Effect of valproic acid on expression of M1/M2 microglia in prefrontal cortex of rats with neuropathic pain / 中华麻醉学杂志

ABSTRACT

Objective:To evaluate the effect of valproic acid on the expression of M1/M2 microglia in the prefrontal cortex of rats with neuropathic pain (NP).Methods:Thirty-six clean-grade healthy male Sprague-Dawley rats, aged 6-7 weeks, weighing 200-230 g, were divided into 3 groups ( n=12 each) using a random number table method: sham operation group (group S), group NP, and valproic acid group (group V). The NP model was established by ligation of the L 5 spinal nerve (SNL) of anesthetized rats.Valproic acid 300 mg/kg was intraperitoneally injected immediately after SNL and every day after ligation, once a day, for 3 consecutive days in group V, while the equal volume of normal saline was given instead of valproic acid in S and NP groups.The mechanical paw withdrawal threshold (MWT) was measured before ligation and at 1, 3, 7, 14, 21 and 28 days after ligation.Sucrose preference test and forced-swim test were performed on day 28 after ligation.After the end of the behavior test, the prefrontal cortex was removed for determination of the expression of cluster of differentiation (CD) 16 and CD206 by Western blot.The ratio of CD206/CD16 was calculated. Results:Compared with group S, the MWT at each time point after ligation and rate of preference for sucrose were significantly decreased, the duration of immobility in forced-swim test was prolonged, the expression of CD16 and CD206 was up-regulated, and the ratio of CD206/CD16 was decreased in group NP ( P<0.05). Compared with group NP, the MWT at each time point after ligation and rate of preference for sucrose were significantly increased, the duration of immobility in forced-swim test was shortened, the expression of CD16 was down-regulated, the expression of CD206 was up-regulated, and the ratio of CD206/CD16 was increased in group V ( P<0.05). Conclusion:The mechanism by which valproic acid improves depression may be related to promoting the expression of M2 microglia and inhibiting the expression of M1 microglia in the prefrontal cortex of rats with NP.