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

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

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 ***
  1. 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