Fig. 1: RIPK1 contributes to the cell inflammation after UVB irradiation by activating NF-κB. | Cell Death Discovery

Fig. 1: RIPK1 contributes to the cell inflammation after UVB irradiation by activating NF-κB.

From: UVB-Induced necroptosis of the skin cells via RIPK3-MLKL activation independent of RIPK1 kinase activity

Fig. 1

A Cell viability of HaCaT cells 24 h after UVB irradiation at varying doses assessed using the CCK-8 assay. Western blotting of RIPK1 (B) and IкBα (C) in HaCaT cells at 24 h after 60 mJ/cm2 UVB irradiation. D Levels of IL-1β, TNF-α, and IL-6 in the medium measured by ELISA 12 h after irradiation of HaCaT cells and 10 µM Nec-1-pretreated HaCaT cells with 60 mJ/cm² UVB; TSZ and LPS treatments serving as positive controls. E Levels of IL-1β, TNF-α, and IL-6 in the medium measured by ELISA 12 h after irradiation of NC HaCaT and RIPK1-KD HaCaT cells with 60 mJ/cm² UVB; TSZ and LPS treatments serving as positive controls. F Western blotting and statistical analysis of the relative protein level of IκBα in NC HaCaT and RIPK1-KD HaCT cells 12 h after 60 mJ/cm2 UVB irradiation. G Western blot analysis of phosphorylated (p)-p65 and total p65 in NC HaCaT and RIPK1-KD HaCT cells 12 h after 60 mJ/cm2 UVB irradiation. TSZ: 20 ng/mL TNF-α + 100 nM SM-164 + 20 μM Z-VAD(OMe)-FMK; LPS: 20 μg/mL LPS; NC negative control; RIPK1-KD: RIPK1-knockdown. Data are presented as mean ± SD, n = 3. P values determined by one-way analysis of variance (ANOVA), *P < 0.05, **P < 0.01.

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