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Fig. 2 | Inflammation and Regeneration

Fig. 2

From: Molecular hydrogen promotes wound healing by inducing early epidermal stem cell proliferation and extracellular matrix deposition

Fig. 2

H2 treatment promoted different ECM components early deposit in the epidermis, dermis and dermis-epidermis-junction of proximal wound. A Representative H&E staining of the truncated region of epidermis at the wound edge at 3 days post-wounding between two groups; graph indicated the widest basal layer of hypertrophic epidermal wound edge. B Masson staining of different regions of wound edge at 3 days post-wounding between two groups. C–H IHC staining showing the expression of ECM components of Col-I, Col-III, Fibronectin, Integrin, Col-XVII, and Laminin, respectively in the wound edge between D3H and D3C groups. I Scheme of a proximal wound section indicating the histological localization of three kinds of collagens: Col-I (dermis), Col-III (epidermis), and Col-XVII (DEJ) expression after H2 treatment during the re-epithelialization process. J Representative image of day 5 post-wounding indicating the moist haling mode possibly triggered by the early ECM deposition induced by H2 treatment. K Overview of mapping of metabolic differences between the 66% H2 and control groups as well as PCA analysis and pathway enrichment of differential metabolomes; R2X = fraction of variance for the model; Q2 = predictive ability of the model. L IHC staining showing the expression of Col-I and Col-III between D11H and D11C groups. Data in A processed unpaired t test, and were plotted as Mean ± SEM. *P value < 0.05; **P value < 0.01; ***P value < 0.001; no stars for P value > 0.05; scale bar = 100 μm. Red line indicates the boundary between the epithelium and dermis. Black arrowhead indicates positive-expressing cell. d, dermis; he, hypertrophic epidermal wound edge; ife, interfollicular epithelium; sm, smooth muscle

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