Apigenin inhibits larval growth of<i>Caenorhabditis elegans</i>through DAF‐16 activation

Kawasaki, Ichiro; Jeong, Myung-Hwan; Oh, Bong-Kyeong; Shim, Yhong–Hee

doi:10.1016/j.febslet.2010.07.026

Cited by 22 publications

(15 citation statements)

References 17 publications

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“…Analogous results were obtained by Bartholome et al [43], where a treatment of 100 μ M EGCG for 48 h increased (2.2-fold) the amount of worms showing predominantly nuclear localisation of DAF-16 in contrast to untreated C. elegans . Similar effects were also found for quercetin [30, 36, 37], myricetin [36, 38], kaempferol, naringenin [36], fisetin [70], and apigenin [81], but not for rutin [37]. Remarkably, a 48 h pretreatment with 100 μ M quercetin enhanced the mean percentage of worms carrying predominantly nuclear DAF-16 by more than three times in contrast to untreated nematodes [30, 36, 37, 70].…”

Section: Modulation Of Representative Redox-sensitive Signalling Psupporting

confidence: 54%

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Caenorhabditis elegansas Model System in Pharmacology and Toxicology: Effects of Flavonoids on Redox-Sensitive Signalling Pathways and Ageing

Koch

Havermann

Büchter

et al. 2014

The Scientific World Journal

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Flavonoids are secondary plant compounds that mediate diverse biological activities, for example, by scavenging free radicals and modulating intracellular signalling pathways. It has been shown in various studies that distinct flavonoid compounds enhance stress resistance and even prolong the life span of organisms. In the last years the model organism C. elegans has gained increasing importance in pharmacological and toxicological sciences due to the availability of various genetically modified nematode strains, the simplicity of modulating genes by RNAi, and the relatively short life span. Several studies have been performed demonstrating that secondary plant compounds influence ageing, stress resistance, and distinct signalling pathways in the nematode. Here we present an overview of the modulating effects of different flavonoids on oxidative stress, redox-sensitive signalling pathways, and life span in C. elegans introducing the usability of this model system for pharmacological and toxicological research.

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Section: Modulation Of Representative Redox-sensitive Signalling Psupporting

confidence: 54%

“…In this context it was shown that Q3M increased (1.38-fold) daf-2 gene expression in the nematode compared to the control. In contrast, apigenin was found to inhibit daf-2 expression [81]. …”

Section: Modulation Of Representative Redox-sensitive Signalling Pmentioning

confidence: 99%

Caenorhabditis elegansas Model System in Pharmacology and Toxicology: Effects of Flavonoids on Redox-Sensitive Signalling Pathways and Ageing

Koch

Havermann

Büchter

et al. 2014

The Scientific World Journal

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“…Regarding the insulin-like signalling pathway, myricetin induced an increase in nuclear DAF-16::GFP translocation (relative DAF-16::GFP localization: DMSO: 6% ± 2%; myricetin: 41% ± 7%) and a reduction in the cytosolic DAF-16::GFP fraction (DMSO: 65% ± 8%; myricetin: 30% ± 4%), respectively (Figure 5A). A nuclear translocation of DAF-16 or target gene expression was reported for different flavonoids, e.g., quercetin [28], apigenin [31], fisetin [29], kaempferol [29] and epigallocatechin-gallate [16]. A shift from cytosolic to nuclear localization of DAF-16 by myricetin (20% cytosolic compared to 70% cytosolic in control nematodes) was previously reported [20].…”

Section: Resultsmentioning

confidence: 84%

Myricetin-Mediated Lifespan Extension in Caenorhabditis elegans Is Modulated by DAF-16

