Resveratrol ameliorates autophagic flux to promote functional recovery in rats after spinal cord injury

Wang, Peng; Jiang, Li; Zhou, Nina; Zhou, Hao; Liu, Huzhe; Zhao, Wenrui; Zhang, Hanxiang; Zhang, Xiang; Hu, Zhenming

doi:10.18632/oncotarget.23877

Cited by 29 publications

(16 citation statements)

References 57 publications

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“…Resveratrol potentiated motoneuron recovery and decreased apoptosis, after spinal cord injury in mice, through promotion of Beclin 1, LC3II and autophagy (Hu et al, 2017). Similar results were reported by Wang P. et al (2018) in rat spinal cord injury, where resveratrol activated AMPK and autophagic flux, and consequently inhibited mTOR pathway, and in vitro in PC12 cells. Moreover, resveratrol induced autophagy, in dopaminergic SH-SY5Y cells challenged with rotenone via haeme oxygenase signaling (Lin et al, 2014).…”

Section: Polyphenolssupporting

confidence: 88%

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Natural Compounds and Autophagy: Allies Against Neurodegeneration

Stacchiotti

Corsetti

2020

Front. Cell Dev. Biol.

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Prolonging the healthy life span and limiting neurological illness are imperative goals in gerontology. Age-related neurodegeneration is progressive and leads to severe diseases affecting motility, memory, cognitive function, and social life. To date, no effective treatments are available for neurodegeneration and irreversible neuronal loss. Bioactive phytochemicals could represent a natural alternative to ensure active aging and slow onset of neurodegenerative diseases in elderly patients. Autophagy or macroautophagy is an evolutionarily conserved clearing process that is needed to remove aggregateprone proteins and organelles in neurons and glia. It also is crucial in synaptic plasticity. Aberrant autophagy has a key role in aging and neurodegeneration. Recent evidence indicates that polyphenols like resveratrol and curcumin, flavonoids, like quercetin, polyamine, like spermidine and sugars, like trehalose, limit brain damage in vitro and in vivo. Their common mechanism of action leads to restoration of efficient autophagy by dismantling misfolded proteins and dysfunctional mitochondria. This review focuses on the role of dietary phytochemicals as modulators of autophagy to fight Alzheimer's and Parkinson's diseases, fronto-temporal dementia, amyotrophic lateral sclerosis, and psychiatric disorders. Currently, most studies have involved in vitro or preclinical animal models, and the therapeutic use of phytochemicals in patients remains limited.

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Section: Polyphenolssupporting

confidence: 88%

“…Resveratrol AD-AβPP/PS1 mice 1% for 10 months-AMPK/Sirtuin Porquet et al, 2014;Guo et al, 2016;Hu et al, 2017;Zhao et al, 2017;Wang P. et al, 2018;Vidoni et al, 2018;Pineda-Ramirez et al, 2020 Brain ischemia rat 1.8 mg/kg-AMPK/Beclin1…”

Section: Polyphenolsmentioning

confidence: 99%

Natural Compounds and Autophagy: Allies Against Neurodegeneration

Stacchiotti

Corsetti

2020

Front. Cell Dev. Biol.

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“…ese shreds of evidence show that AMPK activation is important not only in autophagosome formation but also in autophagosome clearance and can improve the overall autophagic clearance of aberrant proteins. is was corroborated with many other pharmacological studies in which the role of AMPK in autophagic flux is demonstrated [63,70,71]. For instance, Chen et al showed that AMPK activation with metformin enhances the autophagosomes clearance.…”

Section: Ampk and Aβ Metabolismsupporting

confidence: 65%

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

Assefa

Tafere

Wondafrash

et al. 2020

BioMed Research International

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Alzheimer’s disease is a multifactorial neurodegenerative disease characterized by progressive cognitive dysfunction. It is the most common form of dementia. The pathologic hallmarks of the disease include extracellular amyloid plaque, intracellular neurofibrillary tangles, and oxidative stress, to mention some of them. Despite remarkable progress in the understanding of the pathogenesis of the disease, drugs for cure or disease-modifying therapy remain somewhere in the distance. From recent time, the signaling molecule AMPK is gaining enormous attention in the AD drug research. AMPK is a master regulator of cellular energy metabolism, and recent pieces of evidence show that perturbation of its function is highly ascribed in the pathology of AD. Several drugs are known to activate AMPK, but their effect in AD remains to be controversial. In this review, the current shreds of evidence on the effect of AMPK activators in Aβ accumulation, tau aggregation, and oxidative stress are addressed. Positive and negative effects are reported with regard to Aβ and tauopathy but only positive in oxidative stress. We also tried to dissect the molecular interplays where the bewildering effects arise from.

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“…Rapamycin is reported to induce cytoprotective autophagic flux (M. Wang et al, ; P. Wang et al, ; Wu et al, ). Induction of autophagy by rapamycin considerably mitigated the BE1‐induced apoptosis, whereas single treatment with the autophagy inducer had no effect on cell fate.…”

Section: Discussionmentioning

confidence: 99%

1,7‐Bis(4‐hydroxyphenyl)‐4‐hepten‐3‐one from Betula platyphylla induces apoptosis by suppressing autophagy flux and activating the p38 pathway in lung cancer cells

Jung

Song

Son

et al. 2019

Phytotherapy Research

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Betula platyphylla (BP) is frequently administered in the treatment of various human diseases, including cancers. This study was undertaken to investigate the pharmacological function of the active components in BP and the underlying mechanism of its chemotherapeutic effects in human lung cancer cells. We observed that BP extracts and 1,7‐bis(4‐hydroxyphenyl)‐4‐hepten‐3‐one (BE1), one of the components of BP, effectively decreased the cell viability of several lung cancer cell lines. BE1‐treated cells exhibited apoptosis induction and cell cycle arrest at the G2/M phase. Further examination demonstrated that BE1 treatment resulted in suppression of autophagy, as evidenced by increased protein expression levels of both LC3 II and p62/SQSTM1. Interestingly, the pharmacological induction of autophagy with rapamycin remarkably reduced the BE1‐induced apoptosis, indicating that apoptosis induced by BE1 was associated with autophagy inhibition. Our data also demonstrated that BE1 exposure activated the p38 pathway resulting in regulation of the pro‐apoptotic activity. Taken together, we believe that BE1 is a potential anticancer agent for human lung cancer, which exerts its effect by enhancing apoptosis via regulating autophagy and the p38 pathway.

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Resveratrol ameliorates autophagic flux to promote functional recovery in rats after spinal cord injury

Cited by 29 publications

References 57 publications

Natural Compounds and Autophagy: Allies Against Neurodegeneration

Natural Compounds and Autophagy: Allies Against Neurodegeneration

The Bewildering Effect of AMPK Activators in Alzheimer’s Disease: Review of the Current Evidence

1,7‐Bis(4‐hydroxyphenyl)‐4‐hepten‐3‐one from Betula platyphylla induces apoptosis by suppressing autophagy flux and activating the p38 pathway in lung cancer cells

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