Rosa laevigata Michx. Polysaccharide Ameliorates Diabetic Nephropathy in Mice through Inhibiting Ferroptosis and PI3K/AKT Pathway-Mediated Apoptosis and Modulating Tryptophan Metabolism

Zhang, Tianyu; Sun, Wenjuan; Wang, Lixin; Zhang, Hui; Wang, Yuansong; Pan, Baochao; Li, Hanzhou; Ma, Ziang; Xu, Kai; Cui, Huantian; Lv, Shuquan

doi:10.1155/2023/9164883

Cited by 4 publications

(1 citation statement)

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“…Many plant polysaccharides extracts and monosaccharides have certain anti‐inflammatory effects on the skin barrier. 15 , 16 , 17 , 39 , 40 Wound healing and repair involve individual and collective cellular migration processes. 41 We found that PURP at concentrations ranging from 1 to 500 µg/mL had no cytotoxic effects, with cell viabilities greater than 100% (Figure 2A ).…”

Section: Resultsmentioning

confidence: 99%

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

Wang,

et al. 2024

Skin Research and Technology

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BackgroundPlant polysaccharides have various biological activities. However, few studies have been conducted on the skin barrier of Prinsepia utilis Royle polysaccharide extract (PURP).Materials and methodsThe 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.ResultsPURP 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.ConclusionWe 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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