Phospho-RIPK1 (Ser166) Antibody - #AF2398

FIGURE 2 CHBP inhibits necroptosis in random-pattern skin flaps. (a,b) Representative immunohistochemical staining for RIPK3 (brown) in mouse skin tissues from the control, FLAP and FLAP + CHBP groups and quantification of integrated absorbance of RIPK3 signal (n = 6 mice per group). The tissues were counterstained with haematoxylin (blue; scale bar = 100 μm). (c,d) Representative images of immunofluorescence staining of mouse skin samples (DAPI staining of the nuclei) and quantification graph for RIPK1 (green)-positive cells (n = 6 mice per group). Scale bar: 10 μm. Skin samples were harvested from mice in the control, FLAP and FLAP + CHBP groups. (e–g) CHBP treatment attenuated the activation of RIPK1, RIPK3 and MLKL induced by ischaemia–reperfusion injury. The expression of caspase 8 (CASP8) was significantly increased, which has an inhibitory effect on necroptosis. Densitometric quantification is shown (n = 6 mice per group). Data shown are means ± SEM. *P 

Fig. 2: Expression of necroptosis in LPS-induced ALI. a, d, g Validation of protein expression levels of RIPK1, p-RIPK1, RIPK3, p-RIPK3, MLKL, and p-MLKL in mouse lung tissue with ALI using western blotting. b, c, e, f, h, i Quantitative statistical analysis of the western blotting results was performed by measuring the grayscale values of the bands using Image J, with the target bands normalized to the internal reference (β-actin). j Fluorescence microscope images of paraffin tissue sections from mouse lung tissues stained with anti-p-RIPK1 (green), anti-p-RIPK3 (grey), anti-p-MLKL (red), and DAPI (blue) for visualization, with a scale bar indicating 50μm. At least three samples were included in each group, with three randomly selected fields of view from each sample used to measure and analyze the corresponding fluorescence signal intensity. Significance was determined with p-values 

Fig. 2: Expression of necroptosis in LPS-induced ALI. a, d, g Validation of protein expression levels of RIPK1, p-RIPK1, RIPK3, p-RIPK3, MLKL, and p-MLKL in mouse lung tissue with ALI using western blotting. b, c, e, f, h, i Quantitative statistical analysis of the western blotting results was performed by measuring the grayscale values of the bands using Image J, with the target bands normalized to the internal reference (β-actin). j Fluorescence microscope images of paraffin tissue sections from mouse lung tissues stained with anti-p-RIPK1 (green), anti-p-RIPK3 (grey), anti-p-MLKL (red), and DAPI (blue) for visualization, with a scale bar indicating 50μm. At least three samples were included in each group, with three randomly selected fields of view from each sample used to measure and analyze the corresponding fluorescence signal intensity. Significance was determined with p-values 

Fig. 2 Homer1-KD promoted post-ischemic neuronal necroptosis. A, B Representative images A and quantification B of neuronal death based on TUNEL assay in the ischemic penumbra cortex of each group of mice at 8 h after pMCAO. C Effects of Homer1-KD on the expression level of p-RIPK1, p-RIPK3, and p-MLKL in the ischemic penumbra cortex of each group at 8 h after pMCAO. D–G Quantification of result in C. H Representative photographs of p-MLKL-positive neurons of brain tissue in each group at 8 h after pMCAO. I Quantification of result in H. J, K Representative images J and quantification K of primary neuronal death based on TUNEL assay in vitro of different groups at 4 h after OGD. L Effects of Homer1-KD on the expression level of p-RIPK1, p-RIPK3, and p-MLKL of different groups in vitro experiment at 4 h after OGD. M–P Quantification of result in L. For B, D–G, I, K–N: *P