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Pinocembrin Protects SH-SY5Y Cells Against MPP+-Induced Neurotoxicity Through the Mitochondrial Apoptotic Pathway

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Abstract

Pinocembrin (PB), the most abundant flavonoid in propolis, has been proven to have neuroprotective property against neurotoxicity in vivo and in vitro. Our recent study demonstrated the neuroprotective effect of PB against Aβ25–35-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 abrogates the effects of the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) which mimics Parkinson’s disease (PD) with elevation of intracellular reactive oxygen species (ROS) level and apoptotic death. We found that pretreatment of SH-SY5Y cells with PB significantly reduced the MPP+-induced loss of cell viability, the generation of intracellular ROS, apoptotic rate, and the cleavage of caspase-3. PB strikingly inhibited MPP+-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio, and the release of cytochrome c. Overall, these results suggest that PB is intimately involved in inhibiting MPP+-induced loss of mitochondrial function and induction of apoptosis that contributes toward neuronal survival. These data indicated that PB might provide a valuable therapeutic strategy for the treatment of PD.

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Acknowledgments

This work was supported in part by the National Natural Science Foundation of China (81260196 to HW; 81201844 to JZ), Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region (NJYT-13-B20) to HW, Scientific Research Projects in Universities of Inner Mongolia Autonomous Region (NJSZ12306) to HW, and Beijing Natural Science Foundation Proposed Program (7132137) to JG.

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Correspondence to Hongquan Wang.

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Wang, Y., Gao, J., Miao, Y. et al. Pinocembrin Protects SH-SY5Y Cells Against MPP+-Induced Neurotoxicity Through the Mitochondrial Apoptotic Pathway. J Mol Neurosci 53, 537–545 (2014). https://doi.org/10.1007/s12031-013-0219-x

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