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. 2021 Nov 30;9(12):1802. doi: 10.3390/biomedicines9121802

Figure 11.

Figure 11

(A) HaCaT keratinocyte scratch wound closure over time after induction of chronic inflammatory conditions (TNF-α/IFN-γ) and treatment with wIRA or heating w/o wIRA. (B) Evaluation of scratch wound healing in [%]. (C) Gene expression profiles of these HaCaT keratinocytes at specific time points during scratch wound healing after induction of chronic inflammatory conditions (TNF-α/IFN-γ) showed differences for pro-inflammatory cytokine gene expression after 1 h (IL1A, IL6) and 3 h (CXCL8) as well as growth factor gene transcription after 3 h and stress response gene levels after 6 h. In addition, heat shock protein gene expression exhibited alterations after 6 h while AMP gene expression was partly affected at 48 h as well as desmoglein gene expression. Asterisks [*] indicate significant differences in scratch wound healing or transcription level compared to 1 h (* p < 0.05, ** p < 0.01, *** p < 0.001). Hashtags [#] designate significant differences of scratch wound healing or transcription levels at the respective time point compared to the control under optimal conditions (# p < 0.05, ## p < 0.01, ### p < 0.001) while the paragraph character [§] shows significant differences between untreated and treated samples under non-optimal conditions at the respective time point (§ p < 0.05, §§ p < 0.001, §§§ p < 0.001). The plus sign [+] specifies significant differences between wIRA-treated samples and those receiving heating w/o wIRA under non-optimal conditions at the respective time point (+ p < 0.05, ++ p < 0.01).