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五味子乙素通过AMPK/PGC1α/Nrf2信号通路减轻铁死亡,从而抑制脂多糖诱导的子宫内膜炎。

Schisandrin B Inhibits LPS-Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway.

作者信息

Yu Jing, Li Xuewei, Zhou Min, Lu Min, Ruan Zheng, Zou Wenshuang, Yu Shaohui

机构信息

Department of Endocrinology, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin, China.

Department of Gynaecology, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin, China.

出版信息

J Cell Mol Med. 2024 Dec;28(23):e70281. doi: 10.1111/jcmm.70281.

Abstract

Endometritis is one of the common reproductive diseases in human and animal. In recent years, a number of studies have found that Schisandra B (Sch B), as a natural Chinese medicine extract, has antioxidant, anti-inflammatory and other biological activities. Based on the above, in this study, mice were used to conduct an in vivo experiment to investigate the effect and mechanism of Sch B on lipopolysaccharide (LPS)-induced endometritis. Haematoxylin and eosin (H&E) staining was used to detect the pathological changes of uterine tissue and western blot was used to detect the expression levels of signalling pathways and key genes for ferroptosis. The results showed that Sch B significantly inhibited the pathological injury of uterine tissue, myeloperoxidase (MPO) activity, the activation of NF-κB pathway and the production of TNF-α and IL-1β. Furthermore, Sch B effectively inhibited ferroptosis by inhibiting malondialdehyde (MDA) and iron production and promoting the expression of ferroptosis suppressor genes GPX4 and ferritin. In conclusion, Sch B inhibited LPS-induced endometritis through alleviating inflammatory response and ferroptosis via AMPK/PGC1α/Nrf2 signalling pathway.

摘要

子宫内膜炎是人和动物常见的生殖系统疾病之一。近年来,多项研究发现,五味子乙素(Sch B)作为一种天然的中药提取物,具有抗氧化、抗炎等生物学活性。基于此,本研究以小鼠为实验对象,开展体内实验,探究Sch B对脂多糖(LPS)诱导的子宫内膜炎的作用及机制。采用苏木精-伊红(H&E)染色检测子宫组织的病理变化,采用蛋白质免疫印迹法检测铁死亡信号通路及关键基因的表达水平。结果表明,Sch B显著抑制子宫组织的病理损伤、髓过氧化物酶(MPO)活性、NF-κB通路的激活以及TNF-α和IL-1β的产生。此外,Sch B通过抑制丙二醛(MDA)和铁的生成以及促进铁死亡抑制基因GPX4和铁蛋白的表达,有效抑制了铁死亡。综上所述,Sch B通过AMPK/PGC1α/Nrf2信号通路减轻炎症反应和铁死亡,从而抑制LPS诱导的子宫内膜炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bbe/11628352/058f8e717ad4/JCMM-28-e70281-g003.jpg

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