Cordycepin mitigates MPTP-induced Parkinson's disease through inhibiting TLR/NF-κB signaling pathway

Cheng, Chun‐Yan; Zhu, Xiaoying

doi:10.1016/j.lfs.2019.02.037

Cited by 41 publications

(31 citation statements)

References 32 publications

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“…Oxidative stress has been a major area for preclinical research in PD. Many animal studies have tested extracts from various common edible plants with antioxidant activity, such as ginseng, 38 turmeric, 39 and cordyceps sinensis, 40 in reducing onset or symptoms in animal models of PD. Others have focused on antioxidative vitamins, such as vitamin C 41 and vitamin E, 12,42 and found them to reduce the development of PD in these experimental models.…”

Section: Discussionmentioning

confidence: 99%

Dietary Antioxidants and Risk of Parkinson's Disease in the Singapore Chinese Health Study

Ying

Khan

et al. 2020

Movement Disorders

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A BS TRACT: Background: Despite experimental evidence implicating oxidative stress in the pathogenesis of PD, epidemiological studies have provided inconsistent associations between dietary antioxidants and risk of developing PD. Furthermore, no study has been done in any Asian population. Objectives: We examined the associations for intake levels of dietary carotenoids (α-carotene, β-carotene, lycopene, β-cryptoxanthin, and lutein) and vitamins (vitamin A, C and E) and the risk of developing PD. Methods: We used data from the Singapore Chinese Health Study, a population-based prospective cohort of 63,257 men and women aged 45 to 74 years during enrollment in 1993-1998. Antioxidant intake was derived from a validated semiquantitative food frequency questionnaire. Incident cases were identified through followup interviews, hospital records, or PD registries through 31 July 2018. Hazard ratios and corresponding 95% confidence intervals were derived from multivariable Cox proportional hazard regression models with adjustment for other lifestyle and dietary factors. Results: During an average 19.4 years of follow-up, 544 incident PD cases were identified. No association was found for dietary carotenoids, individually or summed. Hazard ratio comparing highest to lowest quartile for total carotenoids was 0.98 (95% confidence interval: 0.76-1.28; P trend = 0.83). There were also no clear dose-dependent associations of dietary vitamins A, C, and E with risk of developing PD (all P trend ≥ 0.10). Sensitive analyses with lag time and excluding supplement use did not materially alter results. Conclusions: Intake of dietary antioxidants, such as carotenoids and vitamins, was not associated with the risk of developing PD in Singaporean Chinese.

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Section: Discussionmentioning

confidence: 99%

Dietary Antioxidants and Risk of Parkinson's Disease in the Singapore Chinese Health Study

Ying

Khan

et al. 2020

Movement Disorders

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“…Several synthetic and natural substances, as summarized in Table 1, are utilized to attenuate dopaminergic neuron loss through suppressing TLR signaling pathway and NF-κB (Café-Mendes et al, 2017;Cheng & Zhu, 2019;Li et al, 2018;Ling et al, 2019;Lv et al, 2019;Xu et al, 2017;Yang et al, 2019;Yu et al, 2016;Zhang & Xu, 2018 ;Zhang et al, 2016 It has been demonstrated that aggregated α-synuclein by binding to CD36 on microglia, which by recruiting Fyn kinase can activate protein kinase C-delta (PKC-δ), thereby propagating translocation of NF-κB p65 subunit to the nucleus. In the nucleus, p65 subunit enhances expression of IL-1β and NLR family pyrin domain containing 3 (NLRP3) inflammasome (Panicker et al, 2019) (Figure 1).…”

Section: Inflammationmentioning

confidence: 99%

“…Several synthetic and natural substances, as summarized in Table 1, are utilized to attenuate dopaminergic neuron loss through suppressing TLR signaling pathway and NF‐κB (Café‐Mendes et al., 2017; Cheng & Zhu, 2019; Li et al., 2018; Ling et al., 2019; Lv et al., 2019; Xu et al., 2017; Yang et al., 2019; Yu et al., 2016; Zhang & Xu, 2018 ; Zhang et al., 2016).…”

