Fucoidan from Undaria pinnatifida Ameliorates Epidermal Barrier Disruption via Keratinocyte Differentiation and CaSR Level Regulation

Chen, Yu; Li, Xue-Nan; Gan, Xiaoshuang; Qi, Junmei; Che, Biao; Tai, Meiling; Gao, Shuang; Zhao, Wengang; Xu, Nuo; Hu, Zhenlin

doi:10.3390/md17120660

Cited by 15 publications

(10 citation statements)

References 45 publications

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“…Fucoidans have been demonstrated to exert antiphotoaging effects against UV irradiation. We found that the fucoidan from UPF can ameliorate epidermal barrier disruption (25). In the present study, we explored the effect of UPF on UV-induced epidermis and dermis aging.…”

Section: Discussionmentioning

confidence: 91%

“…Fucoidan purified from Undaria pinnatifida (UPF) also exerts its photoprotective effect by augmenting the immune response and decreasing the matrix metalloproteinase-1 (MMP-1) level in UVB-irradiated mouse skin although its mechanism remains unknown (24). Based on results of our previous study (25), we hypothesized that UPF exerts antiphotoaging effects against UV irradiation. This study was aimed to explore the effect of UPF on UV-irradiated keratinocytes and fibroblasts and to explore the potential underlying mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of fucoidan purified from Undaria pinnatifida against UV-irradiated skin photoaging

Jing¹,

Guo²,

Zhong³

et al. 2021

Ann Transl Med

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Background: Exposure to ultraviolet (UV) radiation (UVB and UVA) is the most well-known extrinsic factor that induces skin aging. Fucoidan has been shown to possess antiphotoaging effects against UV irradiation and can be used as an ingredient in the pharmaceutical industry. The present study evaluated the photoprotective effect of fucoidan purified from Undaria pinnatifida (UPF) on UV-induced skin photoaging and explored its potential molecular mechanism.Methods: To evaluate the effect of UPF on UV-induced skin aging, HaCaT cells and HFF-1 cells were pretreated with or without UPF and then exposed to UVB and UVA radiation, respectively, and the levels of cellular senescence, reactive oxygen species (ROS) production and mitochondrial dysfunction were evaluated. The mitochondrial ROS (mROS) was stained through MitoSOX, and the confocal microscope was used to capture the images. For further exploration of AMPK/SIRT-1/PGC-1α signaling, western blot was employed. Results:The results demonstrated that pretreatment of HaCaT and HFF-1 cells with UPF ameliorated cellular senescence, ROS and mROS overproduction, and mitochondrial dysfunction caused by UV exposure. This research also revealed that UPF could activate the AMPK/SIRT-1/PGC-1α signaling pathway to promote mitochondrial biogenesis.Conclusions: UPF can ameliorate UV-induced skin photoaging through inhibition of ROS production via the alleviation of mitochondrial dysfunction by regulating the SIRT-1/PGC-1α signaling pathway.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Protective effects of fucoidan purified from Undaria pinnatifida against UV-irradiated skin photoaging

Jing¹,

Guo²,

Zhong³

et al. 2021

Ann Transl Med

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“…In mouse studies, which examined effects of CaSR knockdown (13,17,41), 90% knockdown of the CaSR protein in the epidermis eventually led to disruption of the epidermal permeability barrier. Treatment of immortalized keratinocytes with NPS‐2143 has also been reported to inhibit some measures of cellular differentiation (61). In this study, siRNA knockdown of CaSR in keratinocytes was only 60%.…”

