Schisandrin A ameliorates MPTP-induced Parkinson’s disease in a mouse model via regulation of brain autophagy

Zhi, Yinghao; Jin, Yongxi; Pan, Lulu; Zhang, Aiguo; Liu, Feiwen

doi:10.1007/s12272-019-01186-1

Cited by 24 publications

(15 citation statements)

References 17 publications

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“…Sonia Angeline et al showed that naringenin or sesamol can improve the reduction in parkin expression and impairment of motor function in a rotenone-exposed rat PD model [ 55 ]. In this study, MK effectively reversed the 6-OHDA-induced inhibition of the expression of PINK1 and parkin to decrease dopaminergic neurodegeneration, an effect that was shown previously for carnosic acid [ 9 ], salidroside [ 56 ], schizandrin A [ 57 ], and Ganoderma lucidum extract [ 58 ].…”

Section: Discussionsupporting

confidence: 76%

Maackiain Ameliorates 6-Hydroxydopamine and SNCA Pathologies by Modulating the PINK1/Parkin Pathway in Models of Parkinson’s Disease in Caenorhabditis elegans and the SH-SY5Y Cell Line

Tsai

Liu

et al. 2020

IJMS

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The movement disorder Parkinson’s disease (PD) is the second most frequently diagnosed neurodegenerative disease, and is associated with aging, the environment, and genetic factors. The intracellular aggregation of α-synuclein and the loss of dopaminergic neurons in the substantia nigra pars compacta are the pathological hallmark of PD. At present, there is no successful treatment for PD. Maackiain (MK) is a flavonoid extracted from dried roots of Sophora flavescens Aiton. MK has emerged as a novel agent for PD treatment that acts by inhibiting monoamine oxidase B. In this study, we assessed the neuroprotective potential of MK in Caenorhabditis elegans and investigated possible mechanism of this neuroprotection in the human SH-SY5Y cell line. We found that MK significantly reduced dopaminergic neuron damage in 6-hydroxydopamine (6-OHDA)-exposed worms of the BZ555 strain, with corresponding improvements in food-sensing behavior and life-span. In transgenic worms of strain NL5901 treated with 0.25 mM MK, the accumulation of α-synuclein was diminished by 27% (p < 0.01) compared with that in untreated worms. Moreover, in worms and the SH-SY5Y cell line, we confirmed that the mechanism of MK-mediated protection against PD pathology may include blocking apoptosis, enhancing the ubiquitin-proteasome system, and augmenting autophagy by increasing PINK1/parkin expression. The use of small interfering RNA to downregulate parkin expression in vivo and in vitro could reverse the benefits of MK in PD models. MK may have considerable therapeutic applications in PD.

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Section: Discussionsupporting

confidence: 76%

Maackiain Ameliorates 6-Hydroxydopamine and SNCA Pathologies by Modulating the PINK1/Parkin Pathway in Models of Parkinson’s Disease in Caenorhabditis elegans and the SH-SY5Y Cell Line

Tsai

Liu

et al. 2020

IJMS

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“…Schisandrin increases levels of TH expression and reduces inflammatory cytokines, however reduction of IL-1Beta and TNF-α were not found to be significant in this case. As in PD, MPTP can induce significant decreases in LC3-II , beclin1 , parkin , and PINK1 , all of which significantly resist depletion after treatment with schisandrin A, suggesting it enhances autophagy [ 124 , 125 , 126 ]. As another lignan, 7-hydroxymatairesinol, found in strawberries and sesame seeds, was recently shown to prevent striatal terminal loss and neuroinflammation in the substantia nigra, and decrease levels of microglial and astrocyte markers.…”

Section: Mechanisms Of Neuroprotectionmentioning

confidence: 99%

The Pathology of Parkinson’s Disease and Potential Benefit of Dietary Polyphenols

et al. 2020

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Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by a loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as olfactory impairment, pain, autonomic dysfunction, impaired sleep, fatigue, and behavioral changes. The pathogenesis of PD is believed to involve oxidative stress, disruption to mitochondria, alterations to the protein α-synuclein, and neuroinflammatory processes. There is currently no cure for the disease. Polyphenols are secondary metabolites of plants, which have shown benefit in several experimental models of PD. Intake of polyphenols through diet is also associated with lower PD risk in humans. In this review, we provide an overview of the pathology of PD and the data supporting the potential neuroprotective capacity of increased polyphenols in the diet. Evidence suggests that the intake of dietary polyphenols may inhibit neurodegeneration and the progression of PD. Polyphenols appear to have a positive effect on the gut microbiome, which may decrease inflammation that contributes to the disease. Therefore, a diet rich in polyphenols may decrease the symptoms and increase quality of life in PD patients.

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“…It has been previously shown to protect against acute myocardial ischemia through the phosphoinositide 3-kinase (PI3K)/Akt-NADPH oxidase 2 (NOX2) signaling pathway [ 28 ]. In addition, Schisandrol A has been used to treat neurological disorders in many studies [ 41 , 42 , 43 ]. It has been reported to improve learning and memory impairment and attenuate β-amyloid deposition in a mouse model of Alzheimer’s disease by ameliorating neurotransmitter dysfunction [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Schisandrol A Suppresses Catabolic Factor Expression by Blocking NF-κB Signaling in Osteoarthritis

et al. 2021

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Schisandrol A possesses pharmacological properties and is used to treat various diseases; however, its effects on osteoarthritis (OA) progression remain unclear. Here, we investigated Schisandrol A as a potential therapeutic agent for OA. In vitro, Schisandrol A effects were confirmed based on the levels of expression of catabolic factors (MMPs, ADAMTS5, and Cox2) induced by IL-1β or Schisandrol A treatment in chondrocytes. In vivo, experimental OA in mice was induced using a destabilized medial meniscus (DMM) surgical model or oral gavage of Schisandrol A in a dose-dependent manner, and demonstrated using histological analysis. In vitro and in vivo analyses demonstrated that Schisandrol A inhibition attenuated osteoarthritic cartilage destruction via the regulation of Mmp3, Mmp13, Adamts5, and Cox2 expression. In the NF-κB signaling pathway, Schisandrol A suppressed the degradation of IκB and the phosphorylation of p65 induced by IL-1β. Overall, and Schisandrol A reduced the expression of catabolic factors by blocking NF-κB signaling and prevented cartilage destruction. Therefore, Schisandrol A attenuated OA progression, and can be used to develop novel OA drug therapies.

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Schisandrin A ameliorates MPTP-induced Parkinson’s disease in a mouse model via regulation of brain autophagy

Cited by 24 publications

References 17 publications

Maackiain Ameliorates 6-Hydroxydopamine and SNCA Pathologies by Modulating the PINK1/Parkin Pathway in Models of Parkinson’s Disease in Caenorhabditis elegans and the SH-SY5Y Cell Line

Maackiain Ameliorates 6-Hydroxydopamine and SNCA Pathologies by Modulating the PINK1/Parkin Pathway in Models of Parkinson’s Disease in Caenorhabditis elegans and the SH-SY5Y Cell Line

The Pathology of Parkinson’s Disease and Potential Benefit of Dietary Polyphenols

Schisandrol A Suppresses Catabolic Factor Expression by Blocking NF-κB Signaling in Osteoarthritis

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