Effect of extracts and isolated compounds derived from Retama monosperma (L.) Boiss. on anti-aging gene expression in human keratinocytes and antioxidant activity

Zefzoufi, Manal; Fdil, Rabiaa; Bouamama, Hafida; Gadhi, Chemseddoha; Katakura, Yoshinori; Mouzdahir, Abdelkarim; Sraidi, Khadija

doi:10.1016/j.jep.2021.114451

Cited by 22 publications

(23 citation statements)

References 48 publications

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“…Results obtained on different cell lines show that treatment with quercetin significantly lowers the levels of ROS and inflammatory cytokines, reduces the expression of SA-β gal, p16 and p53 and markedly increases that of the antioxidant enzymes SOD and CAT, regardless of the type of oxidative trigger used to induce senescence [ 258 , 259 , 260 , 261 , 262 ]. In addition to promoting the expression of Nrf2 [ 263 ], the beneficial action of quercetin appears to be mediated by the microRNA-155-5p, which is involved in the regulation of SIRT1 and NF-kB [ 262 , 264 ]. Moreover, as aging is associated with an inefficient protein-degradation (which is required to protect against OS), the effect of quercetin and its derivatives on the restoration of proteasomal functioning is of interest as rejuvenating strategy [ 265 ].…”

Section: Resultsmentioning

confidence: 99%

“…Isoflavonoids. Genistein is a phytoestrogen extracted by soya that is known for its antioxidant and anti-aging properties, although less potent than other flavonoids such as quercetin and kaempferol [ 264 ]. As for other antioxidants, the role of genistein is multiple: it can induce apoptosis acting as a cancer protective compound, but it can also reduce inflammation and OS acting as anti-aging and neurodegenerative protective agent [ 276 ].…”

Section: Resultsmentioning

confidence: 99%

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The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

et al. 2022

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Cellular senescence is an irreversible state of cell cycle arrest occurring in response to stressful stimuli, such as telomere attrition, DNA damage, reactive oxygen species, and oncogenic proteins. Although beneficial and protective in several physiological processes, an excessive senescent cell burden has been involved in various pathological conditions including aging, tissue dysfunction and chronic diseases. Oxidative stress (OS) can drive senescence due to a loss of balance between pro-oxidant stimuli and antioxidant defences. Therefore, the identification and characterization of antioxidant compounds capable of preventing or counteracting the senescent phenotype is of major interest. However, despite the considerable number of studies, a comprehensive overview of the main antioxidant molecules capable of counteracting OS-induced senescence is still lacking. Here, besides a brief description of the molecular mechanisms implicated in OS-mediated aging, we review and discuss the role of enzymes, mitochondria-targeting compounds, vitamins, carotenoids, organosulfur compounds, nitrogen non-protein molecules, minerals, flavonoids, and non-flavonoids as antioxidant compounds with an anti-aging potential, therefore offering insights into innovative lifespan-extending approaches.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

et al. 2022

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“…Meanwhile, Sirtuin 3 (Sirt3), as a major deacetylase in mitochondria is responsible for deacetylation of mitochondrial proteins, including SOD2 [ 21 ]. Interestingly, a recent study in vitro has hinted that kaempferol can promote the expression of Sirt3 [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Sirtuin 3 Plays a Critical Role in the Antidepressant- and Anxiolytic-like Effects of Kaempferol

Wang

Liang

et al. 2022

Antioxidants

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An estimated 20% of women experience depression at some point during menopause. Hormone replacement therapy (HRT), as the main therapy for depression and other menopausal syndromes, comes with a few undesirable side effects and a potential increase in cancer and cardiovascular risk. Consequently, there is a dire need for the development of new therapies to treat menopausal depression. Oxidative stress combined with the decline in sex hormones might explain the occurrence of psychological symptoms characteristic of menopause. Therefore, antioxidants have been suggested as a promising therapy for aging-associated diseases, such as menopausal depression. As a flavonoid antioxidant, kaempferol might have a potential neuroprotective action. Hence, the study was conducted to assess the potential antidepressant action of kaempferol and clarify the underlying mechanism. The results show that kaempferol has potential beneficial effects on VCD-induced rodent model of menopausal depression and produces antioxidant effects as well as increases the deacetylation of superoxide dismutase 2 (SOD2) and the protein level of Sirtuin3 (Sirt3) in the hippocampus. On the contrary, Sirt3 depletion abrogated the antidepressant- and anxiolytic-like effects as well as antioxidant effects of kaempferol. In conclusion, kaempferol might produce antidepressant effects via upregulating the expression of Sirt3, the major deacetylase in mitochondria, and subsequently activate the mitochondrial antioxidases. These findings shed some light on the use of kaempferol or vegetables and herbs that contain kaempferol as a complementary therapy for menopausal depression.

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“…The number of free radicals created and the amount of antioxidants produced in the human body are in balance. 3…”

Section: Introductionmentioning

confidence: 99%

“…The number of free radicals created and the amount of antioxidants produced in the human body are in balance. 3 Human skin serves as the primary barrier against environmental pollutants while also providing external beauty. Extrinsic skin aging, also known as skin photoaging, is caused by prolonged exposure to external stimuli, with UVB and UVB irradiation being one of the most damaging culprits.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and Protective Effect of Acetone Extract of Entada phaseoloides Leaves on UVB-Irradiated Human Epidermal Keratinocytes (HaCaT cells) by Inhibiting COX-2, iNOS, and Caspase-3 Activation

Mittraphab

Matsumoto

Shimizu

2022

Natural Product Communications

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Chronic ultraviolet (UV) exposure produces oxidative stress, molecular damage, and aging-related signal transduction, all of which contribute to skin photoaging. In this study, the antioxidant and anti-inflammatory activities of Entada phaseoloides are reported. High-performance liquid chromatography (HPLC) detected 7 phenolic compounds: gallic acid, protocatechuic acid, 4-hydroxybenzoic acid, quercetin, luteolin, kaempferol, and apigenin. We investigated the antioxidant and protective effect of the acetone extract of E. phaseoloides leaves (AEP) on UVB-irradiated human epidermal keratinocytes (HaCaT cells). AEP showed antioxidant activity in the 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2-azinobis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) assays. AEP at a concentration of 40 μg/mL increased cell survival rate of the UVB-damaged cells. Moreover, AEP blocked gene expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in UVB-induced HaCaT cells and decreased UVB-induced apoptosis in HaCaT cells by regulating the gene expression of caspase-3. These results suggest that AEP has the potential to protect against UVB irradiation and antioxidant.

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Effect of extracts and isolated compounds derived from Retama monosperma (L.) Boiss. on anti-aging gene expression in human keratinocytes and antioxidant activity

Cited by 22 publications

References 48 publications

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

Sirtuin 3 Plays a Critical Role in the Antidepressant- and Anxiolytic-like Effects of Kaempferol

Antioxidant and Protective Effect of Acetone Extract of Entada phaseoloides Leaves on UVB-Irradiated Human Epidermal Keratinocytes (HaCaT cells) by Inhibiting COX-2, iNOS, and Caspase-3 Activation

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