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Apoptosis signal-regulating kinase 1 inhibition attenuates cardiac hypertrophy and cardiorenal fibrosis induced by uremic toxins: Implications for cardiorenal syndrome

Fig 3

Signaling pathway activation in p-cresol sulfate-stimulated neonatal cardiac myocytes.

Representative images and quantification of Western blot analyses of NCMs stimulated with PCS in the absence and presence of (A) 100 μM Probenecid and 1.0 μM G226 for (i) phospho-ASK1, (ii) phospho-p38, (iii) phospho-ERK1/2, (iv) phospho-NF-κB; and (B) 3.0 μM RWJ-67657 and 1.0 μM U0126 for (i) phospho-p38, (ii) phospho-ERK1/2, (iii) phospho-NF-κB and (iv) Pan Actin. Data are presented as mean ± SEM (n = 3). *p<0.05, **p<0.01, ***p<0.001 vs control, #p<0.05, ##p<0.01, ###p<0.001 vs PCS [100 μM], One-way Anova.

Fig 3

doi: https://doi.org/10.1371/journal.pone.0187459.g003