Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 53, Issue 4, Pages 537-545Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-013-0219-x
Keywords
Parkinson's disease; Pinocembrin; MPP+; Oxidative stress; Neuroprotection
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Funding
- National Natural Science Foundation of China [81260196, 81201844]
- Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region [NJYT-13-B20]
- Scientific Research Projects in Universities of Inner Mongolia Autonomous Region [NJSZ12306]
- Beijing Natural Science Foundation Proposed Program [7132137]
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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 A beta(25-35)-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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