Fig. 1
From: Quercetin alleviates incontinence-associated dermatitis via IKK/NF-κB pathway
IAD rat model exhibits skin barrier damage, inflammation, and activation of the NF-κB pathway. (A) Representative macroscopic images showing progressive dorsal skin damage in IAD model rats over 5 days, characterized by increasing erythema, epidermal loss, and rash, compared to minimal changes in control rats. (B) Transepidermal water loss (TEWL) significantly increased in IAD rats in a time-dependent manner over 5 days (n = 6 rats per group, Student’s t-test, **p < 0.01, ***p < 0.001). (C) Western blot images showing elevated protein expression and phosphorylation of NF-κB, IKKα, and IKKβ in IAD skin compared to controls. (D) Densitometric analysis confirms significant upregulation of total and phosphorylated NF-κB, IKKα, and IKKβ in IAD rats (n = 6 rats per group, Student’s t-test, *p < 0.05, **p < 0.01, ***p < 0.001). (E) ELISA shows marked elevation of pro-inflammatory cytokines (IL-1β, IL-6, IFN-γ, TNF-α) in IAD skin homogenates (n = 6 rats per group, Student’s t-test, ***p < 0.001). (F) H&E staining reveals epidermal thinning and increased nucleated cell infiltration in the dermis of IAD rats compared to intact control skin (scale bar = 200 μm). (G) Quantification confirms a significant increase in dermal nucleated cell counts in IAD rats (n = 6 rats per group; 5 random fields per sample, Student’s t-test, ***p < 0.001). (H) Filaggrin immunohistochemical staining shows reduced epidermal filaggrin expression (brown signal) in IAD rats versus controls (scale bar = 200 μm). Epidermal area is outlined by a red dashed line. (I) Quantitative analysis indicates approximately a three-fold decrease in filaggrin-positive area in IAD epidermis (n = 6 rats per group; 5 random fields per sample, Student’s t-test, ***p < 0.001).
