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Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson's Disease.
Chin J Integr Med. 2018 Nov; 24(11):835-843.CJ

Abstract

OBJECTIVE

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).

METHODS

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).

RESULTS

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.

CONCLUSIONS

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.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Liu SM
Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Li XZ
Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, 150040, China. Department of Pharmacy, Guiyang College of Traditional Chinese Medicine, Guiyang, 550025, China.
Zhang SN
Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, 150040, China. Department of Pharmacy, Guiyang College of Traditional Chinese Medicine, Guiyang, 550025, China.
Yang ZM
Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Wang KX
Drug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Lu F
Institute of Traditional Chinese Medicine, Heilongjiang University of Chinese Medicine, Harbin, 150040, China. lufang_19790501@163.com.
Wang CZ
Tang Center for Herbal Medicine Research, and Department of Anesthesia and Critical Care, University of Chicago, Chicago, IL, 60637, USA.
Yuan CS
Tang Center for Herbal Medicine Research, and Department of Anesthesia and Critical Care, University of Chicago, Chicago, IL, 60637, USA.

MeSH

AnimalsEleutherococcusMPTP PoisoningMaleMembrane Potential, MitochondrialMesencephalonMiceMice, Inbred C57BLMitochondrial SwellingNeuroprotective AgentsPlant Extracts

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30090975

Citation

Liu, Shu-Min, et al. "Acanthopanax Senticosus Protects Structure and Function of Mesencephalic Mitochondria in a Mouse Model of Parkinson's Disease." Chinese Journal of Integrative Medicine, vol. 24, no. 11, 2018, pp. 835-843.
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. 2018;24(11):835-843.
Liu, S. M., Li, X. Z., Zhang, S. N., Yang, Z. M., Wang, K. X., Lu, F., Wang, C. Z., & Yuan, C. S. (2018). Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson's Disease. Chinese Journal of Integrative Medicine, 24(11), 835-843. https://doi.org/10.1007/s11655-018-2935-5
Liu SM, et al. Acanthopanax Senticosus Protects Structure and Function of Mesencephalic Mitochondria in a Mouse Model of Parkinson's Disease. Chin J Integr Med. 2018;24(11):835-843. PubMed PMID: 30090975.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acanthopanax senticosus Protects Structure and Function of Mesencephalic Mitochondria in A Mouse Model of Parkinson's Disease. AU - Liu,Shu-Min, AU - Li,Xu-Zhao, AU - Zhang,Shuai-Nan, AU - Yang,Zhi-Ming, AU - Wang,Ke-Xin, AU - Lu,Fang, AU - Wang,Chong-Zhi, AU - Yuan,Chun-Su, Y1 - 2018/08/08/ PY - 2016/06/29/accepted PY - 2018/8/10/pubmed PY - 2019/2/6/medline PY - 2018/8/10/entrez KW - Acanthopanax senticosus Harms KW - Parkinson’s disease KW - mitochondrial dysfunction KW - mitochondrial structural damage KW - oxidative phosphorylation system SP - 835 EP - 843 JF - Chinese journal of integrative medicine JO - Chin J Integr Med VL - 24 IS - 11 N2 - OBJECTIVE: 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). METHODS: 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). RESULTS: 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. CONCLUSIONS: 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. SN - 1672-0415 UR - https://www.unboundmedicine.com/medline/citation/30090975/Acanthopanax_senticosus_Protects_Structure_and_Function_of_Mesencephalic_Mitochondria_in_A_Mouse_Model_of_Parkinson's_Disease_ DB - PRIME DP - Unbound Medicine ER -