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1.南华大学附属第一医院,湖南衡阳421001
2.湖南中医药大学针灸推拿与康复学院, 长沙410208
3.湖南中医药大学第一附属医院,长沙410007
唐艳华,E-mail:tangyanhua2020@qq.com
收稿:2025-01-18,
修回:2025-02-13,
纸质出版:2026-02-25
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薛晓,刘鑫,刘余,等.电针对原发性痛经大鼠A20/NF-κB/NLRP3/GSDMD信号通路的影响[J].针刺研究,2026,51(2):161-168.
XUE Xiao,LIU Xin,LIU Yu,et al.Effect of electroacupuncture on the A20/NF-κB/NLRP3/GSDMD signaling pathway in rats with primary dysmenorrhea[J].Acupuncture Research,2026,51(02):161-168.
薛晓,刘鑫,刘余,等.电针对原发性痛经大鼠A20/NF-κB/NLRP3/GSDMD信号通路的影响[J].针刺研究,2026,51(2):161-168. DOI: 10.13702/j.1000-0607.20250062.
XUE Xiao,LIU Xin,LIU Yu,et al.Effect of electroacupuncture on the A20/NF-κB/NLRP3/GSDMD signaling pathway in rats with primary dysmenorrhea[J].Acupuncture Research,2026,51(02):161-168. DOI: 10.13702/j.1000-0607.20250062.
目的
2
探讨电针“关元”“三阴交”对原发性痛经(PDM)大鼠泛素编辑酶A20(A20)/核转录因子- κB(NF-κB)/核苷酸结合寡聚化结构域样受体蛋白3 (NLRP3)/Gasdermin D 蛋白(GSDMD)信号通路的影响。
方法
2
雌性未孕SD大鼠被随机分为空白组、模型组、电针组、布洛芬组,6只/组。苯甲酸雌二醇和缩宫素联合构建PDM模型。电针组造模同时电针“关元”“三阴交”,每次20 min,每日1次,连续10 d。布洛芬组从造模开始用布洛芬溶液(0.8 mL/只)灌胃治疗,1次/d,连续治疗10 d。扭体反应观察大鼠行为学;HE染色观察子宫病理改变;ELISA法检测血清炎性因子前列腺素F2α(PGF2α)和肿瘤坏死因子-α(TNF-α)的含量;Western blot法检测各组大鼠子宫组织A20、磷酸化核转录因子κB p65(p-NF-κB p65)、NF-κB p65、NLRP3、半胱天冬酶-1(Caspase-1)、白细胞介素1β(IL-1β)、GSDMD、Gasdermin D氮端结构域(GSDMD-N)蛋白表达量。
结果
2
与空白组比较,模型组大鼠扭体次数和评分均增加(
P
<
0.05,
P
<
0.01),并出现扭体潜伏期(
P
<
0.01);与模型组比较,电针组与布洛芬组大鼠扭体次数、评分均降低(
P
<
0.05),且扭体潜伏期增长(
P
<
0.01)。空白组子宫组织的黏膜上皮层完整,无明显水肿;模型组大量宫腔上皮坏死,子宫内膜伴有严重的水肿,中性粒细胞增多;电针组和布洛芬组子宫内膜水肿和炎性病理损伤明显缓解。与空白组比较,模型组大鼠血清PGF2α、TNF-α含量,子宫组织p-NF-κB p65、NF-κB p65、NLRP3、IL-1β、Caspase-1、GSDMD、GSDMD-N蛋白表达均升高(
P
<
0.05,
P
<
0.01),A20蛋白表达量下降(
P
<
0.01);与模型组比较,电针组血清PGF2α、TNF-α含量,子宫组织p-NF-κB p65、NF-κB p65、NLRP3、GSDMD、GSDMD-N蛋白水平均降低(
P
<
0.05,
P
<
0.01),A20蛋白表达量升高(
P
<
0.01)。电针组与布洛芬组上述指标相比差异无统计学意义。
结论
2
电针对PDM大鼠的抗炎机制可能与其启动A20介导的NF-κB信号通路负反馈调控途径,抑制NF-κB/NLRP3/GSDMD信号通路有关。
Objective
2
To observe the effect of electroacupuncture (EA) at “Guanyuan” (CV4) and “Sanyinjiao” (SP6) on the ubiquitin-editing enzyme A20 (A20)/nuclear factor-κB (NF-κB)/NOD-like receptor protein 3 (NLRP3)/Gasdermin D (GSDMD) signaling pathway in rats with primary dysmenorrhea (PDM).
Methods
2
Female naive SD rats were randomly divided into blank, model, EA and medication groups (
n
=6 per group). PDM rat model was established by subcutaneous injection of estradiol benzoate combined with intraperitoneal injection of oxytocin. EA (50 Hz) was applied to CV4 and bilateral SP6 of rats in the EA group, with needles retained for 20 min, once daily for 10 consecutive days. Rats in the medication group received ibuprofen(125 mg/100 mL, 0.8 mL) by gavage for 10 consecutive days. At the 11
th
day, wri
thing behavior of rats was assessed. Uterine pathology was assessed by HE staining. Serum contents of prostaglandin F2α (PGF2α) and tumor necrosis factor-α (TNF-α) were measured by ELISA. Protein expression of A20, phosphorylated NF-κB p65 (p-NF-κB p65), NF-κB p65, NLRP3, Caspase-1, Interleukin (IL)-1β, GSDMD, and GSDMD N-terminal domain (GSDMD-N) in uterine tissue were detected by Western blot.
Results
2
Compared with the blank group, the writhing times, scores, and latency period, the contents of PGF2α and TNF-α in serum, and the protein expression levels of p-NF-κB p65, NF-κB p65, NLRP3, Caspase-1, IL-1β, GSDMD, and GSDMD-N in the uterine tissues of rats in the model group were all significantly increased (
P
<
0.05,
P
<
0.01). In contrast, the expression level of A20 was decreased (
P
<
0.01). Compared with the model group, the writhing times and scores, the contents of PGF2α and TNF-α in serum, and the protein expression levels of p-NF-κB p65, NF-κB p65, NLRP3, GSDMD, and GSDMD-N in rats of the EA and medication groups were all significantly decreased (
P
<
0.05,
P
<
0.01). Conversely, the writhing latency period and the expression level of A20 were significantly increased (
P
<
0.01). After modeling, the endometrial epithelial cells were dead, accompanied by endometrial edema and neutrophil infiltration, which was milder in the EA and the medication groups.
Conclusion
2
EA intervention can effectively relieve inflammatory response in PDM rats, which may be associated with its effect in activating the A20-mediated NF-κB negative feedback pathway and inhibiting the NF-κB/NLRP3/GSDMD signaling pathway.
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