[Effects of electroacupuncture with different waveforms on NLRP3 inflammasome and pyroptosis in the cerebral cortex of rats with cerebral ischemia-reperfusion injury].
摘要
Objective: To observe the effects of electroacupuncture (EA) with different waveforms on nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome and pyroptosis in the cerebral cortex of rats with cerebral ischemia-reperfusion injury (CIRI), and explore the potential mechanisms of EA in treating CIRI. Methods: A total of 70 male SD rats were selected. Twelve rats were randomly assigned to a sham operation group, while the remaining rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) model by reforming Longa method. Forty-eight successfully modeled rats were randomly divided into a model group, an EA-continuous wave (EA-A) group, an EA-discontinuous wave (EA-B) group, and an EA-dense-disperse wave (EA-C) group, with 12 rats in each group. EA was performed at "Baihui" (GV20), "Dazhui" (GV14), and bilateral "Zusanli" (ST36) once daily for 20 min for 7 d. The EA-A group used a continuous wave (15 Hz), the EA-B group used a discontinuous wave (15 Hz with 1.5 s intervals), and the EA-C group used a dense-disperse wave (alternating 3 Hz/15 Hz). Neurological deficit scores were recorded before and after intervention. After intervention, TTC staining was used to assess cerebral infarct volume. HE staining was performed to observe the morphological changes in the ischemic cortical brain tissue. ELISA was used to measure interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels in the ischemic cortex. Western blot was used to detect the protein expression of NLRP3, Caspase-1, gasdermin D (GSDMD), and apoptosis-associated speck-like protein (ASC), and qRT-PCR was used to detect the mRNA expression of NLRP3, Caspase-1, GSDMD and ASC. Results: <0.01). Conclusion: Different EA waveforms could all alleviate neurological deficits and reduce cerebral infarct volume in CIRI rats. The mechanism may be related to inhibition of NLRP3 inflammasome-mediated pyroptosis.