Section: Discussionmentioning

confidence: 99%

UV‐induced DNA Damage in Skin is Reduced by CaSR Inhibition

Yang

Rybchyn

Silva

et al. 2022

Photochem & Photobiology

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The epidermis maintains a cellular calcium gradient that supports keratinocyte differentiation from its basal layers (low) to outer layers (high) leading to the development of the stratum corneum, which resists penetration of UV radiation. The calcium-sensing receptor (CaSR) expressed in keratinocytes responds to the calcium gradient with signals that promote differentiation. In this study, we investigated whether the CaSR is involved more directly in protection from UV damage in studies of human keratinocytes in primary culture and in mouse skin studied in vivo. siRNA-directed reductions in CaSR protein levels in human keratinocytes significantly reduced UV-induced direct cyclobutane pyrimidine dimers (CPD) by ~80% and oxidative DNA damage (8-OHdG) by ~65% compared with control transfected cells. Similarly, in untransfected cells, the CaSR negative modulator, NPS-2143 (500 nM), reduced UV-induced CPD and 8-OHdG by ~70%. NPS-2143 also enhanced DNA repair and reduced reactive oxygen species (ROS) by ~35% in UV-exposed keratinocytes, consistent with reduced DNA damage after UV exposure. Topical application of NPS-2143 also protected hairless Skh: hr1 mice from UV-induced CPD, oxidative DNA damage and inflammation, similar to the reductions observed in response to the well-known photoprotection agent 1,25(OH) 2 D 3 (calcitriol). Thus, negative modulators of the CaSR offer a new approach to reducing UV-induced skin damage.

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“…11 Chen et al have demonstrated that fucoidan can regulate calcium levels in the body, thereby augmenting the sensitivity of keratinocytes to calcium ions, inducing keratinocyte differentiation under low calcium levels, and promoting epidermal barrier repair. 12 Moreover, studies have revealed that fucoidan mitigates lipid peroxidation, enhances antioxidant enzyme activity, suppresses the expression of inflammatory factors, and interacts with growth factors to promote dermal wound healing. 13,14 Recent research has suggested that fucoidan can regulate heparin-binding growth factors, such as FGF-2, to generate angiogenesis in vitro.…”

Section: Introductionmentioning

confidence: 99%

Fucoidan promotes angiogenesis and accelerates wound healing through AKT/Nrf2/HIF‐1α signalling pathway

Wen,

Yang,

Wang

et al. 2023

International Wound Journal

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After skin injury, wound repair involves a complex process in which angiogenesis plays a crucial role. Previous research has indicated that fucoidan may aid in wound healing; we therefore hypothesised that fucoidan may speed up the process by promoting angiogenesis. In this study, we investigated the potential molecular mechanism underlying fucoidan's ability to accelerate wound healing by promoting angiogenesis. Using a full‐cut wound model, we observed that fucoidan significantly intensified wound closure and promoted granulation formation and collagen deposition. Immunofluorescence staining revealed that fucoidan also promoted wound angiogenesis, specifically by accelerating the migration of new blood vessels to the middle area of the wound. Furthermore, fucoidan demonstrated the ability to enhance the proliferation of human umbilical vein endothelial cells (HUVECs) damaged by hydrogen peroxide (H2O2) and to improve the formation of endothelial tubes. Mechanistic studies revealed that fucoidan upregulated the protein levels of the AKT/Nrf2/HIF‐1α signalling pathway, which plays a crucial role in angiogenesis. This was further confirmed using the inhibitor LY294002, which reversed the promotion of endothelial tube formation by fucoidan. Overall, our findings suggest that fucoidan can promote angiogenesis via the AKT/Nrf2/HIF‐1α signalling pathway and accelerate wound healing.

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Fucoidan from Undaria pinnatifida Ameliorates Epidermal Barrier Disruption via Keratinocyte Differentiation and CaSR Level Regulation

Cited by 15 publications

References 45 publications

Protective effects of fucoidan purified from Undaria pinnatifida against UV-irradiated skin photoaging

Protective effects of fucoidan purified from Undaria pinnatifida against UV-irradiated skin photoaging

UV‐induced DNA Damage in Skin is Reduced by CaSR Inhibition

Fucoidan promotes angiogenesis and accelerates wound healing through AKT/Nrf2/HIF‐1α signalling pathway

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