Abstract
Purpose: To investigate the role and mechanism of action of breviscapine (Brp) in 1-methyl-4- phenylpyridinium ion (MPP+)-induced cell injury in human neuroblastoma cell line, SH-SY5Y.Methods: The injury on SH-SY5Y cells was induced using MPP+. Cell viability and apoptotic ability were determined by CCK8 assay and Annexin V/PI staining, respectively. Protein expressions of nuclear factor E2-related factor 2 (Nrf2) and its related downstream proteins - hemeoxygenase 1(HO-1) and NAD(P)H-quinoneoxido reductase 1(NQO1), were determined using Western blotting.Results: Brp dose-dependently attenuated MPP+ induced reduction in the viability of SH SY5Y cells, but alleviated MPP+-induced oxidative stress (OS) and cell injury, as evidenced by the levels of reactive oxygen species (ROS), tyrosine hydroxylase (TH), lactic dehydrogenase (LDH), and dopaminetransporter (DAT) (p < 0.05). Brp decreased the amount of apoptotic cells induced by MPP+, as well as the protein levels of Bax and cleaved-caspase 3, and also induced the activation of Nrf2 signaling pathway (p < 0.05).Conclusion: Brp alleviates MPP+-induced cellular damage and cell apoptosis in SH-SY5Y cells by activating Nrf2 pathway. Thus, Brp is a potential therapeutic candidate for the treatment of PD.
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