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. 2014 Jul 21;111(31):11455–11460. doi: 10.1073/pnas.1404267111

Fig. 1.

Fig. 1.

Prolactin/female sex constrains hepatocellular IL-1β responses in vitro and in vivo. (A) PRL preconditioning in AML12 hepatocytes reduces IL-1β phosphorylation of p38 MAPK, NF-κB p65/RelA, and AKT. (B) IL-1β induction of APR genes is diminished in PRL-preconditioned hepatocytes. (C) Decreased phosphorylation of p38 MAPK, NF-κB p65/RelA, and AKT but not STAT3, JNK, or ERK1/2 in IL-1β–challenged female versus male mouse liver. (D) Muted induction of inflammatory and tumor-associated genes in IL-1β–challenged females versus males. Data are expressed as mean ± SEM (n = 5 per sex); *P < 0.05, Student t test.