Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway.
Galuteolin suppresses proliferation and inflammation in TNF-α-induced RA-FLS cells by activating HMOX1 to regulate IKKβ/NF-κB pathway.
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DOI：
10.1186/s13018-020-02004-x
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发表时间：
2020-10-21
影响因子：
2.6
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Guan Y;Zhao X;Liu W;Wang Y
Galuteolin(Galu)是从金银花中提取和纯化的物质。本研究旨在探讨GALU对肿瘤坏死因子-α诱导的RA-FLS细胞(滑膜细胞)的影响，并从抗细胞凋亡和抗炎的角度揭示其潜在的分子机制。α刺激后，用CCK-8比色法检测细胞增殖情况。采用原位末端标记法检测细胞凋亡率。免疫印迹法检测Iκκβ、p-p65、p65、p-IκB、IκB、裂解半胱氨酸天冬氨酸蛋白酶3、半胱氨酸天冬氨酸蛋白酶3、Bcl2、bax的表达。用RT-PCR方法检测HO-1的表达。用双抗体夹心酶联免疫吸附试验检测促炎症细胞因子IL-1、β、IL-6、IL-8和MMP1的含量。Galu以剂量依赖的方式显著抑制细胞增殖。此外，Galu还能明显促进RA-FLS细胞的凋亡率，上调HO-1、caspase-3和Bax的表达水平，降低Bcl2的表达水平。此外，GALU还能明显抑制RA-κκβ细胞中I-κ、p-p65和p-I-β的表达，并显著降低促炎因子IL-1、IL-6、IL-8和MMP1的表达水平。Galuteolin通过抑制细胞凋亡和炎症，对肿瘤坏死因子-α诱导的RA-FLS细胞具有保护作用，对类风湿关节炎的临床应用具有指导意义。
Galuteolin (Galu) is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the effects of Galu on the TNF-α-induced RA-FLS cells (synoviocytes) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis and anti-inflammation. After TNF-α stimulation, cell proliferation of RA-FLS was assessed by CCK-8 assay. TUNEL staining was used to detect the apoptosis. Western blot was used to detect the expressions of Iκκβ, p-p65, p65, p-IκB, IκB, Cleaved-caspase3, Caspase-3, Bcl-2, and Bax. HO-1 were determined by RT-PCR. The contents of pro-inflammatory cytokines IL-1β, IL-6, IL-8, and MMP-1 were determined by ELISA. Galu significantly suppressed cell proliferation in a dose-dependent manner. Additionally, Galu obviously promotes cell apoptosis rate of RA-FLS cells and elevated the expression levels of HO-1, caspase-3, and Bax, while reducing the expression level of Bcl-2. Furthermore, Galu apparently inhibited the levels of Iκκβ, p-p65, and p-IκB. Moreover, Galu also significantly reduced the levels of pro-inflammatory factors IL-1β, IL-6, IL-8, and MMP-1 in RA-FLS cells. Galuteolin exerts protective effects against TNF-α-induced RA-FLS cells by inhibiting apoptosis and inflammation, which can guide the clinical use of rheumatoid arthritis.
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