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Berberine inhibits the LPS-induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

机译:小ber碱抑制LPS / TLR4信号通路介导的LPS诱导的子宫腺肌病组织间质细胞增殖和炎症反应

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摘要

A previous study by our group has demonstrated that lipopolysaccharide (LPS) induces adenomyosis through stimulating inflammatory cell proliferation and invasive growth of stromal cells via Toll-like receptor 4 (TLR4) signaling. The present study aimed to investigate the effects of berberine (BBR) on LPS-induced ectopic endometrial stromal cells (EESCs) isolated from patients with adenomyosis. The viability of EESCs treated with LPS or LPS plus BBR was detected by a cell counting kit-8 assay, and the cell cycle distribution and apoptosis were evaluated by flow cytometry. The effect of BBR on the expression of key molecules of inflammatory proliferation and invasive growth of LPS-induced EESCs was also evaluated. BBR significantly inhibited the LPS-induced proliferation of EESCs in a dose- and time-dependent manner. BBR induced cell cycle arrest in G0/G1 phase and enhanced apoptosis of LPS-induced EESCs. Furthermore, BBR inhibited the expression of interleukin (IL)-6, IL-8, transforming growth factor-β, epithelial growth factor, vascular endothelial growth factor and matrix metalloproteinase 2 in LPS-induced EESCs. To the best of our knowledge, the present study was the first to demonstrate that BBR has a protective effect on ameliorating the LPS-induced progression of adenomyosis. This result may provide a novel therapeutic strategy for the clinical treatment of the disease.
机译:我们小组先前的研究表明,脂多糖(LPS)通过Toll样受体4(TLR4)信号刺激炎症细胞增殖和基质细胞的侵袭性生长来诱导腺肌病。本研究旨在调查小ber碱(BBR)对LPS诱导的子宫腺肌病患者异位子宫内膜间质细胞(EESCs)的影响。用细胞计数试剂盒8法检测用LPS或LPS加BBR处理的EESC的活力,并通过流式细胞术评估细胞周期分布和凋亡。还评估了BBR对LPS诱导的EESCs炎症增殖和侵袭性生长关键分子表达的影响。 BBR以剂量和时间依赖性方式显着抑制LPS诱导的EESC增殖。 BBR诱导细胞周期停滞在G0 / G1期,并增强LPS诱导的EESC的凋亡。此外,BBR抑制LPS诱导的EESCs中白介素(IL)-6,IL-8,转化生长因子-β,上皮生长因子,血管内皮生长因子和基质金属蛋白酶2的表达。就我们所知,本研究首次证明BBR对改善LPS诱导的子宫腺肌病进展具有保护作用。该结果可以为疾病的临床治疗提供新颖的治疗策略。

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