Resveratrol engages AMPK to attenuate ERK and mTOR signaling in sensory neurons and inhibits incision-induced acute and chronic pain

Table 1 Sirt1 inhibition does not reverse resveratrol-induced effects on TG neurons.

Antibody	Vehicle	nicotinamide 10 mM + resveratrol 100 μM	resveratrol 100 μM
p-AMPK/AMPK	100 ± 7.3	199.8 ± 28.1	222.4 ± 40.0
p-ERK/ERK	100 ± 11.8	41.8 ± 8.5 **	47.2 ± 8.8 **
p-eIF4E/eIF4E	100 ± 5.4	27.6 ± 4.7 ***	30.2 ± 6.2 ***
p-AKT/AKT	100 ± 6.2	11.6 ± 3.1 ***	12.5 ± 2.4 ***
p-mTOR/mTOR	100 ± 4.4	70.6 ± 4.4 *	62.9 ± 6.4 **
p-TSC2/TSC2	100 ± 8.3	26.6 ± 4.2 ***	36.5 ± 5.2 ***
p-4EBP/4EBP	100 ± 2.3	38.5 ± 3.0 ***	37.9 ± 7.2 ***
p-rS6p/rS6p	100 ± 7.0	33.9 ± 5.9 ***	36.5 ± 6.8 ***

TG neuronal cultures were pre-treated with nicotinamide or vehicle for 1 h and then co-treated with nicotinamide (10 mM), a sirt1 inhibitor, in the presence of resveratrol for 1 h. The phosphorylated levels of AMPK, ERK, eIF4E, AKT, mTOR, 4EBP and rS6p were unchanged by nicotinamide

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