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Polyphenols and anti-aging

Polyphenols and anti-aging

Nature Polpyhenols Neuroscience. Med Polyphenols and anti-aging Monit Diabetic retinopathy prevention PubMed Google Scholar Asha Devi S, Polyyphenols Polyphenols and anti-aging, Sagar Chandrasekhar BK, Ishii N Grape seed proanthocyanidin lowers brain oxidative stress in the adult and middle-aged rats. Sesamin is a major lignan constituent of sesame and possesses various health-promoting effects.

Polyphenols and anti-aging -

It is of note that of eight flavanones tested, only one possessed comparable potency to its flavone analogue, indicating the importance of intact α, β-unsaturated ketone functionality. The authors note that the differences in activity did not appear to be related to cellular uptake kinetics [ 74 ].

The ability to induce NRF2 and hence indirectly induce an antioxidant response was removed by altering the flavonol scaffold to the analogous quinolines, hence removing the α, β-unsaturated functionality while maintaining a planar ring system.

In a multi-target medicinal chemistry campaign of the flavonol scaffold, several compounds were found to maintain GSH levels following the addition of glutamate [ 75 ]. Induction of NRF2 was assessed to determine whether these activities correlated over the series; the parent compound fisetin entry 15h was found to induce NRF2 activity, as well as flavonol 15i and chalcone derivatives 15j , 15k.

However, activity is lost upon replacement to the quinoline scaffold e. Several flavonoid derivatives can still result in inhibition of KEAP1 despite not possessing a Michael acceptor per se.

Catechol groups can undergo oxidation under physiological conditions to produce quinones, as depicted in entry This can be achieved over several steps through various mechanisms, such as oxidation with ROS or redox metalloenzymes, if the cellular environment permits it.

Compounds of this class can increase NRF2 activity in vivo [ 79 ]. NRF2 can similarly be modified by other α, β-unsaturated ketone-containing natural products such as chalcones, from which flavonoids are structurally derived [ 86 ]. Notably these compounds exhibit activity while not containing any hydroxyl groups.

A library of fifty-nine chalcones scaffold of entry 17a were synthesized and screened at µM for their ability to modulate NRF2 signalling, as determined by measuring the fold change in expression of ARE-driven genes GCLM and NQO1 [ 87 ]. Ortho-CF 3 17b reliably improved potency of the compounds in terms of fold induction, as compared with meta and para, potentially indicating that a negative inductive effect increases the reactivity of the α, β-unsaturated ketone.

Attempts to recapitulate this by substitution of the CF 3 group for NO 2 17d rendered the compounds cytotoxic [ 87 ]. The pattern of methoxy substitution on the phenyl ring did not show a consistent or discernible SAR profile: the most potent induction of NRF2 in vitro was seen with the unsubstituted ortho-CF 3 derivative 17b , but disubstituted 17f emerged as the most potent of the series when the compounds were examined in vivo in mouse small intestine following gavage 6- and fold upregulation for GCLM and NQO1 respectively compared to vehicle control [ 87 ].

Piperlongumine PL, 18a is a natural product chalcone-derivative with demonstrated cytoprotective effects against H 2 O 2 or 6-OHDA-induced oxidative stress; the protective mechanism is probably mediated through NRF2 signalling [ 88 ] As with the parent chalcone scaffold, retention of the exocyclic trans double bond was found to be necessary for cytoprotection against oxidative stress, as demonstrated by pairwise analysis of compounds 18b and 18c.

The olefin present in the lactam ring in parent PL 18a was not required for potent activation of the antioxidant response. Structures 18b and 18d were identified as the most potent derivatives lacking innate cytotoxicity and were shown to induce the nuclear accumulation of NRF2, with a concomitant upregulation of the antioxidant response.

Knockdown of NRF2 ablated the cytoprotective effect of these compounds, demonstrating their action through the NRF2 axis [ 88 ]. The ability of both stilbenoids and flavonoids to directly scavenge free radical species is dependent on the presence of a labile hydrogen within the polyphenol, usually from OH, to donate to ROS, and also on the resultant stability of the polyphenol radical once formed.

Masking of critical OH groups required for reactivity with ROS ablates potency. Similarly, antioxidant activity of polyphenols is also decreased by destabilisation of the resultant radical through removal of the stilbenoid π-bond olefin or imine , removing scaffold-defining features of flavonols, or substitution on phenyl groups with substituents that destabilise the radical.

