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      Prinsepia utilis Royle polysaccharides promote skin barrier repair through the Claudin family

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          Abstract

          Background

          Plant polysaccharides have various biological activities. However, few studies have been conducted on the skin barrier of Prinsepia utilis Royle polysaccharide extract (PURP).

          Materials and methods

          The proportions of polysaccharides, monosaccharides and proteins were determined by extracting polysaccharides from fruit meal using water. The healing rate was measured by cell scratch assays. SDS‐damaged reconstructed human epidermal models, an acetone–ether‐induced mouse model and an IL‐4‐induced cellular inflammation model were used to detect the effects of polysaccharides on the phenotype, HA, TEWL, and TEER, with further characterizations performed using QRT‐PCR, Western blotting, immunofluorescence (IF) assays.

          Results

          PURP contained 35.73% polysaccharides and 11.1% proteins. PURP promoted cell migration and increased skin thickness in a reconstructed human epidermis model. The TEWL significantly decreased, and the HA content significantly increased. PURP significantly increased the TEER and decreased the permeability of the SDS‐damaged reconstructed human epidermis model. Claudin‐3, Claudin‐4, and Claudin‐5 were significantly upregulated. IF and Western blot analysis revealed that the Claudin‐4 level significantly increased after treatment with PURP. Claudin‐1, Claudin‐3, Claudin‐4, and Claudin‐5 gene expression and IF and immunohistochemical staining were significantly increased in mice treated with acetone–ether. PURP promoted the expression of Claudin‐1, Claudin‐3, Claudin‐4, and Claudin‐5 after treatment with 100 ng/mL IL‐4. PURP also downregulated the expression of NO, IL6, TNFα and NFκB in Raw 264.7 cells and in a mouse model.

          Conclusion

          We hypothesize that PURP may repair the skin barrier by promoting the expression of the claudin family and can assist in skin therapy.

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          Most cited references68

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          Inflammatory responses and inflammation-associated diseases in organs

          Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease. Both infectious and non-infectious agents and cell damage activate inflammatory cells and trigger inflammatory signaling pathways, most commonly the NF-κB, MAPK, and JAK-STAT pathways. Here, we review inflammatory responses within organs, focusing on the etiology of inflammation, inflammatory response mechanisms, resolution of inflammation, and organ-specific inflammatory responses.
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            • Record: found
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            Tight junction proteins.

            A fundamental function of epithelia and endothelia is to separate different compartments within the organism and to regulate the exchange of substances between them. The tight junction (TJ) constitutes the barrier both to the passage of ions and molecules through the paracellular pathway and to the movement of proteins and lipids between the apical and the basolateral domains of the plasma membrane. In recent years more than 40 different proteins have been discovered to be located at the TJs of epithelia, endothelia and myelinated cells. This unprecedented expansion of information has changed our view of TJs from merely a paracellular barrier to a complex structure involved in signaling cascades that control cell growth and differentiation. Both cortical and transmembrane proteins integrate TJs. Among the former are scaffolding proteins containing PDZ domains, tumor suppressors, transcription factors and proteins involved in vesicle transport. To date two components of the TJ filaments have been identified: occludin and claudin. The latter is a protein family with more than 20 members. Both occludin and claudins are integral proteins capable of interacting adhesively with complementary molecules on adjacent cells and of co-polymerizing laterally. These advancements in the knowledge of the molecular structure of TJ support previous physiological models that exhibited TJ as dynamic structures that present distinct permeability and morphological characteristics in different tissues and in response to changing natural, pathological or experimental conditions.
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              Skin hydration: a review on its molecular mechanisms.

              Water is absolutely essential for the normal functioning of the skin and especially its outer layer, the stratum corneum (SC). Loss of water from the skin must be carefully regulated, a function dependent on the complex nature of the SC. The retention of water in the SC is dependent on two major components: (1) the presence of natural hygroscopic agents within the corneocytes (collectively referred to as natural moisturizing factor) and (2) the SC intercellular lipids orderly arranged to form a barrier to transepidermal water loss (TEWL). The water content of the SC is necessary for proper SC maturation and skin desquamation. Increased TEWL impairs enzymatic functions required for normal desquamation resulting in the visible appearance of dry, flaky skin. There have been recent discoveries regarding the complex mechanisms of skin hydration. In particular, it has been discovered that glycerol, a well-known cosmetic ingredient, exists in the SC as a natural endogenous humectant. Hyaluronan, which has been regarded mainly as dermal component, is found in the epidermis and is important for maintaining normal SC structure and epidermal barrier function. More importantly, the discovery of the existence of the water-transporting protein aquaporin-3 in the viable epidermis and the presence of tight junction structures at the junction between the stratum granulosum and SC have brought new insights into the mechanisms of skin water distribution and barrier function.
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                Author and article information

                Contributors
                susiewbcc@outlook.com
                Journal
                Skin Res Technol
                Skin Res Technol
                10.1111/(ISSN)1600-0846
                SRT
                Skin Research and Technology
                John Wiley and Sons Inc. (Hoboken )
                0909-752X
                1600-0846
                08 July 2024
                July 2024
                : 30
                : 7 ( doiID: 10.1111/srt.v30.7 )
                : e13848
                Affiliations
                [ 1 ] Yunnan Botanee Biotechnology Group Co., Ltd. Yunnan China
                [ 2 ] Yunnan Characteristic Plant Extraction Laboratory Yunnan Yunke Characteristic Plant Extraction Laboratory Co., Ltd. Kunming China
                Author notes
                [*] [* ] Correspondence

                Li He, Yunnan Characteristic Plant Extraction Laboratory, Yunnan Yunke Characteristic Plant Extraction Laboratory Co., Ltd., Kunming 650106, China.

                Email: susiewbcc@ 123456outlook.com

                Author information
                https://orcid.org/0000-0002-7912-1053
                https://orcid.org/0000-0002-3601-3036
                Article
                SRT13848
                10.1111/srt.13848
                11231044
                38978226
                3c49d2d1-5504-4d05-8ae7-681e932a061d
                © 2024 The Authors. Skin Research and Technology published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 10 April 2024
                : 16 June 2024
                Page count
                Figures: 8, Tables: 0, Pages: 15, Words: 7689
                Funding
                Funded by: The High‐Level Talent Promotion and Training Project of Kunming
                Award ID: 2022SCP008
                Funded by: Independent Research Fund of the Yunnan Characteristic Plant Extraction Laboratory
                Award ID: 2022YKZY001
                Categories
                Original Article
                Original Article
                Custom metadata
                2.0
                July 2024
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.4.5 mode:remove_FC converted:09.07.2024

                cell model,claudin,mouse model,polysaccharides,reconstructed human epidermis model,skin barrier

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