Abstract

Objective To evaluate the role of autophagy in the development of inflammatory pain in the rats. Methods Twenty-four healthy adult male Sprague-Dawley rats, weighing 180-240 g, were randomly divided into 4 groups (n=6 each) by using a random number table: control group (group C), inflammatory pain group (group IP), dimethyl sulfoxide (DMSO) group (group D), and rapamycin (autophagy inducer) group (group R). Inflammatory pain was produced by injecting 50 μl bee venom into the plantar surface of the left hindpaw.In group C, 0.9% normal saline was injected into the plantar surface of the left hindpaw.In group D, 2% DMSO was injected through a gastric tube into the stomach 1 ml per day for 3 consecutive days, and the model was established at 1 h after injection on 3rd day.In group R, rapamycin 10 mg/kg (in 2% DMSO) was injected through a gastric tube into stomach 1 ml per day for 3 consecutive days, and the model was established at 1 h after injection on 3rd day.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 2 h after the model was established.After measurement of the pain threshold, the dorsal horn of the spinal cord was removed for determination of the expression of microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ), Beclin-1 and p62 by Western blot. Results Compared with group C, the MWT was significantly decreased, the TWL was significantly shortened in IP and D groups, and the expression of LC3Ⅱ, Beclin-1 and p62 in the dorsal horn of the spinal cord was significantly up-regulated in IP, D and R groups (P 0.05). Conclusion Autophagy disorders are involved in the development of inflammatory pain in the rats. Key words: Autophagy; Inflammatory; Pain

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call