Fig. 4: The treatment of dexamethasone reduced keratinocytes necroptosis and relieved DNCB-motivated dermatitis. | Cell Death Discovery

Fig. 4: The treatment of dexamethasone reduced keratinocytes necroptosis and relieved DNCB-motivated dermatitis.

From: Necroptosis-mediated HMGB1 secretion of keratinocytes as a key step for inflammation development in contact hypersensitivity

Fig. 4

A Flowchart of the treatment of dexamethasone for CHS murine model. B The skin appearance of CHS mice before and after the topical application of vehicle or dexamethasone. The samples of unmotivated tissue were taken from the left ears of the mice in the vehicle group (indicated by gray arrow). Other tissue samples were indicated by blue arrow. C, D The improvement of skin manifestation after the treatment of dexamethasone was evaluated by Dermatitis Score, ear weight and thickness. (n = 7). E The histology feature of tissue from different group of mice was showed by H&E staining (20× magnification). Red arrow indicated skin necrosis. ∗p < 0.05. F CD4 + , CD8 + or MPO + cells infiltrating in ear tissue of different mice group were detected by immunohistochemistry assay. Scale bar represents 150 μm. G Quantitative analysis of CD4 + , CD8 + or MPO + cells in the skin tissues from the different mice group. (n = 7). ∗p < 0.05. H The level of keratinocyte death was determined by TUNEL staining. (n = 7). I The phosphorylation levels of RIPK1, RIPK3 and MLKL in mice treated with topical dexamethasone therapy were detected by western blotting. Statistical analysis of the interested protein was shown (n = 3). J The phosphorylation of MLKL was detected by immunofluorescence staining (green). (n = 7). Scale bar represents 100 μm. ∗p < 0.05.

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