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川芎嗪对子宫内膜异位症大鼠的氧化应激和NLRP3依赖性细胞焦亡具有保护作用。

Tetramethylpyrazine Confers Protection Against Oxidative Stress and NLRP3-Dependent Pyroptosis in Rats with Endometriosis.

作者信息

Xu Ke, Zhang Mingzhe, Zou Xiaofeng, Wang Mingyang

机构信息

Department of Gynecology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.

出版信息

Organogenesis. 2025 Dec;21(1):2460261. doi: 10.1080/15476278.2025.2460261. Epub 2025 Feb 18.

Abstract

Tetramethylpyrazine (TMP) has been confirmed to suppress inflammation in endometriosis (EMs). Herein, this study investigated whether and how TMP affected NLRP3 inflammasomes and oxidative stress in EMs. After establishment of an EMs rat model, rats were treated with different concentrations of TMP. The size of endometriotic lesions and the latency and frequency of torsion in rats were recorded, followed by the measurement of relevant indicators (TNF-α, IL-6, IL-2, IL-10, MDA, SOD, GSH, CAT, ROS, NLRP3, ASC, GSDMD, caspase-1, Nrf2, and HO-1). The study experimentally determined that TMP treatment markedly decreased the size of endometriotic lesions and improved torsion in rats with EMs. The levels of inflammatory proteins, oxidative stress markers, NLRP3 inflammasome, and pyroptotic proteins were elevated in rats with EMs, all of which were reversed upon TMP treatment. Additionally, the activities of SOD, GSH, and CAT were lowered in rats with EMs, which were partly abrogated by TMP treatment. Furthermore, the downregulation of Nrf2 and HO-1 was counteracted by TMP treatment. To sum up, TMP represses excessive oxidative stress, NLRP3 inflammasome activation, and pyroptosis in rats with EMs. Additionally, TMP may activate the Nrf2/HO-1 pathway.

摘要

川芎嗪(TMP)已被证实可抑制子宫内膜异位症(EMs)中的炎症。在此,本研究调查了TMP是否以及如何影响EMs中的NLRP3炎性小体和氧化应激。建立EMs大鼠模型后,用不同浓度的TMP对大鼠进行治疗。记录大鼠子宫内膜异位病变的大小以及扭转的潜伏期和频率,随后测量相关指标(TNF-α、IL-6、IL-2、IL-10、MDA、SOD、GSH、CAT、ROS、NLRP3、ASC、GSDMD、caspase-1、Nrf2和HO-1)。该研究通过实验确定,TMP治疗可显著减小EMs大鼠的子宫内膜异位病变大小并改善扭转情况。EMs大鼠中炎症蛋白、氧化应激标志物、NLRP3炎性小体和焦亡蛋白的水平升高,而TMP治疗后这些指标均有所逆转。此外,EMs大鼠中SOD、GSH和CAT的活性降低,TMP治疗可部分消除这种降低。此外,TMP治疗可抵消Nrf2和HO-1的下调。综上所述,TMP可抑制EMs大鼠中过度的氧化应激、NLRP3炎性小体激活和焦亡。此外,TMP可能激活Nrf2/HO-1通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1e7/11845083/0e0ed8950547/KOGG_A_2460261_F0001_OC.jpg

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