Exogenous Tetranectin Protects Against 1-Methyl-4-Phenylpyridine–Induced Neurotoxicity by Inhibiting Apoptosis and Autophagy Through Ribosomal Protein S6 Kinase Beta-1

Xie, Qiang; Liu, Meng; Yan, Yu‐Feng; Shen, Xiao Li; Wang, Ersong

doi:10.1016/j.wneu.2018.10.058

Cited by 8 publications

(2 citation statements)

References 31 publications

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“…Studies have shown that autophagy plays an important role in protecting body from cancer, infection, neurodegeneration, type 2 diabetes, aging and so on [11][12][13] . Artemisinin(ART), extracted from the stems and leaves of Artemisia annua, has been used as an antimalarial drug for a long time and have saved millions of lives 14,15 .…”

Section: Introductionmentioning

confidence: 99%

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Yan

Lai

et al. 2020

Preprint

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Background Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's. The drugs currently used to treat PD cannot inhibit the development of PD, and long-term use produces severe drug resistance and adverse reaction. Artemisinin (ART) is an active ingredient of Artemisia annua and has a neuroprotective effect, but the mechanism is still unclear. This study was designed to investigate the neuroprotective effect of ART in MPP+-treated SH-SY5Y cells. Results There was no significant cytotoxicity when the ART concentration was under. 40 µM. The 20 µM ART for 24 h could increase the cell viability by reducing oxidative stress and cell apoptosis in MPP+-treated SH-SY5Y cell. In addition, immunoblot and immunofluorescence results showed that MPP+ treatment increased the expression of Beclin1, LC3II/LC3I and decreased the expression of P62, while ART can reverse the changes caused by MPP+. Discussion More and more researches reported that ART and its derivates have neuroprotective effects through anti-oxidant and anti-apoptosis. we found that pre-treated cells with 20 µM ART for 4 h could significantly increase the viability in Parkinson's disease cell model. The oxidative stress and apoptosis were the main reason for the degeneration of dopaminergic neurons, while artemisinin can attenuate oxidative stress and apoptosis in MPP+-lesioned dopaminergic neurons. The levels of autophagy proteins LC3II/I, Beclin1 and P62 also showed that MPP + increased the autophagy level, and pre-treatment with ART decreased the autophagy level, which may be the pathological mechanism for artemisinin to reduce oxidative stress damage and apoptosis. Conclusions These results indicate that ART exerts a positive effect on MPP+-treated SH-SY5Y cells in terms of anti-oxidative stress and anti-apoptosis. These effects may be related to autophagy. These findings contribute to a better understanding of the critical role of ART in PD treatment.

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Section: Introductionmentioning

confidence: 99%

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Yan

Lai

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…In adverse environments such as oxidative stress, the body initiates various of defense mechanisms, such as increasing the levels of antioxidants, degrading speci c misfolded proteins through the ubiquitin-proteasome system, and degrading damaged proteins and organelles through autophagy. Studies have shown that autophagy plays an important role in protecting body from cancer, infection, neurodegeneration, type 2 diabetes, aging and so on [11][12][13] . Artemisinin(ART), extracted from the stems and leaves of Artemisia annua, has been used as an antimalarial drug for a long time and have saved millions of lives 14,15 .…”

Section: Introductionmentioning

confidence: 99%

Artemisinin Attenuated Oxidative Stress and Apoptosis by Inhibiting Autophagy in MPP+-treated SH-SY5Y Cell 

Yan

Lai

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's. The drugs currently used to treat PD cannot inhibit the development of PD, and long-term use produces severe drug resistance and adverse reaction. Artemisinin (ART) is an active ingredient of Artemisia annua and has a neuroprotective effect, but the mechanism is still unclear. This study was designed to investigate the neuroprotective effect of ART in MPP+-treated SH-SY5Y cells. Results There was no significant cytotoxicity when the ART concentration was under. 40μM. The 20μM ART for 24h could increase the cell viability by reducing oxidative stress and cell apoptosis in MPP+-treated SH-SY5Y cell. In addition, immunoblot and immunofluorescence results showed that MPP+ treatment increased the expression of Beclin1, LC3II/LC3I and decreased the expression of P62, while ART can reverse the changes caused by MPP+. Discussion More and more researches reported that ART and its derivates have neuroprotective effects through anti-oxidant and anti-apoptosis. we found that pre-treated cells with 20μM ART for 4h could significantly increase the viability in Parkinson's disease cell model. The oxidative stress and apoptosis were the main reason for the degeneration of dopaminergic neurons, while artemisinin can attenuate oxidative stress and apoptosis in MPP+-lesioned dopaminergic neurons. The levels of autophagy proteins LC3II/I, Beclin1 and P62 also showed that MPP+ increased the autophagy level, and pre-treatment with ART decreased the autophagy level, which may be the pathological mechanism for artemisinin to reduce oxidative stress damage and apoptosis. Conclusions These results indicate that ART exerts a positive effect on MPP+-treated SH-SY5Y cells in terms of anti-oxidative stress and anti-apoptosis. These effects may be related to autophagy. These findings contribute to a better understanding of the critical role of ART in PD treatment.

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Exogenous Tetranectin Alleviates Pre-formed-fibrils-induced Synucleinopathies in SH-SY5Y Cells by Activating the Plasminogen Activation System

et al. 2022

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Exogenous Tetranectin Protects Against 1-Methyl-4-Phenylpyridine–Induced Neurotoxicity by Inhibiting Apoptosis and Autophagy Through Ribosomal Protein S6 Kinase Beta-1

Cited by 8 publications

References 31 publications

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Artemisinin Attenuated Oxidative Stress and Apoptosis by Inhibiting Autophagy in MPP+-treated SH-SY5Y Cell

Exogenous Tetranectin Alleviates Pre-formed-fibrils-induced Synucleinopathies in SH-SY5Y Cells by Activating the Plasminogen Activation System

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Exogenous Tetranectin Protects Against 1-Methyl-4-Phenylpyridine–Induced Neurotoxicity by Inhibiting Apoptosis and Autophagy Through Ribosomal Protein S6 Kinase Beta-1

Cited by 8 publications

References 31 publications

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cell

Artemisinin Attenuated Oxidative Stress and Apoptosis by Inhibiting Autophagy in MPP+-treated SH-SY5Y&nbsp;Cell&nbsp;

Exogenous Tetranectin Alleviates Pre-formed-fibrils-induced Synucleinopathies in SH-SY5Y Cells by Activating the Plasminogen Activation System

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Artemisinin Attenuated Oxidative Stress and Apoptosis by Inhibiting Autophagy in MPP+-treated SH-SY5Y Cell