[1]宣智博,单葳葳,吴限,等.基于多组学探讨电针对重症肌无力模型大鼠骨骼肌泛凋亡的机制研究[J].卒中与神经疾病杂志,2025,32(02):169-176.[doi:10.3969/j.issn.1007-0478.2025.02.011]
 Xuan Zhibo*,Shan Weiwei,Wu Xian,et al.A multi-omics-based investigation of the electroacupuncture mechanism on PANoptosis in skeletal muscle of rats modeled with myasthenia gravis[J].Stroke and Nervous Diseases,2025,32(02):169-176.[doi:10.3969/j.issn.1007-0478.2025.02.011]
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基于多组学探讨电针对重症肌无力模型大鼠骨骼肌泛凋亡的机制研究()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第32卷
期数:
2025年02期
页码:
169-176
栏目:
论著
出版日期:
2025-04-20

文章信息/Info

Title:
A multi-omics-based investigation of the electroacupuncture mechanism on PANoptosis in skeletal muscle of rats modeled with myasthenia gravis
文章编号:
1007-0478(2025)02-0169-08
作者:
宣智博单葳葳吴限杨华森姜益常胡梦婉
150006 哈尔滨,黑龙江中医药大学(宣智博 杨华森 胡梦婉); 黑龙江中医药大学附属第一医院[单葳葳 吴限(通信作者)姜益常]
Author(s):
Xuan Zhibo* Shan Weiwei Wu Xian et al.
Heilongjiang University of Chinese Medicine, Harbin Heilongjiang 150006
关键词:
重症肌无力 多组学 电针 泛凋亡 动物实验 骨骼肌
Keywords:
Myasthenia Gravis Multi-Omics Electroacupuncture PANoptosis Animal Experiment Skeletal Muscle
分类号:
R746.1
DOI:
10.3969/j.issn.1007-0478.2025.02.011
文献标志码:
A
摘要:
目的 基于转录-蛋白多组学联合探讨电针治疗重症肌无力(Myasthenia gravis,MG)模型大鼠骨骼肌泛凋亡的相关机制。方法 采用基因表达总览(Gene expression omnibus,GEO)数据库基因表达综合系列(Gene expression omnibus series,GSE)227835作为转录组学研究样本,分析获得MG泛凋亡关键基因; 采用大鼠乙酰胆碱受体-α亚基97-116肽段制备实验性自身免疫性重症肌无力模型(Experimental autoimmune myasthenia gravis model,EAMG),将造模成功的大鼠随机分为模型组、电针组和西药组; 治疗结束后检测各组大鼠Lemmon评分、肌电图、血清抗乙酰胆碱受体抗体(Anti-acetylcholine receptor antibody,AChR-Ab)水平、骨骼肌中泛凋亡关键基因的蛋白表达水平。结果 分析获得2000个突变基因,其中13个与泛凋亡相关,最终筛选获得MG泛凋亡关键基因为半胱氨酸天冬氨酸特异性蛋白酶(Cysteine aspartate specific protease,CASP)1、CASP3、黑色素瘤缺乏因子2(Absent in melanoma 2,AIM)2; 治疗前电针组、模型组、西药组重复电刺激衰减率、Lemmon评分较对照组高(P<0.05),而3组间无明显差异(P>0.05); 与治疗前比较,治疗后西药组及电针组衰减率、Lemmon评分均降低(P<0.05); 治疗后西药组、电针组及模型组的Lemmon评分、衰减率、血清AChR-Ab水平、CASP1,CASP3,AIM2蛋白表达水平均高于对照组(P<0.05),其中电针组及西药组上述指标低于模型组(P<0.05),西药组低于电针组(P<0.05)。结论 MG泛凋亡关键基因为CASP1,CASP3,AIM2; 电针可有效减轻MG模型大鼠症状,其机制可能是通过降低CASP1,CASP3,AIM2的表达水平来抑制细胞泛凋亡反应,进而降低机体免疫反应和炎性因子水平,起到治疗MG模型大鼠的作用。
Abstract:
ObjectiveTo explore the mechanisms of PANoptosis related to electroacupuncture treatment in rats with Myasthenia gravis(MG)through a combined transcriptomic and proteomic approach.Methods The GEO database GSE227835 was utilized as the transcriptomic research sample to analyze key genes associated with PANoptosis in MG. A rat model of Experimental autoimmune myasthenia gravis(EAMG)was established using the acetylcholine receptor α subunit peptide segment 97-116. The successfully modeled rats were randomly divided into control group, model group, electroacupuncture group, and western medicine group. After treatment, the Lemmon score, electromyography, serum AChR-Ab levels, and protein expression levels of key PANoptosis genes in skeletal muscle were assessed for each group.Results A total of 2000 mutated genes were analyzed, of which 13 were related to PANoptosis. The key PANoptosis genes identified in MG were CASP1, CASP3, and AIM2. Before treatment, the electroacupuncture group, model group, and western medicine group had higher repetitive electrical stimulation attenuation rates and Lemmon scores compared to the control group(P<0.05), with no statistical differences among the three groups(P>0.05). Compared to pre-treatment values, the attenuation rates and Lemmon scores in the western medicine and electroacupuncture groups were significantly reduced(P<0.05). After treatment, the Lemmon scores, attenuation rates, serum AChR-Ab levels, and protein expression levels of CASP1, CASP3, and AIM2 in the western medicine group, electroacupuncture group, and model group were all higher than those in the control group(P<0.05), with the electroacupuncture and western medicine groups showing lower values than the model group(P<0.05), and the western medicine group lower than the electroacupuncture group(P<0.05).Conclusion The key PANoptosis genes in MG are CASP1, CASP3, and AIM2. Electroacupuncture effectively alleviates symptoms in MG modeled rats, potentially by reducing the expression levels of CASP1, CASP3, and AIM2, thereby inhibiting cellular PANoptosis responses and subsequently lowering immune responses and inflammatory factor levels, contributing to the treatment of MG in modeled rats.

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备注/Memo

备注/Memo:
基金项目:第七批全国老中医药专家学术经验继承项目[国中医药人教函(2022)76号]
更新日期/Last Update: 2025-04-20