Pinocembrin attenuates MPP+-induced neurotoxicity by the induction of heme oxygenase-1 through ERK1/2 pathway. (26th January 2016)

• Record Type: Journal Article
• Authors: Wang, Hongquan; Wang, Yumin; Zhao, Linan; Cui, Qifu; Wang, Yuehua; Du, Guanhua
• Is Part Of: Neuroscience letters. Volume 612(2016)
• Page Start: 104
• Page End: 109
• Publication Date: 2016-01-26
• Subjects: Parkinson's disease -- Pinocembrin -- MPP+ -- Heme oxygenase-1 -- Neuroprotection; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.11.048
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Pinocembrin exerts a neuroprotective effect against MPP + -induced neurotoxicity in SH-SY5Y cells. Pinocembrin induces expression of heme oxygenase-1 through ERK1/2 pathway. Pinocembrin attenuates MPP + -induced neurotoxicity by the induction of heme oxygenase-1 expression. Abstract: Our recent study demonstrated that pinocembrin (PB), the most abundant flavonoid in propolis, has neuroprotective effect against 1-methyl-4-phenylpyridinium (MPP + )-induced SH-SY5Y neurotoxicity. However, the mechanism as how PB can induce neuroprotection is not known. In the present study, we demonstrate here that PB increased heme oxygenase-1 (HO-1) expression, which conferred protection against MPP + -induced cytotoxicity, because the inhibitor of HO-1 zinc protoporphyrin-IX attenuated the neuroprotection of PB. PB induced the phosphorylation of ERK1/2, and its cytoprotective effect was abolished by ERK1/2 inhibitors. Meanwhile, we have shown that MPP + induce the expression in a concentration-dependent manner in SH-SY5Y cells, which was further enhanced by PB. Taken together, the results suggest that PB enhances HO-1 expression to suppress MPP + -induced oxidative damage via ERK1/2 signaling pathways. These results revealed the mechanisms of PB enhances HO-1 expression, and contribute to shed some light on the mechanisms whereby PB inhibits the MPP + -induced neurotoxicity. These data indicated that PB might provide a valuable therapeutic strategy for the treatment of PD.