FOLLOWUS
Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson’s Disease
- Chinese Journal of Integrative Medicine Vol. 24, Issue 11, Pages: 835-843(2018)
- Affiliations：
1. Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine,Harbin,China
2. Department of Pharmacy, Guiyang College of Traditional Chinese Medicine,Guiyang,China
3. Institute of Traditional Chinese Medicine, Heilongjiang University of Chinese Medicine,Harbin,China
4. Tang Center for Herbal Medicine Research, and Department of Anesthesia and Critical Care, University of Chicago,Chicago,USA
- Author bio：
- Funds：Supported by the National Natural Science Foundation of China (No. 81270056), China Postdoctoral Science Foundation (No. 2013T60398), Scientific Research grants of Postdoctoral Researchers Settled in Heilongjiang (No. LBH-Q13160), Outstanding Talents Cultivation Fund of Heilongjiang University of Chinese Medicine (No. 2013jc01), and the Outstanding Innovative Talent Support Programs of Heilongjiang University of Chinese Medicine
DOI：10.1007/s11655-018-2935-5
CLC：Published：2018，
Published Online：8 August 2018，
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Liu, Sm., Li, Xz., Zhang, Sn. et al. Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson’s Disease., Chin. J. Integr. Med. 24, 835–843 (2018). https://doi.org/10.1007/s11655-018-2935-5
Shu-min Liu, Xu-zhao Li, Shuai-nan Zhang, et al. Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson’s Disease. [J]. Chinese Journal of Integrative Medicine 24(11):835-843(2018)
Liu, Sm., Li, Xz., Zhang, Sn. et al. Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson’s Disease., Chin. J. Integr. Med. 24, 835–843 (2018). https://doi.org/10.1007/s11655-018-2935-5 DOI：
Shu-min Liu, Xu-zhao Li, Shuai-nan Zhang, et al. Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson’s Disease. [J]. Chinese Journal of Integrative Medicine 24(11):835-843(2018) DOI： 10.1007/s11655-018-2935-5.
摘要
To investigate the neuro-protective effects of Acanthopanax senticosus Harms (EAS) on mesencephalic mitochondria and the mechanism of action
using a mouse model of Parkinson’s disease (PD). The chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms (EAS) was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group
the MPTP model group
and the EAS treated group with MPTP (MPTP+EAS group
10 in each group). The MPTP model group and the MPTP+EAS group received MPTP-HCl (30 mg/kg i.p) once a day for 5 days. The control group received an equal volume of saline (20 mL/kg i.p) once a day for 5 days. Induced by 1-methyl-4-phenyl-1
2
3
6-tetrahydropyridine hydrochloride daily (MPTP-HCl
30 mg/kg) for 5 days
the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model
including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2 (NDUFV2)
mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1 (MT-ND1)
succinate dehydrogenase complex subunit A (SDHA)
and succinate dehydrogenase cytochrome b560 subunit (SDHC). After treatment with EAS
the behavioral changes induced by MPTP were attenuated significantly (P<0.05). EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential (both P<0.05)
which was supported by an ultra-structural level analysis. The changes in reactive oxygen species (ROS)
malonic dialdehyde (MDA)
oxidative phosphorylation (OXPHOS) system 4 subunits levels and PD-related proteins expressions (parkin
Pink1
DJ-1
α-synuclein
and Lrrk2) reverted to near normal levels (all P<0.05)
based on the results of immune-histological and Western blotting observations. The neuro-protective effects of EAS are linked to protecting mice against MPTP-induced mitochondrial dysfunction and structural damage. Therefore
EAS is a promising candidate for the prevention or treatment of mitochondrial neurodegenerative disorders
such as PD.
Abstract
To investigate the neuro-protective effects of Acanthopanax senticosus Harms (EAS) on mesencephalic mitochondria and the mechanism of action
using a mouse model of Parkinson’s disease (PD). The chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms (EAS) was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group
the MPTP model group
and the EAS treated group with MPTP (MPTP+EAS group
10 in each group). The MPTP model group and the MPTP+EAS group received MPTP-HCl (30 mg/kg i.p) once a day for 5 days. The control group received an equal volume of saline (20 mL/kg i.p) once a day for 5 days. Induced by 1-methyl-4-phenyl-1
2
3
6-tetrahydropyridine hydrochloride daily (MPTP-HCl
30 mg/kg) for 5 days
the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model
including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2 (NDUFV2)
mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1 (MT-ND1)
succinate dehydrogenase complex subunit A (SDHA)
and succinate dehydrogenase cytochrome b560 subunit (SDHC). After treatment with EAS
the behavioral changes induced by MPTP were attenuated significantly (P<0.05). EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential (both P<0.05)
which was supported by an ultra-structural level analysis. The changes in reactive oxygen species (ROS)
malonic dialdehyde (MDA)
oxidative phosphorylation (OXPHOS) system 4 subunits levels and PD-related proteins expressions (parkin
Pink1
DJ-1
α-synuclein
and Lrrk2) reverted to near normal levels (all P<0.05)
based on the results of immune-histological and Western blotting observations. The neuro-protective effects of EAS are linked to protecting mice against MPTP-induced mitochondrial dysfunction and structural damage. Therefore
EAS is a promising candidate for the prevention or treatment of mitochondrial neurodegenerative disorders
such as PD.
关键词
Acanthopanax senticosus HarmsParkinson’s diseasemitochondrial dysfunctionmitochondrial structural damageoxidative phosphorylation system
Keywords
Acanthopanax senticosus HarmsParkinson’s diseasemitochondrial dysfunctionmitochondrial structural damageoxidative phosphorylation system
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