Ferulic acid delayed amyloid β-induced pathological symptoms by autophagy pathway via a fasting-like effect in Caenorhabditis elegans

Wang, Ningbo; Zhou, Yanjun; Zhao, Longhe; Wang, Cai-ding; Ma, Wuli; Ge, Guangfei; Wang, Yu; Ullah, Inam; Muhammad, Fahim; Alwayli, Dhafer; Zhi, Dejuan; Li, Hongyu

doi:10.1016/j.fct.2020.111808

Cited by 26 publications

(16 citation statements)

References 57 publications

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“…Extracts of Kushui rose [ 121 ], Greek mountain tea [ 108 ], Chinese liquorice [ 97 ], and the leaves of coconut [ 124 ], G. biloba [ 99 ] and G. uralensis [ 97 ] reduced Aβ deposits in the CL2006 strain. A similar effect was reported for several compounds isolated from G. uralensis extract including glycyrrhetinic acid, isoliquiritigenin, glycyrrhizic acid and its aglycon [ 97 ], as well as ferulic acid [ 146 ], otophylloside B [ 138 ] and oleuropein aglycone [ 135 ]. This protective effect was also reported for extracts of strawberry [ 112 ] and the brown macroalga P. gymnospora [ 123 ] in the CL4176 strain.…”

Section: Effects Of Natural Products In Caenorhabditis Eleg...supporting

confidence: 75%

“…Other compounds were isolated from non-tested products, including several sequisterpenoids (nardochinin A, B, C and D) from the underground parts of Nardostachys chinensis Batal ethanolic extract [ 133 ], sesamin, sesamol and sesamolin from sesame ( Sesamun indicum L.) seeds [ 134 ], oleuropein aglycone from extra virgin olive oil [ 135 ], magnolol from Magnolia genus especies [ 136 ], several sesquiterpene lactones (salcastanins, nubiol, nubdienolide, and nubenolide) from Salvia castanea [ 137 ], otophylloside B from Cynanchum otophyllum L. [ 138 ], betalains from red-beet ( Beta vulgaris L.) [ 139 ], gossypol from cotton plant ( Gossypium arboreum L.) [ 140 ], cyclotides from butterfly pea [ 141 ], resveratrol from red wine [ 142 ] and withanolide A from the root of ashwagandha ( Withania somnifera (L.) Dunal) [ 143 ]. Likewise, some well-known bioactive molecules that can be found in multiple sources such as quercetin [ 144 , 145 ], ferulic acid [ 146 ], caffeine [ 110 ], morin [ 140 ], gallic acid, ellagic acid [ 114 ] and caffeic acid [ 147 ] were also tested in the mentioned assays.…”

Section: Effects Of Natural Products In Caenorhabditis Eleg...mentioning

confidence: 99%

“…These were ginkgolide A [ 99 ], G. zeylanicum extract [ 100 ], tiger milk mushroom extract [ 131 ], cyclotides from butterfly pea [ 141 ], and otophylloside B [ 138 ]. Other authors have reported that sensitivity to exogenous serotonin was improved by ferulic acid [ 146 ], caffeic acid [ 147 ], A. tatarinowii Schott oil [ 105 ], ginkgolide A [ 99 ], sesamin, sesamolin [ 134 ], Kushui rose essential oil and geraniol (both isolated from Kushui rose essential oil) [ 121 ] and β-citronellol [ 121 ]. However, red rose [ 118 ] extract, sesamol [ 134 ] and the rest of the compounds isolated from G. biloba leaf extract, ginkgolide B, C and J, bilobalide B and flavonoids [ 99 ] had no effect on chemotaxis.…”

Section: Effects Of Natural Products In Caenorhabditis Eleg...mentioning

confidence: 99%

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Natural Bioactive Products and Alzheimer’s Disease Pathology: Lessons from Caenorhabditis elegans Transgenic Models

Navarro-Hortal¹,

Romero-Márquez²,

Osta³

et al. 2022

Diseases

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Alzheimer’s disease (AD) is an age-dependent, progressive disorder affecting millions of people. Currently, the therapeutics for AD only treat the symptoms. Although they have been used to discover new products of interest for this disease, mammalian models used to investigate the molecular determinants of this disease are often prohibitively expensive, time-consuming and very complex. On the other hand, cell cultures lack the organism complexity involved in AD. Given the highly conserved neurological pathways between mammals and invertebrates, Caenorhabditis elegans has emerged as a powerful tool for the investigation of the pathophysiology of human AD. Numerous models of both Tau- and Aβ-induced toxicity, the two prime components observed to correlate with AD pathology and the ease of performing RNA interference for any gene in the C. elegans genome, allow for the identification of multiple therapeutic targets. The effects of many natural products in main AD hallmarks using these models suggest promising health-promoting effects. However, the way in which they exert such effects is not entirely clear. One of the reasons is that various possible therapeutic targets have not been evaluated in many studies. The present review aims to explore shared therapeutical targets and the potential of each of them for AD treatment or prevention.

