Electroacupuncture alleviates intrauterine adhesion through regulating autophagy in rats.

IF 3.6 2区 医学 Q2 DEVELOPMENTAL BIOLOGY
Jingyu Liu, Qian Zhu, Yan Pan, Sainan Hao, Zhaoxian Wang, Chuting Cui, Junwei Li, Yueying Huang, Liangjun Xia, Tiancheng Xu, Jie Cheng, Jie Shen, Youbing Xia
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引用次数: 0

Abstract

Autophagy is a well-conserved metabolic system that maintains homeostasis by relying on lysosomal breakdown. The endometrium of patients with intrauterine adhesion (IUA) and an animal model exhibits impaired autophagy. Autophagy is negatively correlated with inflammation. Activation of autophagy can inhibit the inflammatory response, while defects in autophagy will activate the inflammatory response. Here, we studied whether electroacupuncture (EA) inhibits inflammation and promotes endometrial injury repair by activating endometrial autophagy. The IUA animal model was established by mechanical injury plus lipopolysaccharide infection. EA stimulation was applied to the acupoints Guanyuan (CV4), bilateral Sanyinjiao (SP6), and Zusanli (ST36). The results indicated that EA could improve endometrial morphology, attenuate endometrial fibers, and enhance endometrial receptivity in the rat. EA could increase the autophagosomes of endometrial epithelial cells, increase the levels of LC3 and Beclin1, and decrease the level of p62. Additionally, EA may also suppress the nuclear factor kappa-B (NF-κB) signaling pathway and reduce the release of inflammatory factors. Additionally, the effect of EA was comparable to that of the autophagy agonist rapamycin, and the autophagy inhibitor 3-methyladenine reversed the therapeutic effect of EA. Therefore, we assume that EA may facilitate endometrial healing by activating autophagy and reducing NF-κB signal pathway-mediated inflammation.

电针通过调节大鼠的自噬来减轻宫内粘连。
自噬是一个非常保守的代谢系统,依靠溶酶体的分解来维持体内平衡。子宫内粘连(IUA)患者的子宫内膜和动物模型都表现出自噬受损。自噬与炎症呈负相关。激活自噬可以抑制炎症反应,而自噬缺陷会激活炎症反应。在这里,我们研究了电针(EA)是否通过激活子宫内膜自噬来抑制炎症并促进子宫内膜损伤修复。采用机械损伤加脂多糖(LPS)感染建立IUA动物模型。电针穴位分别为关元、三阴交、足三里。结果表明,电针能改善大鼠子宫内膜形态,减弱子宫内膜纤维,增强子宫内膜容受性。电针可增加子宫内膜上皮细胞的自噬体,增加LC3和Beclin1的水平,降低p62的水平。此外,EA还可能抑制核因子(NF)-κB信号通路,减少炎症因子的释放。此外,EA的效果与自噬激动剂雷帕霉素相当,自噬抑制剂3-甲基腺嘌呤逆转了EA的治疗效果。因此,我们认为EA可能通过激活自噬和减少NF-κB信号通路介导的炎症来促进子宫内膜愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Molecular human reproduction
Molecular human reproduction 生物-发育生物学
CiteScore
8.30
自引率
0.00%
发文量
37
审稿时长
6-12 weeks
期刊介绍: MHR publishes original research reports, commentaries and reviews on topics in the basic science of reproduction, including: reproductive tract physiology and pathology; gonad function and gametogenesis; fertilization; embryo development; implantation; and pregnancy and parturition. Irrespective of the study subject, research papers should have a mechanistic aspect.
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