A bibenzyl compound 20C protects rats against 6-OHDA-induced damage by regulating adaptive immunity associated molecules

Wang, Shuo; Han, Qi-Wen; Zhou, Tian-Tian; Zhang, Chenglu; Zhu, Cheng‐Gang; Zhou, Xin; Chen, Nai‐Hong; Yuan, Yu‐He; Shi, Jian‐Gong

doi:10.1016/j.intimp.2020.107269

Cited by 6 publications

(6 citation statements)

References 49 publications

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“…Further scavenging assay showed that 12 had a stronger 1,1-diphenyl-2-picrylhydrazyl radical (DPPH·), oxidative radical and •OH scavenging ability than vitamin C ( Supporting Information Fig. S22a−d ), demonstrating that such neuroprotective activity of bibenzyls was related to their antioxidative stress effects 48 , although the intensity of 12 in scavenging O 2 ‒ · was weaker than vitamin C ( Fig. S22e ).…”

Section: Resultsmentioning

confidence: 99%

Structural diversification of bioactive bibenzyls through modular co-culture leading to the discovery of a novel neuroprotective agent

Liu

Sui

et al. 2023

Acta Pharmaceutica Sinica B

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Section: Resultsmentioning

confidence: 99%

Structural diversification of bioactive bibenzyls through modular co-culture leading to the discovery of a novel neuroprotective agent

Liu

Sui

et al. 2023

Acta Pharmaceutica Sinica B

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“…Nitrified α-syn exists widely in LBs and insoluble components involved in the brain. α-Syn possesses four tyrosines (Y39, Y125, Y133, and Y136) that can be post-translationally modified by nitration, especially at Y125, which plays a key role in the accumulation and precipitation of α-syn under nitrative stress. − Also, a report showed that a bibenzyl compound 20C (a traditional Chinese medicine extract) can not only inhibit the activity of inducible nitric oxide synthase (iNOS) induced by 6-OHDA but also inhibit the adaptive immunity mediated by nitrated-α-synuclein . Meanwhile, in the midbrain of PD mice, simvastatin increased DA neurons and reduced protein tyrosine nitration, thereby providing a novel antioxidant mechanism .…”

Section: Ptms Of α-Synmentioning

confidence: 99%

“…110−112 Also, a report showed that a bibenzyl compound 20C (a traditional Chinese medicine extract) can not only inhibit the activity of inducible nitric oxide synthase (iNOS) induced by 6-OHDA but also inhibit the adaptive immunity mediated by nitrated-α-synuclein. 113 Meanwhile, in the midbrain of PD mice, simvastatin increased DA neurons and reduced protein tyrosine nitration, thereby providing a novel antioxidant mechanism. 114 Furthermore, Danielson et al 115 indicated that it has been verified that the nitrification of Y-39 could reduce binding of α-syn to synthetic vesicles which may accelerate oligomerization, and a mutation in this residue leads to increased formation of α-syn fibrils and neurotoxicity.…”

Section: Nitrationmentioning

confidence: 99%

Effects of α-Synuclein-Associated Post-Translational Modifications in Parkinson’s Disease

Wang

Yung

et al. 2021

ACS Chem. Neurosci.

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α-Synuclein (α-syn), a small highly conserved presynaptic protein containing 140 amino acids, is thought to be the main pathological hallmark in related neurodegenerative disorders. Although the normal function of α-syn is closely involved in the regulation of vesicular neurotransmission in these diseases, the underlying mechanisms of post-translational modifications (PTMs) of α-syn in the pathogenesis of Parkinson's disease (PD) have not been fully characterized. The pathological accumulation of misfolded α-syn has a critical role in PD pathogenesis. Recent studies of factors contributing to α-syn-associated aggregation and misfolding have expanded our understanding of the PD disease process. In this Review, we summarize the structure and physiological function of α-syn, and we further highlight the major PTMs (namely phosphorylation, ubiquitination, nitration, acetylation, truncation, SUMOylation, and O-GlcNAcylation) of α-syn and the effects of these modifications on α-syn aggregation, which may elucidate mechanisms for PD pathogenesis and lay a theoretical foundation for clinical treatment of PD.

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“…Furthermore, MPO inhibitors have beneficial effects in the treatment of neurodegenerative diseases such as PDD (Maki et al, 2019 ). Bibenzyl compound 20C, a Chinese medicinal extract, can inhibit the adaptive immune response mediated by nitration of α-syn (Wang et al, 2021 ), which may inhibit oxidative stress and neuronal death. Iron-induced oxidative stress is the most common harmful reaction, and excessive iron content is associated with an increase in nitration stress, which leads to increases in the tyrosine nitration level.…”

Section: The Interaction Between Aβ Tau α-Syn and Ironmentioning

confidence: 99%

Parkinson’s Disease Dementia: Synergistic Effects of Alpha-Synuclein, Tau, Beta-Amyloid, and Iron

Han

Fan

et al. 2021

Front. Aging Neurosci.

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Parkinson’s disease dementia (PDD) is a common complication of Parkinson’s disease that seriously affects patients’ health and quality of life. At present, the process and pathological mechanisms of PDD remain controversial, which hinders the development of treatments. An increasing number of clinical studies have shown that alpha-synuclein (α-syn), tau, beta-amyloid (Aβ), and iron are closely associated with PDD severity. Thus, we inferred the vicious cycle that causes oxidative stress (OS), due to the synergistic effects of α-syn, tau, Aβ, and, iron, and which plays a pivotal role in the mechanism underlying PDD. First, iron-mediated reactive oxygen species (ROS) production can lead to neuronal protein accumulation (e.g., α-syn andAβ) and cytotoxicity. In addition, regulation of post-translational modification of α-syn by iron affects the aggregation or oligomer formation of α-syn. Iron promotes tau aggregation and neurofibrillary tangles (NFTs) formation. High levels of iron, α-syn, Aβ, tau, and NFTs can cause severe OS and neuroinflammation, which lead to cell death. Then, the increasing formation of α-syn, Aβ, and NFTs further increase iron levels, which promotes the spread of α-syn and Aβ in the central and peripheral nervous systems. Finally, iron-induced neurotoxicity promotes the activation of glycogen synthase kinase 3β (GSK3β) related pathways in the synaptic terminals, which in turn play an important role in the pathological synergistic effects of α-syn, tau and Aβ. Thus, as the central factor regulating this vicious cycle, GSK3β is a potential target for the prevention and treatment of PDD; this is worthy of future study.

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A bibenzyl compound 20C protects rats against 6-OHDA-induced damage by regulating adaptive immunity associated molecules

Cited by 6 publications

References 49 publications

Structural diversification of bioactive bibenzyls through modular co-culture leading to the discovery of a novel neuroprotective agent

Structural diversification of bioactive bibenzyls through modular co-culture leading to the discovery of a novel neuroprotective agent

Effects of α-Synuclein-Associated Post-Translational Modifications in Parkinson’s Disease

Parkinson’s Disease Dementia: Synergistic Effects of Alpha-Synuclein, Tau, Beta-Amyloid, and Iron

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