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Vitexin protects dopaminergic neurons in MPTP-induced Parkinson's disease through PI3K/Akt signaling pathway.
Drug Des Devel Ther. 2018; 12:565-573.DD

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease which is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc).

Methods

In this study, the neuroprotective effect of vitexin (Vit), a flavonoid compound isolated from Crataegus pinnatifida Bunge was examined in PD models both in vitro and in vivo.

Results

On SH-SY5Y cells, methyl-4-phenylpyridine (MPP+) treatment suppressed cell viability, induced apoptosis, and increased Bax/Bcl-2 ratio and caspase-3 activity. However, Vit improved these parameters induced by MPP+ treatment significantly. Further study disclosed that Vit enhanced the phosphorylation of PI3K and Akt which was downregulated by MPP+ in SH-SY5Y cells, the effect of which could be blocked by PI3K inhibitor LY294002 and activated by PI3K activator IGF-1. Moreover, results from the pole test and traction test suggested that Vit pretreatment prevented bradykinesia and alleviated the initial lesions caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in MPTP-treated mouse PD model. Vit also enhanced the activation of PI3K and Akt and suppressed the ratio of Bax/Bcl-2 and caspase-3 activity in MPTP-treated mice.

Conclusion

Taken together, this study demonstrated that Vit protected dopaminergic neurons against MPP+/MPTP-induced neurotoxicity through the activation of PI3K/Akt signaling pathway. Our findings may facilitate the clinical application of Vit in the therapy of PD.

Authors+Show Affiliations

Department of Neurology, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China.Department of Neurology, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China.Department of Neurology, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29588573

Citation

Hu, Ming, et al. "Vitexin Protects Dopaminergic Neurons in MPTP-induced Parkinson's Disease Through PI3K/Akt Signaling Pathway." Drug Design, Development and Therapy, vol. 12, 2018, pp. 565-573.
Hu M, Li F, Wang W. Vitexin protects dopaminergic neurons in MPTP-induced Parkinson's disease through PI3K/Akt signaling pathway. Drug Des Devel Ther. 2018;12:565-573.
Hu, M., Li, F., & Wang, W. (2018). Vitexin protects dopaminergic neurons in MPTP-induced Parkinson's disease through PI3K/Akt signaling pathway. Drug Design, Development and Therapy, 12, 565-573. https://doi.org/10.2147/DDDT.S156920
Hu M, Li F, Wang W. Vitexin Protects Dopaminergic Neurons in MPTP-induced Parkinson's Disease Through PI3K/Akt Signaling Pathway. Drug Des Devel Ther. 2018;12:565-573. PubMed PMID: 29588573.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitexin protects dopaminergic neurons in MPTP-induced Parkinson's disease through PI3K/Akt signaling pathway. AU - Hu,Ming, AU - Li,Fangming, AU - Wang,Weidong, Y1 - 2018/03/16/ PY - 2018/3/29/entrez PY - 2018/3/29/pubmed PY - 2018/9/18/medline KW - MPTP KW - PI3K/Akt KW - Parkinson’s disease KW - neuroprotective KW - vitexin SP - 565 EP - 573 JF - Drug design, development and therapy JO - Drug Des Devel Ther VL - 12 N2 - : Parkinson's disease (PD) is a progressive neurodegenerative disease which is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Methods: In this study, the neuroprotective effect of vitexin (Vit), a flavonoid compound isolated from Crataegus pinnatifida Bunge was examined in PD models both in vitro and in vivo. Results: On SH-SY5Y cells, methyl-4-phenylpyridine (MPP+) treatment suppressed cell viability, induced apoptosis, and increased Bax/Bcl-2 ratio and caspase-3 activity. However, Vit improved these parameters induced by MPP+ treatment significantly. Further study disclosed that Vit enhanced the phosphorylation of PI3K and Akt which was downregulated by MPP+ in SH-SY5Y cells, the effect of which could be blocked by PI3K inhibitor LY294002 and activated by PI3K activator IGF-1. Moreover, results from the pole test and traction test suggested that Vit pretreatment prevented bradykinesia and alleviated the initial lesions caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in MPTP-treated mouse PD model. Vit also enhanced the activation of PI3K and Akt and suppressed the ratio of Bax/Bcl-2 and caspase-3 activity in MPTP-treated mice. Conclusion: Taken together, this study demonstrated that Vit protected dopaminergic neurons against MPP+/MPTP-induced neurotoxicity through the activation of PI3K/Akt signaling pathway. Our findings may facilitate the clinical application of Vit in the therapy of PD. SN - 1177-8881 UR - https://www.unboundmedicine.com/medline/citation/29588573/Vitexin_protects_dopaminergic_neurons_in_MPTP_induced_Parkinson's_disease_through_PI3K/Akt_signaling_pathway_ L2 - https://dx.doi.org/10.2147/DDDT.S156920 DB - PRIME DP - Unbound Medicine ER -