Büchter

Ackermann

Havermann

et al. 2013

IJMS

106

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Myricetin is a naturally occurring flavonol found in many plant based food sources. It increases the lifespan of Caenorhabditis elegans, but the molecular mechanisms are not yet fully understood. We have investigated the impact of this flavonoid on the transcription factors DAF-16 (C. elegans FoxO homologue) and SKN-1 (Nrf2 homologue), which have crucial functions in the regulation of ageing. Myricetin is rapidly assimilated by the nematode, causes a nuclear translocation of DAF-16 but not of SKN-1, and finally prolongs the mean adult lifespan of C. elegans by 32.9%. The lifespan prolongation was associated with a decrease in the accumulation of reactive oxygen species (ROS) detected by DCF. Myricetin also decreases the formation of lipofuscin, a pigment consisting of highly oxidized and cross-linked proteins that is considered as a biomarker of ageing in diverse species. The lifespan extension was completely abolished in a daf-16 loss-of-function mutant strain (CF1038). Consistently with this result, myricetin was also not able to diminish stress-induced ROS accumulation in the mutant. These results strongly indicate that the pro-longevity effect of myricetin is dependent on DAF-16 and not on direct anti-oxidative effects of the flavonoid.

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“…Among the herbal PAK1-blockers, apigenin from the CAPE-based propolis or camomile flowers is the first that has been proven to extend the lifespan of nematode (C. elegans) in a FOXO-dependent manner [14]. Apigenin is a flavonoid that blocks PAK1 by directly down-regulating PI-3 kinase [15].…”

Section: Apigeninmentioning

confidence: 99%

Natural or Synthetic Anti-Melanogenic Compounds That Block the PDGFR-EGFR-PAK1-MITF-Tyrosinase Signaling Pathway

Miyata¹,

Pham-Thi²,

Ahn³

2017

J Dermatol Res Ther

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A natural sleeping pill and "elixir" (longevity-promoter) called "Melatonin" is one of the first natural anti-melanogenic compounds, and originally derived from bovine pineal glands. However, currently the majority of melatonin product in the market is chemically synthesized. Since then a wide variety of anti-melanogenic compounds such as curcumin, CAPE (Caffeic Acid Phenethyl Ester), and Artepillin C (ARC) were identified in nature as well as chemically synthesized compounds such as Gleevec. These anti-melanogenic compounds share a series of interesting biological properties such as anti-cancer, anti-inflammatory, anti-ageing (longevity-promoting), immune-boosting, anti-malaria, and anti-diabetic activities. However, the precise molecular mechanism underlying their anti-melanogenic action has remained to be clarified until recently. Finally we found the first clue to understanding of the "melanogenic" signalling pathway involving the major oncogenic/ageing kinase called PAK1 (RAC/CDC42-activated kinase 1) By siRNA-based silencing of PAK1 gene in murine melanoma cell line (B16F10): (i) The major growth hormone in serum called PDGF (Platelet-Derived Growth Factor) is essential for the inducible melanogenesis, but not for the exponential growth per se, and (ii) This cytokine activates its receptor called PDGFR, a Tyr-kinase on the cell surface, and induces another cell surface receptor Tyr-kinase called EGFR (Epidermal Growth Factor Receptor), to form a heterodimer with PDGFR, activating the down-stream melanogenic/oncogenic signalling pathway involving PAK1 and eventually MITF (Microphthalmia-Associated Transcription Factor) essential for expression of Tyrosinase and its Related Protein (TRP) genes. Melatonin and many other anti-melanogenic compounds block PAK1 directly or indirectly, and eventually down-regulate tyrosinase or TRP which is essential for melanin biosynthesis from an amino acid called tyrosine.

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Apigenin inhibits larval growth ofCaenorhabditis elegansthrough DAF‐16 activation

Cited by 22 publications

References 17 publications

Caenorhabditis elegansas Model System in Pharmacology and Toxicology: Effects of Flavonoids on Redox-Sensitive Signalling Pathways and Ageing

Caenorhabditis elegansas Model System in Pharmacology and Toxicology: Effects of Flavonoids on Redox-Sensitive Signalling Pathways and Ageing

Myricetin-Mediated Lifespan Extension in Caenorhabditis elegans Is Modulated by DAF-16

Natural or Synthetic Anti-Melanogenic Compounds That Block the PDGFR-EGFR-PAK1-MITF-Tyrosinase Signaling Pathway

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