ERK inhibitor), brusatol (specific Nrf2 inhibitor) and SnPP (specific HO-1 inhibitor) deprived almost all the effects of QMA in MCAO rats and OGD-treated PC12 cells. These data suggested that the protective actions of QMA on the cerebral ischemia may be related to activation of endogenous cytoprotective mechanism via ERK and Akt activated Nrf2/HO-1 signaling pathway.

Pubmed ID: 30550742

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Cell Signaling Technology (tool)

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Privately held company that develops and produces antibodies, ELISA kits, ChIP kits, proteomic kits, and other related reagents used to study cell signaling pathways that impact human health.

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SNPP (tool)

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THIS RESOURCE IS NO LONGER IN SERVICE, documented September 29, 2016. A dynamic general database management system to manage high-throughput SNP genotyping data. It provides several functions, including data importing with comparison, Mendelian inheritance check within pedigrees, data compiling and exporting. Furthermore, SNPP may generate files for repeat genotyping and transform them into files that can be executed by a liquid handling system.

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