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姜黄素通过下调磷脂酰肌醇 3-激酶/蛋白激酶 B 信号通路缓解大鼠类风湿性关节炎。

Galangin alleviates rheumatoid arthritis in rats by downregulating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway.

机构信息

Orthopedics and Traumatology, Nanchang Hongdu Hospital of Traditional Chinese Medicine, Nanchang, Jiangxi, China.

College of Traditional Chinese Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, China.

出版信息

Bioengineered. 2022 Apr;13(4):11192-11201. doi: 10.1080/21655979.2022.2062969.

DOI:10.1080/21655979.2022.2062969
PMID:35485325
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9208502/
Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease that greatly affect patients' quality of life. Galangin extract is renowned for its anti-proliferative and anti-oxidative characteristics. However, galangin cytotoxicity studies are presently inadequate. We aimed to investigate the therapeutic potential of galangin on RA by investigating the PI3K/AKT signaling pathway.Fibroblast-like synovial cells (FLSs) were exposed to lipopolysaccharide (LPS) to establish an RA model . An ELISA assay was used to detect the levels of IL-1β, TNF-α, and IL-6. Cell viability and apoptosis were determined by CCK8/EdU and flow cytometry assays. A western blot assay was used to analyze the protein expression levels. An RA rat model was established to evaluate the function of galangin through histopathological examination. Our results found that galangin induced apoptosis, inhibited cell proliferation, and increased cell invasion of rheumatoid arthritis fibroblast-like synovial cells (RAFLSs). Galangin inactivated the PI3K/AKT signaling pathway and the inflammatory response. An agonist of PI3K signaling, 740Y-P, restored the cellular functions of RAFLSs. Moreover, galangin suppressed the development of RA . Galangin effected its anti-arthritic influence through the PI3K/AKT signaling pathway. Galangin has potential as an alternative treatment for RA.

摘要

类风湿关节炎(RA)是一种慢性自身免疫性疾病,极大地影响了患者的生活质量。高良姜素提取物以其抗增殖和抗氧化特性而闻名。然而,目前对高良姜素的细胞毒性研究还不够充分。我们旨在通过研究 PI3K/AKT 信号通路来研究高良姜素治疗 RA 的潜力。用脂多糖(LPS)处理成纤维样滑膜细胞(FLSs)以建立 RA 模型。通过 ELISA 检测 IL-1β、TNF-α 和 IL-6 的水平。通过 CCK8/EdU 和流式细胞术检测细胞活力和细胞凋亡。通过 Western blot 分析蛋白表达水平。通过组织病理学检查评估高良姜素在 RA 大鼠模型中的作用。我们的结果发现,高良姜素诱导 RA 成纤维样滑膜细胞(RAFLSs)凋亡、抑制细胞增殖和增加细胞侵袭。高良姜素抑制了 PI3K/AKT 信号通路和炎症反应。PI3K 信号通路的激动剂 740Y-P 恢复了 RAFLSs 的细胞功能。此外,高良姜素抑制了 RA 的发展。高良姜素通过 PI3K/AKT 信号通路发挥其抗关节炎作用。高良姜素具有作为 RA 替代治疗的潜力。

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