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Quote : 王强,王玥.电针内关、百会通过NLRP3/ASC/Caspase-1通路干预局灶性脑缺血再灌注损伤大鼠的作用研究[J].湖南中医药大学学报英文版,2022,42(8):1335-1340.[Click to copy ]
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电针内关、百会通过NLRP3/ASC/Caspase-1通路干预局灶性脑缺血再灌注损伤大鼠的作用研究
王强,王玥
(湖南省脑科医院, 湖南 长沙 410007;湖南中医药大学附属第一医院, 湖南 长沙 410007)
摘要:
    目的 通过NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)/凋亡相关斑点样蛋白(apoptosis-associated speck-like protein containing CARD,ASC)/半胱天冬酶-1(Caspase-1)通路探讨电针内关、百会对局灶性脑缺血再灌注损伤大鼠的干预作用及机制。方法 Sprague-Dawley大鼠30只,随机分为对照组、假手术组、模型组、尼莫地平组、电针组,每组6只。模型组、尼莫地平组、电针组予以大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)造模,成功后尼莫地平组予10.8 mg/kg尼莫地平片灌胃,电针组予以针刺内关、百会,对照组、假手术组均给予0.9%生理盐水灌胃,干预14 d。采用Longa评分进行神经功能评定,采用ELISA法检测血清白介素-1β(interleukin-1 beta,IL-1β)含量,免疫荧光测定NLRP3、ASC、Caspase-1阳性表达。结果 造模后,模型组、尼莫地平组、电针组Longa评分明显升高,与对照组、假手术组相比,差异有统计学意义(P<0.05);干预后,尼莫地平组、电针组Longa评分低于模型组(P<0.05),而尼莫地平组、电针组之间的Longa评分差异无统计学意义(P>0.05)。干预后,模型组大鼠IL-1β含量高于对照组、假手术组(P<0.01);尼莫地平组、电针组大鼠IL-1β含量低于模型组(P<0.05)。干预后,模型组ASC、Caspase-1及NLRP3的表达明显高于对照组、假手术组(P<0.01);与模型组比较,尼莫地平组、电针组ASC、Caspase-1及NLRP3的表达明显降低(P<0.01)。结论 电针内关、百会可改善局灶性脑缺血再灌注损伤大鼠运动功能,可能与调控NLRP3/ASC/Caspase-1信号通路、降低IL-1β表达有关。
关键词:  脑缺血  局灶性  电针  内关  百会  NLRP3  ASC  Caspase-1
DOI:10.3969/j.issn.1674-070X.2022.08.016
Received:February 08, 2022  
基金项目:湖南省自然科学基金项目(2020JJ8066);湖南省重点研发项目(2020SK2123)。
Effect of electroacupuncture at Neiguang (“PC6”) and Baihui (“DU20”) on focal cerebral ischemia-reperfusion injury through NLRP3/ASC/Caspase-1 pathway in rats
WANG Qiang,WANG Yue
(Hunan Brain Hospital, Changsha, Hunan 410007, China;The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China)
Abstract:
    Objective To investigate the effect and mechanism of electroacupuncture at Neiguan ("PC6") and Baihui ("DU20") on focal cerebral ischemia-reperfusion injury in rats through NOD-like receptor thermal protein domain associated protein 3, (NLRP3)/apoptosis-associated speck-like protein containing CARD (ASC)/Caspase-1 pathway. Methods Thirty Sprague-Dawley rats were randomly divided into control group, sham operation group, model group, nimodipine group and electroacupuncture group, with 6 rats in each group. Middle cerebral artery occlusion (MCAO) was performed in the model group, nimodipine group, and electroacupuncture group. After success, the nimodipine group was given nimodipine 10.8 mg/kg intragastric administration, while electroacupuncture group was given Neiguan ("PC6") and Baihui ("DU20") acupuncture, the control group and the sham operation group were given 0.9% normal saline by gavage for 14 d. Longa score was used to evaluate neurological function. The level of interleukin-1 beta (IL-1β) in serum was measured by ELISA and the expression of NLRP3, ASC, Caspase-1 was detected by immunofluorescence. Results After modeling, Longa scores of model group, nimodipine group and electroacupuncture group were significantly higher than those of control group and sham operation group (P<0.05), after intervention, Longa score in nimodipine group and electroacupuncture group was lower than that in model group (P<0.05), but there was no significant difference in Longa score between nimodipine group and electroacupuncture group. After intervention, the content of IL-1 β in model group was higher than that in control group and sham operation group (P<0.01), and the content of IL-1 β in nimodipine group and electroacupuncture group was lower than that in model group (P<0.05). After intervention, the expression of ASC, Caspase-1 and NLRP3 in model group was significantly higher than that in control group and sham operation group (P<0.01). Compared with model group, the expression of ASC, Caspase-1 and NLRP3 in nimodipine group, electroacupuncture group was significantly lower (P<0.01). Conclusion Electroacupuncture at Neiguan ("PC6") and Baihui ("DU20") can improve the motor function of rats with focal cerebral ischemia-reperfusion injury, which may be related to regulating the NLRP3/ASC/Caspase-1 signaling pathway and decreasing the expression of IL-1β.
Key words:  cerebral ischemia  focal  electroacupuncture  Neiguan ("PC6")  Baihui ("DU20")  NLRP3  ASC  Caspase-1
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