With regards to NRF2 activation, α, β-unsaturated carbonyl groups appear to be necessary for polyphenols to act as indirect antioxidants though activation of NRF2. Soft electrophiles are preferred since the mechanism is through reaction with KEAP1 cysteine residues R-SH being a soft nucleophile.

To our knowledge, it has not been conclusively demonstrated whether the less reactive α, β-unsaturated carbonyl groups that are present in the scaffold react directly with KEAP1, or whether said scaffold serves to stabilise the formation of more reactive quinone species in the neighbouring phenol ring, which would subsequently react with KEAP1.

Regardless of mechanism, the strong dependence on the presence of the α, β-unsaturated carbonyls for efficacy is notable. Flavonoids containing imines and ketones retain some potency. Modifications enhancing electrophilic reactivity appear to also enhance in vitro potency for NRF2 activation.

Sensitivity of various structural features towards modification are described in Fig. Summary of key features of polyphenols that contribute to direct or indirect antioxidant activity through ROS scavenging or NRF2 upregulation upper and lower panels respectively.

Black dotted boxes indicate catechol and olefin groups; red indicates important groups also outlined with pale grey dotted ovals.

Age-related diseases ARDs are complex, systems-dependent phenomena; drugs that act on individual protein targets are therefore unlikely to be effective in disease modification.

By contrast, compounds that possess beneficial polypharmacology, i. target multiple therapeutic pathways simultaneously, will have a higher likelihood of robustly modulating ARDs. Polyphenolics such as stilbenoids, flavonoids and chalcones are polypharmacologically active in several ARD-relevant biological processes, particularly oxidative stress, inflammation and cellular senescence.

The pharmacophores for direct and indirect modulation of oxidative stress, through scavenging of ROS or upregulation of NRF2 activity respectively, are overlapping in some areas and discrete in others, but both direct and indirect activities are likely to be important in the overall molecular mechanisms of these compounds in vivo.

Additionally, there are other contributing mechanisms by which specific sub-classes of polyphenolics may affect ROS homeostasis not discussed here, such as inhibition of xanthine oxidase [ 42 ].

This complexity mirrors that of the multiple interacting biochemical pathways involved in generating the complex phenotype of biological ageing. In drug design campaigns for anti-ageing therapeutics, we therefore caution against optimising for efficacy in one particular facet of biochemical activity e.

in vitro quenching of ROS without reflecting the complexity of the biological system [ 89 ] such as that represented by cell and organismal ageing. Moreover, while transformed cancer cell lines are widely used in drug screening presumably because of ease of culture and immortality , they are far from ideal as a platform for testing drugs for amelioration of ageing phenotypes; such immortal cells do not age and their biochemical signalling pathways can be highly abnormal.

Such screening programmes are likely to highlight agents with beneficial polypharmacological properties that may prove to have therapeutic benefit in vivo. Polyphenolic natural products therefore represent strong starting points for medicinal chemistry optimisation campaigns in anti-ageing therapeutics.

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J Med Chem 60 23 — Download references. AR is funded by Elysium Health through a personal Oxford-Elysium Fellowship for drug discovery for age-related diseases. The funders had no involvement in the design of the study, in collection, analysis and interpretation of data, or writing of the manuscript.

Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK. You can also search for this author in PubMed Google Scholar. AR conducted the review of the literature; AR and LSC co-wrote the manuscript.

Both authors read and approved the final manuscript. Our collection was open to a broad selection of content related to polyphenols and ageing, such as:. Lizzy Ostler University of Brighton. Submission is open to everyone. Before submitting your manuscript, please ensure you have carefully read the submission guidelines for BMC Chemistry.

Information about our article-processing charges and waivers can be found here. Ageing, and particularly the onset of age-related diseases, is associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage.

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Do you ever wish you Post-Workout Supplement turn back Polyphfnols clock Po,yphenols Polyphenols and anti-aging down the aging process? Well, there might be a way to do just that with the Poltphenols of polyphenols! In this article, we will delve deep into the world of polyphenols and explore how they can work wonders for your anti-aging journey. So, grab a cup of tea, sit back, and let's dive in! Before we talk about the benefits of polyphenols, let's first get to know these mighty compounds a little better.


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