化学
STAT蛋白
磷脂酰肌醇
激活剂(遗传学)
炎症
激酶
细胞内
PI3K/AKT/mTOR通路
细胞生物学
肿瘤坏死因子α
Janus激酶2
细胞因子
贾纳斯激酶
兴奋剂
分子生物学
氨基酸
信号转导
药理学
细胞外基质
促炎细胞因子
伤口愈合
生物化学
状态5
信使核糖核酸
癌症研究
细胞粘附
细胞生长
作用机理
车站3
细胞凋亡
内分泌学
斯达
内科学
细胞
白细胞介素
粘附
细胞迁移
作者
Xinyuan Ye,Shen Yh,Ronghua Bao,Yu-Ling Liu,Qiuru Ren,Quan-Long Zhang,Lu-Ping Qin,Qiao-Yan Zhang
出处
期刊:PubMed
[National Institutes of Health]
日期:2025-10-01
卷期号:50 (20): 5811-5819
标识
DOI:10.19540/j.cnki.cjcmm.20250609.701
摘要
This study aims to explore the effects and mechanism of Jintiange Capsules-containing serum(JTG-CS) on fibroblast-like synoviocytes(FLS) in human rheumatoid arthritis. The blank serum from SD rats and low, medium, and high-dose JTG-CS samples were prepared. Ultra-high performance liquid chromatography-tandem mass spectrometry(UHPLC-MS/MS) was employed to determine the amino acid composition and content in the blank serum and JTG-CS. Tumor necrosis factor-α(TNF-α) was used to stimulate FLS for the modeling of inflammation. The proliferation of FLS was determined by the CCK-8 assay. The migration and invasion of FLS were examined by wound healing and Transwell assays. The protein expression of FLS was analyzed by Western blot. JTG-CS significantly inhibited the proliferation, migration, wound healing, and invasion of FLS stimulated by TNF-α, down-regulated the expression of intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), matrix metalloproteinase(MMP)2, and MMP3, lowered the levels of TNF-α, interleukin(IL)-6, and IL-1β, and inhibited the activation of phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt), nuclear factor(NF)-κB, and Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3) pathways. The treatment with the PI3K agonist reversed the inhibitory effects of JTG-CS on inflammatory cytokines and invasion of FLS stimulated by TNF-α. Compared with the blank serum, JTG-CS showed increased content of 46 amino acids and decreased content of 20 amino acids. JTG-CS inhibited the proliferation, migration, invasion, and inflammation of FLS stimulated by TNF-α by inhibiting the activation of the PI3K/Akt pathway.
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