Section: Evidence Into Involvement Of Nf‐κb Family In Pdmentioning

confidence: 99%

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Dolatshahi

Hameghavandi

Sabahi

et al. 2021

Eur J of Neuroscience

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Parkinson's disease (PD) is the second most common neurodegenerative disease and the most common movement disorder, which causes morbidity and mortality and imposes a large burden (Kowal et al., 2013). Sporadic form of PD occurs more abundantly in aging population and causes symptoms like rigidity, bradykinesia, akinesia, resting tremor, motor imbalance, etc (Davie, 2008). It is characterized by selective degeneration and progressive loss of dopaminergic (DA) neurons in substantia nigra pars compacta (SNpc) which give rise to axonal processes innervating striatum (Surmeier, 2018). A myriad of etiologies contribute to DA neuron loss including inflammation, oxidative stress, autophagy, neurotransmission alterations, metabolic changes, etc. However, the

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“…Rosmarinic acid could attenuate inflammatory responses by suppressing the HMGB1/TLR4/NF-κB signaling pathways, which may contribute to its anti-PD activity (Lv et al, 2019). Cordycepin mitigates MPTP-induced inflammatory response in PD by inhibiting the TLR/NF-κB signaling pathway (Cheng and Zhu, 2019). The knockdown of cathepsin D can protect dopaminergic neurons from neuroinflammation-mediated neurotoxicity via inhibition of the NF-κB signaling pathway in a PD model (Gan et al, 2018).…”

Section: The Role Of Nf-κb In Neuroinflammation In Pdmentioning

confidence: 99%

Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements

Yao

Koc

et al. 2021

Front. Cell Dev. Biol.

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Parkinson’s disease (PD) is one of the most prevalent neurodegenerative aging disorders characterized by motor and non-motor symptoms due to the selective loss of midbrain dopaminergic (DA) neurons. The decreased viability of DA neurons slowly results in the appearance of motor symptoms such as rigidity, bradykinesia, resting tremor, and postural instability. These symptoms largely depend on DA nigrostriatal denervation. Pharmacological and surgical interventions are the main treatment for improving clinical symptoms, but it has not been possible to cure PD. Furthermore, the cause of neurodegeneration remains unclear. One of the possible neurodegeneration mechanisms is a chronic inflammation of the central nervous system, which is mediated by microglial cells. Impaired or dead DA neurons can directly lead to microglia activation, producing a large number of reactive oxygen species and pro-inflammatory cytokines. These cytotoxic factors contribute to the apoptosis and death of DA neurons, and the pathological process of neuroinflammation aggravates the primary morbid process and exacerbates ongoing neurodegeneration. Therefore, anti-inflammatory treatment exerts a robust neuroprotective effect in a mouse model of PD. Since discovering the first mutation in the α-synuclein gene (SNCA), which can cause disease-causing, PD has involved many genes and loci such as LRRK2, Parkin, SNCA, and PINK1. In this article, we summarize the critical descriptions of the genetic factors involved in PD’s occurrence and development (such as LRRK2, SNCA, Parkin, PINK1, and inflammasome), and these factors play a crucial role in neuroinflammation. Regulation of these signaling pathways and molecular factors related to these genetic factors can vastly improve the neuroinflammation of PD.

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Cordycepin mitigates MPTP-induced Parkinson's disease through inhibiting TLR/NF-κB signaling pathway

Cited by 41 publications

References 32 publications

Dietary Antioxidants and Risk of Parkinson's Disease in the Singapore Chinese Health Study

Dietary Antioxidants and Risk of Parkinson's Disease in the Singapore Chinese Health Study

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Genetic Imaging of Neuroinflammation in Parkinson’s Disease: Recent Advancements

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