Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease

Chien Wei Feng; Han Chun Hung; Shi Ying Huang; Chun Hong Chen; Yun Ru Chen; Chun Yu Chen; San Nan Yang; Hui Min David Wang; Ping Jyun Sung; Jyh Horng Sheu; Kuan Hao Tsui; Wu Fu Chen; Zhi Hong Wen

doi:10.3390/md14100187

Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease

Chien Wei Feng
, Han Chun Hung
, Shi Ying Huang
, Chun Hong Chen
, Yun Ru Chen
, Chun Yu Chen
, San Nan Yang
, Hui Min David Wang
, Ping Jyun Sung
, Jyh Horng Sheu
, Kuan Hao Tsui
, Wu Fu Chen^*
, Zhi Hong Wen

^*Corresponding author for this work

National Sun Yat-sen University
Academia Sinica Taiwan HQ
Quanzhou Normal University
Academia Sinica - Genomics Research Center
I-Shou University
National Chung Hsing University
Kaohsiung Medical University
China Medical University Taichung
National Dong Hwa University
National Museum of Marine Biology and Aquarium, Taiwan
Veterans General Hospital-Kaohsiung Taiwan
National Yang Ming Chiao Tung University
Tajen University
Chang Gung University

Research output: Contribution to journal › Journal Article › peer-review

52 Scopus citations

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.

Original language	English
Article number	187
Journal	Marine Drugs
Volume	14
Issue number	10
DOIs	https://doi.org/10.3390/md14100187
State	Published - 10 2016
Externally published	Yes

Bibliographical note

Publisher Copyright:
© 2016 by the authors.

Keywords

CREB
DJ-1
HO-1
Neuroprotection
Parkinson's disease
Zebrafish

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10.3390/md14100187

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Feng, C. W., Hung, H. C., Huang, S. Y., Chen, C. H., Chen, Y. R., Chen, C. Y., Yang, S. N., Wang, H. M. D., Sung, P. J., Sheu, J. H., Tsui, K. H., Chen, W. F., & Wen, Z. H. (2016). Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease. Marine Drugs, 14(10), Article 187. https://doi.org/10.3390/md14100187

@article{15270d96e4c548558b1a4407c5009b63,

title = "Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease",

abstract = "Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.",

keywords = "CREB, DJ-1, HO-1, Neuroprotection, Parkinson's disease, Zebrafish",

author = "Feng, \{Chien Wei\} and Hung, \{Han Chun\} and Huang, \{Shi Ying\} and Chen, \{Chun Hong\} and Chen, \{Yun Ru\} and Chen, \{Chun Yu\} and Yang, \{San Nan\} and Wang, \{Hui Min David\} and Sung, \{Ping Jyun\} and Sheu, \{Jyh Horng\} and Tsui, \{Kuan Hao\} and Chen, \{Wu Fu\} and Wen, \{Zhi Hong\}",

note = "Publisher Copyright: {\textcopyright} 2016 by the authors.",

year = "2016",

month = oct,

doi = "10.3390/md14100187",

language = "英语",

volume = "14",

journal = "Marine Drugs",

issn = "1660-3397",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

number = "10",

}

Feng, CW, Hung, HC, Huang, SY, Chen, CH, Chen, YR, Chen, CY, Yang, SN, Wang, HMD, Sung, PJ, Sheu, JH, Tsui, KH, Chen, WF & Wen, ZH 2016, 'Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease', Marine Drugs, vol. 14, no. 10, 187. https://doi.org/10.3390/md14100187

TY - JOUR

T1 - Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease

AU - Feng, Chien Wei

AU - Hung, Han Chun

AU - Huang, Shi Ying

AU - Chen, Chun Hong

AU - Chen, Yun Ru

AU - Chen, Chun Yu

AU - Yang, San Nan

AU - Wang, Hui Min David

AU - Sung, Ping Jyun

AU - Sheu, Jyh Horng

AU - Tsui, Kuan Hao

AU - Chen, Wu Fu

AU - Wen, Zhi Hong

PY - 2016/10

Y1 - 2016/10

N2 - Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.

AB - Parkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, bradykinesia, and gait impairment. In a previous study, we found that the marine-derived compound 11-dehydrosinulariolide (11-de) upregulates the Akt/PI3K pathway to protect cells against 6-hydroxydopamine (6-OHDA)-mediated damage. In the present study, SH-SY5Y, zebrafish and rats were used to examine the therapeutic effect of 11-de. The results revealed the mechanism by which 11-de exerts its therapeutic effect: the compound increases cytosolic or mitochondrial DJ-1 expression, and then activates the downstream Akt/PI3K, p-CREB, and Nrf2/HO-1 pathways. Additionally, we found that 11-de could reverse the 6-OHDA-induced downregulation of total swimming distance in a zebrafish model of PD. Using a rat model of PD, we showed that a 6-OHDA-induced increase in the number of turns, and increased time spent by rats on the beam, could be reversed by 11-de treatment. Lastly, we showed that 6-OHDA-induced attenuation in tyrosine hydroxylase (TH), a dopaminergic neuronal marker, in zebrafish and rat models of PD could also be reversed by treatment with 11-de. Moreover, the patterns of DJ-1 expression observed in this study in the zebrafish and rat models of PD corroborated the trend noted in previous in vitro studies.

KW - CREB

KW - DJ-1

KW - HO-1

KW - Neuroprotection

KW - Parkinson's disease

KW - Zebrafish

UR - https://www.scopus.com/pages/publications/84992724459

U2 - 10.3390/md14100187

DO - 10.3390/md14100187

M3 - 文章

C2 - 27763504

AN - SCOPUS:84992724459

SN - 1660-3397

VL - 14

JO - Marine Drugs

JF - Marine Drugs

IS - 10

M1 - 187

ER -

Neuroprotective effect of the marine-derived compound 11-dehydrosinulariolide through DJ-1-related pathway in in vitro and in vivo models of Parkinson's disease

Abstract

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Keywords

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