ABSTRACT
Objective To evaluate the role of spinal AMP-activated protein kinase (AMPK) signaling pathway in reduction of neuropathic pain (NP) by dexmedetomidine in rats.Methods One hundred twenty adult male Sprague-Dawley rats, weighing 180-220 g, were randomly divided into 4 groups (n=30 each) using a random number table: sham operation group (group S);group NP;dexmedetomidine group (group Dex) and AMPK inhibitor group (group AI).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 350 mg/kg.The right sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread in NP and Dex groups.In group Dex, dexmedetomidine 50 μg/kg was injected intraperitoneally once a day starting from the end of operation until the animals were sacrificed.In group AI, AMPK inhibitor Compound C 20 mg/kg was injected intraperitoneally at the end of operation, and the other treatments were similar to those previously described in group Dex.The equal volume of normal saline was given instead of dexmedetomidine in S and NP groups.The mechanical paw withdrawal threshold to von Frey filament stimulation (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before operation (baseline) and 2, 8 and 14 days after operation (T0-3).Results Compared with group S, the MWT was significantly decreased, and the TWL was shortened at T1-3 in NP, Dex and AI groups (P＜0.05).Compared with group NP, the MWT was significantly increased, and the TWL was prolonged at T1-3 in group Dex (P＜0.05) , and no significant change was found in MWT and TWL in group AI (P＞0.05).Conclusion Spinal AMPK signaling pathway is involved in reduction of NP by dexmedetomidine in rats.