Effect of electroacupuncture pretreatment on expression of NLRP3 in neurons during cerebral ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of electroacupuncture (EA) pretreatment on NODlike receptor pyrin domain-containing 3 (NLRP3) in neurons during cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male Sprage-Dawley rats,aged 7 weeks,weighing 250-280 g,were randomly divided into 3 groups (n =18 each) using a random number tablesham operation group (group S),group I/R,and EA pretreatment group (group E).Cerebral I/R was induced by occlusion of the right middle cerebral artery for 90 min using a nylon thread inserted into the internal carotid artery and advanced intracranially to block the blood flow,followed by reperfusion.In group E,the acupoint Baihui was stimulated with an electric stimulator (sparse-dense wave,frequency 2 Hz/15 Hz,intensity ≤ 1 mA) for 30 min once a day for 5 consecutive days,and the model of cerebral I/R was established at 24 h after the last stimulation.At 72 h of reperfusion,neurological function was assessed and scored.The rats were then sacrificed,and their brains were removed for determination of cerebral infarct volume (using TTC staining),expression of NLRP3,caspase-1 and interleukin-1beta (IL-1β) in brain tissues (by Western blot),and expression of NLRP3 protein in neurons (by immunofluorescence histochemistry).The percentage of cerebral infarct volume was calculated.Results Compared with group S,the percentage of cerebral infarct volume and neurological scores were significantly decreased,and the expression of NLRP3,caspase-1 and IL-1β in brain tissues was significantly up-regulated in group I/R (P＜0.05).Compared with group I/R,the percentage of cerebral infarct volume and neurological scores were significantly increased,and the expression of NLRP3,caspase-1 and IL-1β in brain tissues was significantly down-regulated ingroup E (P＜0.05).Conclusion The mechanism by which EA pretreatment reduces inflammatory responses during cerebral I/R injury may be related to down-regulation of NLRP3 expression in neurons in rats.