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Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells

BACKGROUND: Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. Paeonolum, a main component isolated fr...

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Autores principales: Lu, Xi-Lin, Lin, Yue-Hao, Wu, Qi, Su, Feng-Juan, Ye, Cheng-Hui, Shi, Lei, He, Bai-Xuan, Huang, Fei-Wen, Pei, Zhong, Yao, Xiao-Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422610/
https://www.ncbi.nlm.nih.gov/pubmed/25925762
http://dx.doi.org/10.1186/s12906-015-0661-0
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author Lu, Xi-Lin
Lin, Yue-Hao
Wu, Qi
Su, Feng-Juan
Ye, Cheng-Hui
Shi, Lei
He, Bai-Xuan
Huang, Fei-Wen
Pei, Zhong
Yao, Xiao-Li
author_facet Lu, Xi-Lin
Lin, Yue-Hao
Wu, Qi
Su, Feng-Juan
Ye, Cheng-Hui
Shi, Lei
He, Bai-Xuan
Huang, Fei-Wen
Pei, Zhong
Yao, Xiao-Li
author_sort Lu, Xi-Lin
collection PubMed
description BACKGROUND: Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. Paeonolum, a main component isolated from Moutan cortex, has potent antioxidant ability. Here, we have examined the effects of paeonolum against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells. METHODS: The overall viability and neurodegeneration of DA neurons was assessed in ETvmat2:green fluorescent protein (GFP) transgenic zebrafish, in which most monoaminergic neurons are labeled by GFP. Damage to PC12 cells was measured using a cell viability assay and assessment of nuclear morphology. Intracellular reactive oxygen species (ROS) and the level of total GSH were assessed. The mitochondrial cell death pathway including mitochondrial membrane potential, cytochrome C release and caspase-3 activity were also examined in PC12 cells. RESULTS: Paeonolum protected against MPP(+)-induced DA neurodegeneration and locomotor dysfunction in zebrafish in a concentration-dependent manner. Similar neuroprotection was replicated in the PC12 cellular model of MPP(+) toxicity. Paeonolum attenuated MPP(+)-induced intracellular ROS accumulation and restored the level of total GSH in PC12 cells. Furthermore, paeonolum significantly inhibited the mitochondrial cell death pathway induced by MPP(+). CONCLUSIONS: Collectively, the present study demonstrates that paeonolum protects zebrafish and PC12 cells against MPP(+)-induced neurotoxicity.
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spelling pubmed-44226102015-05-07 Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells Lu, Xi-Lin Lin, Yue-Hao Wu, Qi Su, Feng-Juan Ye, Cheng-Hui Shi, Lei He, Bai-Xuan Huang, Fei-Wen Pei, Zhong Yao, Xiao-Li BMC Complement Altern Med Research Article BACKGROUND: Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting 2% of the population aged over 65 years old. Mitochondrial defects and oxidative stress actively participate in degeneration of dopaminergic (DA) neurons in PD. Paeonolum, a main component isolated from Moutan cortex, has potent antioxidant ability. Here, we have examined the effects of paeonolum against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells. METHODS: The overall viability and neurodegeneration of DA neurons was assessed in ETvmat2:green fluorescent protein (GFP) transgenic zebrafish, in which most monoaminergic neurons are labeled by GFP. Damage to PC12 cells was measured using a cell viability assay and assessment of nuclear morphology. Intracellular reactive oxygen species (ROS) and the level of total GSH were assessed. The mitochondrial cell death pathway including mitochondrial membrane potential, cytochrome C release and caspase-3 activity were also examined in PC12 cells. RESULTS: Paeonolum protected against MPP(+)-induced DA neurodegeneration and locomotor dysfunction in zebrafish in a concentration-dependent manner. Similar neuroprotection was replicated in the PC12 cellular model of MPP(+) toxicity. Paeonolum attenuated MPP(+)-induced intracellular ROS accumulation and restored the level of total GSH in PC12 cells. Furthermore, paeonolum significantly inhibited the mitochondrial cell death pathway induced by MPP(+). CONCLUSIONS: Collectively, the present study demonstrates that paeonolum protects zebrafish and PC12 cells against MPP(+)-induced neurotoxicity. BioMed Central 2015-04-29 /pmc/articles/PMC4422610/ /pubmed/25925762 http://dx.doi.org/10.1186/s12906-015-0661-0 Text en © Lu et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Lu, Xi-Lin
Lin, Yue-Hao
Wu, Qi
Su, Feng-Juan
Ye, Cheng-Hui
Shi, Lei
He, Bai-Xuan
Huang, Fei-Wen
Pei, Zhong
Yao, Xiao-Li
Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title_full Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title_fullStr Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title_full_unstemmed Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title_short Paeonolum protects against MPP(+)-induced neurotoxicity in zebrafish and PC12 cells
title_sort paeonolum protects against mpp(+)-induced neurotoxicity in zebrafish and pc12 cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422610/
https://www.ncbi.nlm.nih.gov/pubmed/25925762
http://dx.doi.org/10.1186/s12906-015-0661-0
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