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Glycyrrhizin-Based Hydrogels Accelerate Wound Healing of Normoglycemic and Diabetic Mouse Skin.

ABSTRACT: Efficient wound repair is crucial for mammalian survival. Healing of skin wounds is severely hampered in diabetic patients, resulting in chronic non-healing wounds that are difficult to treat. High-mobility group box 1 (HMGB1) is an important signaling molecule that is released during wounding, thereby delaying regenerative responses in the skin. Here, we show that dissolving glycyrrhizin, a potent HMGB1 inhibitor, in water results in the formation of a hydrogel with remarkable rheological properties. We demonstrate that these glycyrrhizin-based hydrogels accelerate cutaneous wound closure in normoglycemic and diabetic mice by influencing keratinocyte migration. To facilitate topical application of glycyrrhizin hydrogels on cutaneous wounds, several concentrations of glycyrrhizinic acid in water were tested for their rheological, structural, and biological properties. By varying the concentration of glycyrrhizin, these hydrogel properties can be readily tuned, enabling customized wound care.

SUBMITTER: Mees MA

PROVIDER: S-EPMC9861362 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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Glycyrrhizin-Based Hydrogels Accelerate Wound Healing of Normoglycemic and Diabetic Mouse Skin.

Mees Maarten A MA Boone Fleur F Bouwen Thomas T Vanaerschot Frederik F Titeca Charlotte C Vikkula Hanna-Kaisa HK Catrysse Leen L Vananroye Anja A Koos Erin E Alexandris Stelios S Rosenfeldt Sabine S Eyley Samuel S Koetz Joachim J van Loo Geert G Thielemans Wim W Hoste Esther E

Pharmaceutics 20221221 1

Efficient wound repair is crucial for mammalian survival. Healing of skin wounds is severely hampered in diabetic patients, resulting in chronic non-healing wounds that are difficult to treat. High-mobility group box 1 (HMGB1) is an important signaling molecule that is released during wounding, thereby delaying regenerative responses in the skin. Here, we show that dissolving glycyrrhizin, a potent HMGB1 inhibitor, in water results in the formation of a hydrogel with remarkable rheological prope ...[more]

PMID: 36678656

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Project description:BackgroundReactive oxygen species (ROS) are increased in diabetic conditions and play a causal role in diabetic foot ulcers (DFU). We previously showed that ROS up-regulate miR-200c expression, that in turns causes apoptosis, senescence, ROS upregulation and nitric oxide decrease, leading to endothelial disfunction.MethodsThe aim of this study is to dissect miR-200c role in DFU and to explore the potential role of anti-miR-200c and antioxidant catalase (CAT) in promoting wound healing (WH). miR-200c inhibition and CAT treatment were performed either in immortalized keratinocytes (HaCaT) or in primary fibroblasts (FBs) and keratinocytes (KCs) deriving from diabetic patients (pts) undergoing amputations. Primary cells deriving from pts undergoing saphenectomies were used as controls. The miR-200c blockade was performed either via lentiviral particles bearing an anti-miR-200c sequence or locked nucleic acid (LNA) anti-miR-200c oligos. Equine CAT was administered on cell medium. The WH assay was performed in vivo on diabetic (db/db) mice by a topical treatment with CAT and LNA anti-miR-200c on wounds dissolved in a Pluronic gel mixture, administered every three days.ResultsWe found that miR-200c levels were increased by different stimuli known to induce ROS, such as ultraviolet radiation (UV), hydrogen peroxide (H2O2), and high glucose in HaCaT. miR-200c was also upregulated in skin biopsies, in FBs and KCs isolated from pts with DFU vs controls. Forced miR-200c expression induced ROS in both FBs and KCs, and CAT reduced it. miR-200c inhibition improved WH in HaCaT, both under basal conditions and after UV and H2O2 treatment, and the simultaneous treatment with CAT accelerated it. miR-200c inhibition accelerated WH in KCs of DFU pts, increasing its protein targets: sirtuin 1 (SIRT1), the transcription factors FOXO1 and ZEB1 and decreasing p66Shc phosphorylation at Ser-36, that is induced by ROS, and the co-treatment with CAT showed synergistic effects in reducing ROS and cytotoxicity. Interestingly, CAT treatment decreased miR-200c expression in FBs and KCs of DFU pts. Topical administration of anti-miR-200c and CAT in a WH model of diabetic mice accelerated closure.ConclusionsAnti-miR-200c and CAT could be considered a novel treatment for DFU and, possibly, for other types of non-diabetic skin ulcers.

Dataset Information

Glycyrrhizin-Based Hydrogels Accelerate Wound Healing of Normoglycemic and Diabetic Mouse Skin.

Publications

Glycyrrhizin-Based Hydrogels Accelerate Wound Healing of Normoglycemic and Diabetic Mouse Skin.

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