Hesperetin attenuates <scp>UVA‐induced</scp> photodamage in human dermal fibroblast cells

Lu, Zhiyu; Xia, Qingyue; Cheng, Yuxin; Lü, Qian; Li, Yueyue; Zeng, Ni; Luan, Xingbao; Li, Yuan; Fan, Lipan; Luo, Dan

doi:10.1111/jocd.15230

Cited by 7 publications

(4 citation statements)

References 41 publications

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“…Hesperidin and hesperetin (10 µM) decreased MMP-1 levels in physiologically aged NHDFs by approximately 20%, which is consistent with the study by Santhanam et al [ 21 ], in which hesperidin also decreased the levels of MMP-1 as well as MMP-3 and MMP-9 in UVB-irradiated human fibroblasts. Additionally, the study by Lu et al (2022) showed that pretreatment with hesperetin suppressed the UVA-induced inflammatory response by downregulating MMP-1, IL-6, and cyclooxygenase 2 [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…In physiologically aged NHDFs, the level of IL-8 decreased mainly after rhamnose treatment. The fact that hesperidin and hesperetin can regulate oxidative stress and inflammatory activity by down-regulating IL-1β, IL-6, and tumor necrosis factor α (TNF-α), has already been published in a number of studies on skin cells exposed to UVA or UVB radiation [ 30 , 33 , 34 ]. Huang et al (2018) postulated that hesperetin decreased the secretion of IL-6 by infected RAW 264.7 [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

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Hesperidin, Hesperetin, Rutinose, and Rhamnose Act as Skin Anti-Aging Agents

et al. 2023

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Aging is a complex physiological process that can be accelerated by chemical (high blood glucose levels) or physical (solar exposure) factors. It is accompanied by the accumulation of altered molecules in the human body. The accumulation of oxidatively modified and glycated proteins is associated with inflammation and the progression of chronic diseases (aging). The use of antiglycating agents is one of the recent approaches in the preventive strategy of aging and natural compounds seem to be promising candidates. Our study focused on the anti-aging effect of the flavonoid hesperetin, its glycoside hesperidin and its carbohydrate moieties rutinose and rhamnose on young and physiologically aged normal human dermal fibroblasts (NHDFs). The anti-aging activity of the test compounds was evaluated by measuring matrix metalloproteinases (MMPs) and inflammatory interleukins by ELISA. The modulation of elastase, hyaluronidase, and collagenase activity by the tested substances was evaluated spectrophotometrically by tube tests. Rutinose and rhamnose inhibited the activity of pure elastase, hyaluronidase, and collagenase. Hesperidin and hesperetin inhibited elastase and hyaluronidase activity. In skin aging models, MMP-1 and MMP-2 levels were reduced after application of all tested substances. Collagen I production was increased after the application of rhamnose and rutinose.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hesperidin, Hesperetin, Rutinose, and Rhamnose Act as Skin Anti-Aging Agents

et al. 2023

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“…Out of these, benzophenone, avobenzone, oxybenzone, sulisobenzone, octisalate, octinoxate, octocrylene, cinoxate, and homosalate are the famous UVA filters 36 . Thus, considering the current escalation in skin cancer cases, there is a greater need to develop newer UVA filters with effective photoprotection and a safer toxicological profile 37 .…”

Section: Discussionmentioning

confidence: 99%

Probing photoprotection properties of lipophilic chain conjugated thiourea-aryl group molecules to attenuate ultraviolet-A induced cellular and DNA damages

Rana

Fatima

Yaqoob

et al. 2022

Sci Rep

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Ultraviolet-A (UVA) radiation is a major contributor to reactive oxygen species (ROS), reactive nitrite species (RNS), inflammation, and DNA damage, which causes photoaging and photocarcinogenesis. This study aimed to evaluate the UVA protective potential of lipophilic chain conjugated thiourea-substituted aryl group molecules against UVA-induced cellular damages in human dermal fibroblasts (BJ cell line). We tested a series of nineteen (19) molecules for UVA photoprotection, from which 2′,5′-dichlorophenyl-substituted molecule DD-04 showed remarkable UVA protection properties compared to the reference (benzophenone). The results indicate that DD-04 significantly reduced intracellular ROS and nitric oxide (NO) as compared to the UVA-irradiated control (p < 0.001). Moreover, the compound DD-04 showed anti-inflammatory activity as it significantly reduced the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) pro-inflammatory cytokines produced by THP-1 (human monocytic) cells (p < 0.05). DNA damage was also prevented by DD-04 treatment in the presence of UVA. It was observed that DD-04 significantly reduced the number of cyclobutane pyrimidine dimers (CPDs) when compared to the UVA-irradiated control (p < 0.001). Finally, the DNA strand breaks were checked and a single intact DNA band was seen upon treatment with DD-04 in the presence of UVA. In conclusion, DD-04 can be considered a potential candidate UVA filter due to its photoprotective potential.