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Section: Effects Of Natural Products In Caenorhabditis Eleg...supporting

confidence: 75%

Section: Effects Of Natural Products In Caenorhabditis Eleg...mentioning

confidence: 99%

Section: Effects Of Natural Products In Caenorhabditis Eleg...mentioning

confidence: 99%

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Natural Bioactive Products and Alzheimer’s Disease Pathology: Lessons from Caenorhabditis elegans Transgenic Models

Navarro-Hortal¹,

Romero-Márquez²,

Osta³

et al. 2022

Diseases

View full text Add to dashboard Cite

show abstract

“…DAF-16/FOXO and HLH-30/TFEB can form a complex combinatorial transcription factor to promote stress resistance and lifespan in the same genetic pathway [41]. Recently research teams reported that FA can significantly activate the nuclear localization of HLH-30::GFP against amyloid-beta (Aβ) toxicity in C. elegans [42]. DAF-16 and HLH-30 are aging-regulatory transcription factors of significant importance and co-regulate several target genes in the promotion of lifespan [41].…”

Section: Hlh-30 Was Required For Fa-mediated Lifespan Extensionmentioning

confidence: 99%

Ferulic Acid Supplementation Increases Lifespan and Stress Resistance via Insulin/IGF-1 Signaling Pathway in C. elegans

Meng

et al. 2021

IJMS

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Ferulic acid (FA) is a naturally-occurring well-known potent antioxidant and free radical scavenger. FA supplementation is an effective strategy to delay aging, but the underlying mechanism remains unknown. In the present study, we examined the effects of FA on lifespan extension and its mechanism of FA in Caenorhabditis elegans (C. elegans). Results suggested that FA increased the lifespan of C. elegans, rather than altering the growth of E. coli OP50. Meanwhile, FA promoted the healthspan of C. elegans by improving locomotion and reducing fat accumulation and polyQ aggregation. FA increased the resistance to heat and oxidative stress through reducing ROS. The upregulating of the expression of the hlh-30, skn-1, and hsf-1 were involved in the FA-mediated lifespan extension. Furthermore, FA treatment had no impact on the lifespan of daf-2, hlh-30, skn-1, and hsf-1 mutants, confirming that insulin/IGF-1 signaling pathway and multiple longevity mechanisms were associated with the longevity mechanism of FA. We further found that mitochondrial signaling pathway was modulation involved in FA-mediated lifespan extension. With the results from RNA-seq results and mutants lifespan assay. These findings contribute to our knowledge of the lifespan extension and underlying mechanism of action of FA in C. elegans.

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“…Likewise, FA administration to AD-like rats model attenuated performance impairment and memory deficits induced by Aβ deposits [125,126]. In a recent research using C. elegans AD model worms, FA ameliorated Aβ-induced pathological symptoms by the autophagy pathway via a fasting-like effect [127]. Although most of these studies are in animal models or in vitro, they are promising by demonstrating that ferulic acid may be able to effectively fight against neurodegenerative diseases caused by protein misfolding or pathological aggregation while exerting protective effects against insulin impairments.…”

Section: Ferulic Acidmentioning

confidence: 92%

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

2022

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It has become increasingly apparent that defective insulin signaling may increase the risk for developing Alzheimer’s disease (AD), influence neurodegeneration through promotion of amyloid formation or by increasing inflammatory responses to intraneuronal β-amyloid. Recent work has demonstrated that hyperglycemia is linked to cognitive decline, with elevated levels of glucose causing oxidative stress in vulnerable tissues such as the brain. The ability of β-amyloid peptide to form β-sheet-rich aggregates and induce apoptosis has made amyloid fibrils a leading target for the development of novel pharmacotherapies used in managing and treatment of neuropathological conditions such as AD-related cognitive decline. Additionally, deposits of β-sheets folded amylin, a glucose homeostasis regulator, are also present in diabetic patients. Thus, therapeutic compounds capable of reducing intracellular protein aggregation in models of neurodegenerative disorders may prove useful in ameliorating type 2 diabetes mellitus symptoms. Furthermore, both diabetes and neurodegenerative conditions, such as AD, are characterized by chronic inflammatory responses accompanied by the presence of dysregulated inflammatory biomarkers. This review presents current evidence describing the role of various small bioactive molecules known to ameliorate amyloidosis and subsequent effects in prevention and development of diabetes and AD. It also highlights the potential efficacy of peptide–drug conjugates capable of targeting intracellular targets.

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Ferulic acid delayed amyloid β-induced pathological symptoms by autophagy pathway via a fasting-like effect in Caenorhabditis elegans

Cited by 26 publications

References 57 publications

Natural Bioactive Products and Alzheimer’s Disease Pathology: Lessons from Caenorhabditis elegans Transgenic Models

Natural Bioactive Products and Alzheimer’s Disease Pathology: Lessons from Caenorhabditis elegans Transgenic Models

Ferulic Acid Supplementation Increases Lifespan and Stress Resistance via Insulin/IGF-1 Signaling Pathway in C. elegans

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

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