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. 2016 Jan 20;24(3):157–170. doi: 10.1089/ars.2014.6120

FIG. 4.

FIG. 4.

AMPK and NLRP3 inflammasome modulation by CR. N=10 per group. (A) Evolution of pain sensitivity in AL and CR mice treated with sunitinib evaluated in the hot plate test at 55°C. Sunitinib treatment started after 1 month of AL and CR. Data are shown as change of withdrawal latency with respect to the control group. Negative and positive values represent hyperalgesia and analgesia, respectively. (B) Evolution of weight in AL and CR mice treated with sunitinib. (C) Protein levels of phosphorylated AMPK, NLRP3, and matured IL-1β (p17) from sunitinib-treated mice after 15 days of treatment. (D) IL-1β in serum levels from mice treated with sunitinib after 15 days of treatment in AL or CR conditions. *p<0.001 between vehicle and sunitinib-treated mice. (E) Evolution of pain sensitivity in AL and CR mice treated with compound C evaluated in the hot plate test at 55°C. (F) IL-1β in serum levels from mice treated with compound C after 15 days of treatment in AL or CR conditions. *p<0.001 between vehicle and compound C-treated mice. AL, ad libitum; CR, caloric restriction.

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