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“…All of the above promote skin health [ 11 ]. In human dermal fibroblast cells, hesperetin alleviates UVA-induced damage, including suppressing cell death, reducing oxidative stress, and decreasing the expression of matrix metalloproteinases (MMPs) and pro-inflammatory cytokines [ 12 ]. In rats, topical treatment with hesperetin-based hydrogels protects against UV-induced skin damage [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Hesperetin activates CISD2 to attenuate senescence in human keratinocytes from an older person and rejuvenates naturally aged skin in mice

Shen,

Chang,

Yeh

et al. 2024

J Biomed Sci

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Background CDGSH iron-sulfur domain-containing protein 2 (CISD2), a pro-longevity gene, mediates healthspan in mammals. CISD2 is down-regulated during aging. Furthermore, a persistently high level of CISD2 promotes longevity and ameliorates an age-related skin phenotype in transgenic mice. Here we translate the genetic evidence into a pharmaceutical application using a potent CISD2 activator, hesperetin, which enhances CISD2 expression in HEK001 human keratinocytes from an older person. We also treated naturally aged mice in order to study the activator’s anti-aging efficacy. Methods We studied the biological effects of hesperetin on aging skin using, firstly, a cell-based platform, namely a HEK001 human keratinocyte cell line established from an older person. Secondly, we used a mouse model, namely old mice at 21-month old. In the latter case, we investigate the anti-aging efficacy of hesperetin on ultraviolet B (UVB)-induced photoaging and naturally aged skin. Furthermore, to identify the underlying mechanisms and potential biological pathways involved in this process we carried out transcriptomic analysis. Finally, CISD2 knockdown HEK001 keratinocytes and Cisd2 knockout mice were used to study the Cisd2-dependent effects of hesperetin on skin aging. Results Four findings are pinpointed. Firstly, in human skin, CISD2 is mainly expressed in proliferating keratinocytes from the epidermal basal layer and, furthermore, CISD2 is down-regulated in the sun-exposed epidermis. Secondly, in HEK001 human keratinocytes from an older person, hesperetin enhances mitochondrial function and protects against reactive oxygen species-induced oxidative stress via increased CISD2 expression; this enhancement is CISD2-dependent. Additionally, hesperetin alleviates UVB-induced damage and suppresses matrix metalloproteinase-1 expression, the latter being a major indicator of UVB-induced damage in keratinocytes. Thirdly, transcriptomic analysis revealed that hesperetin modulates a panel of differentially expressed genes that are associated with mitochondrial function, redox homeostasis, keratinocyte function, and inflammation in order to attenuate senescence. Intriguingly, hesperetin activates two known longevity-associated regulators, namely FOXO3a and FOXM1, in order to suppress the senescence-associated secretory phenotype. Finally, in mouse skin, hesperetin enhances CISD2 expression to ameliorate UVB-induced photoaging and this occurs via a mechanism involving CISD2. Most strikingly, late-life treatment with hesperetin started at 21-month old and lasting for 5 months, is able to retard skin aging and rejuvenate naturally aged skin in mice. Conclusions Our results reveal that a pharmacological elevation of CISD2 expression at a late-life stage using hesperetin treatment is a feasible approach to effectively mitigating both intrinsic and extrinsic skin aging and that hesperetin could act as a functional food or as a skincare product for fighting skin aging.

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Hesperetin attenuates UVA‐induced photodamage in human dermal fibroblast cells

Cited by 7 publications

References 41 publications

Hesperidin, Hesperetin, Rutinose, and Rhamnose Act as Skin Anti-Aging Agents

Hesperidin, Hesperetin, Rutinose, and Rhamnose Act as Skin Anti-Aging Agents

Probing photoprotection properties of lipophilic chain conjugated thiourea-aryl group molecules to attenuate ultraviolet-A induced cellular and DNA damages

Hesperetin activates CISD2 to attenuate senescence in human keratinocytes from an older person and rejuvenates naturally aged skin in mice

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