自噬
电针
炎症
足三里
促炎细胞因子
生物
内科学
内分泌学
子宫内膜
髓过氧化物酶
自噬体
脂多糖
细胞生物学
医学
细胞凋亡
针灸科
病理
生物化学
替代医学
作者
Jingyu Liu,Qian Zhu,Pan Yan,Sai-Nan Hao,Zhaoxian Wang,Chu-Ting Cui,Junwei Li,Yueying Huang,Liangjun Xia,Tiancheng Xu,Jie Cheng,Jie Shen,Youbing Xia
出处
期刊:Molecular human reproduction
[Oxford University Press]
日期:2023-11-01
卷期号:29 (11)
被引量:2
标识
DOI:10.1093/molehr/gaad037
摘要
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.
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