Pinocembrin Protects SH-SY5Y Cells Against MPP+-Induced Neurotoxicity Through the Mitochondrial Apoptotic Pathway |
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Authors: | Yumin Wang Junhong Gao Yingchun Miao Qifu Cui Weili Zhao Junyi Zhang Hongquan Wang |
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Institution: | 1. Chifeng Medical College, Chifeng University, Chifeng, 024005, People’s Republic of China 2. Department of Oncology, The Affiliated Hospital of Chifeng University, Chifeng, 024005, People’s Republic of China 3. Institute of Acupuncture, China Academy of Chinese Medical Sciences, Beijing, 100700, People’s Republic of China 4. Department of Geriatrics, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, People’s Republic of China 5. Department of Neurology, The Affiliated Hospital of Chifeng University, Chifeng, 024005, People’s Republic of China 6. Department of Neurology, The Affiliated Hospital, Chifeng Medical College, Chifeng University, Chifeng, 024005, Inner Mongolia, People’s Republic of China
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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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