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甘草酸通过抑制体内和体外的 PI3K/AKT/NF-κB 信号通路抑制骨关节炎的发展。

Glycyrrhizin inhibits osteoarthritis development through suppressing the PI3K/AKT/NF-κB signaling pathway in vivo and in vitro.

机构信息

Department of Orthopaedic surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325000, China.

出版信息

Food Funct. 2020 Mar 1;11(3):2126-2136. doi: 10.1039/c9fo02241d. Epub 2020 Feb 19.

DOI:10.1039/c9fo02241d
PMID:32073014
Abstract

Osteoarthritis (OA) is a serious and frequently occurring disease in the elderly, characterized by cartilage degeneration and proliferation of bone structure. Glycyrrhizin, a compound extracted from licorice, has been reported to have various important biological activities, such as antioxidant properties and anti-inflammatory action. However, it has not been reported whether glycyrrhizin has a positive effect on OA development. Our study aimed to evaluate the effects of glycyrrhizin on human OA chondrocytes. In the present study, we discovered that glycyrrhizin remarkably suppressed the interleukin (IL)-1β-induced level of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) and the production of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOs), metalloproteinase3 (MMP3), metalloproteinase13 (MMP13) and a disintegrin and metalloproteinase with thrombospondin motifs5 (ADAMTS5). In addition, glycyrrhizin inverted the degradation of aggrecan and collagen II. Moreover, it significantly inhibited IL-1β-stimulated PI3K/AKT phosphorylation and NF-κB mobilization in human OA chondrocytes. In vivo, glycyrrhizin treatment prevented the destruction of cartilage in mice OA models. In summary, all the results demonstrate that glycyrrhizin may be a potential therapeutic approach for OA.

摘要

骨关节炎(OA)是一种常见于老年人的严重疾病,其特征为软骨退化和骨结构增生。甘草酸是从甘草中提取的一种化合物,已被报道具有多种重要的生物学活性,如抗氧化和抗炎作用。然而,尚未有报道表明甘草酸对 OA 发展有积极影响。我们的研究旨在评估甘草酸对人 OA 软骨细胞的作用。在本研究中,我们发现甘草酸可显著抑制白细胞介素(IL)-1β诱导的一氧化氮(NO)、前列腺素 E2(PGE2)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平以及环氧合酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)、基质金属蛋白酶 3(MMP3)、基质金属蛋白酶 13(MMP13)和整合素金属蛋白酶与凝血酶敏感蛋白 5(ADAMTS5)的产生。此外,甘草酸可逆转聚集蛋白聚糖和 II 型胶原的降解。而且,它可显著抑制 IL-1β刺激的人 OA 软骨细胞中 PI3K/AKT 磷酸化和 NF-κB 转移。在体内,甘草酸治疗可防止小鼠 OA 模型中软骨的破坏。总之,所有结果表明甘草酸可能是 OA 的一种潜在治疗方法。

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