☆ 4.5 Article

Hyperoside Reduces Rotenone-induced Neuronal Injury by Suppressing Autophagy

NEUROCHEMICAL RESEARCH (2021)

Journal

NEUROCHEMICAL RESEARCH

Volume 46, Issue 12, Pages 3149-3158

Publisher

SPRINGER/PLENUM PUBLISHERS

DOI: 10.1007/s11064-021-03404-z

Keywords

Hyperoside; Rotenone; Parkinson's disease; Autophagy; Neuroprotective

Funding

National Natural Science Foundation of China [81703978, 81102552]
Central Government Guided Local Funding Projects for Science and Technology Development [YDZX20201400001483]
Outstanding Youth Talents Program of Shanxi Province [[2019]35]
Natural Science Foundation of Shanxi Province [201901D111334]
Returned Chinese Scholars Technology Activities Preferred Project, Shanxi Province of China [20200026]
Shanxi Scholarship Council [2021-142]
Shanxi university Science and technology innovation Project [2019L0724]
Young Scientist Cultivation Program Project, Shanxi University of Chinese Medicine [2021PY-QN-03]

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Abstract

Hyperoside has shown neuroprotective effects in rotenone-induced PD rat model and SH-SY5Y cell model by affecting autophagy pathways, providing potential therapeutic benefits for Parkinson's disease treatment.

Hyperoside has a variety of pharmacological activities, including anti-liver injury, anti-depression, anti-inflammatory, and anti-cancer activities. However, the effect of hyperoside on Parkinson's disease (PD) is still unclear. Therefore, we tried to study the therapeutic effect and mechanism of hyperoside on PD in vivo and in vitro models. Rotenone was used to induce PD rat model and SH-SY5Y cell injury model, and hyperoside was used for intervention. Immunohistochemistry, animal behavior assays, TUNEL and Western blot were constructed to observe the protective effect and related mechanisms of hyperoside in vivo. Cell counting kit-8 (CCK-8), flow cytometry, Rh123 staining and Western blot were used for in vitro assays. Rapamycin (RAP) pretreatment was used in rescue experiments to verify the relationship between hyperoside and autophagy in rotenone-induced SH-SY5Y cells. Hyperoside promoted the number of tyrosine hydroxylase (TH)-positive cells, improved the behavioral defects of rats, and inhibited cell apoptosis in vivo. Different concentrations of hyperoside had no significant effect on SH-SY5Y cell viability, but dramatically reversed the rotenone-induced decrease in cell viability, increased apoptosis and loss of cell mitochondrial membrane potential in vitro. Additionally, hyperoside reversed the regulation of rotenone on the Beclin1, LC3II, Bax, cleaved caspase 3, Cyc and Bcl-2 expressions in rat SNpc tissues and SH-SY5Y cells, while promoted the regulation of rotenone on the P62 and alpha-synuclcin. Furthermore, RAP reversed the effect of hyperoside on rotenone-induced SH-SY5Y cells. Hyperoside may play a neuroprotective effect in rotenone-induced PD rat model and SH-SY5Y cell model by affecting autophagy.

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Neuroprotective and therapeutic effects of calcitriol in rotenone-induced Parkinson's disease rat model

Alshimaa Magdy, Eman A. E. Farrag, Shereen Mohamed Hamed, Zienab Abdallah, Eman Mohamad El Nashar, Mansour Abdullah Alghamdi, Amira A. H. Ali, Marwa Abd El-kader

Summary: Parkinson's disease (PD) is the second most common neurodegenerative disease, and current treatment strategies only provide symptomatic relief. Recent studies have shown that calcitriol, a form of vitamin D3, has neuroprotective effects in PD by modulating autophagy and the Sirt1/NF-kappa B pathway. This study demonstrated that calcitriol administration improved behavioral impairments and dopaminergic neuron depletion in a rotenone-induced PD model, and attenuated neuroinflammation and autophagy dysfunction. These findings suggest that calcitriol may have a neuroprotective and restorative effect in PD.

FRONTIERS IN CELLULAR NEUROSCIENCE (2022)