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Background Neuroinflammation plays a prominent role in the pathogenesis of Parkinson’s disease (PD), and microglial activation contributes to initiating and maintaining brain inflammation and neuronal death. 5-Lipoxygenase (5LOX) is a key enzyme catalyzing arachidonic acid to produce cysteinyl leukotrienes (CysLTs). CysLTs are potent proinflammatory mediators, and their actions are mediated by activating CysLT receptors. We recently reported that rotenone time- and concentration-dependently induced 5-LOX translocation into the nuclear envelope (a key event for 5-LOX activation) and cell injury in PC12 cells, and the 5-LOX selective inhibitor zileuton attenuated rotenone-induced 5-LOX activation and cell injury. To determine the role of 5-LOX pathway in microglial-dependent neuroinflammation, we investigated the changes of 5-LOX and CysLT1 receptor in a cell model of PD induced by specific mitochondrial complex I inhibitors (rotenone or 1-methyl-4-phenylpyridinium (MPP + )) in BV2 microglial cells. Methods BV2 cells, a murine BV2 microglia cell line, were cultured in media with or without rotenone (0.1, 0.3, 1, 3, 10 nM) or MPP + (0.003, 0.01, 0.03, 0.1, 0.3 μM) for 24

Involvement of 5-lipoxygenase/cysteinyl leukotriene receptor 1 in rotenone- and MPP+-induced BV2 microglial activation