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丹皮酚提取物对 LPS 处理的巨噬细胞炎症和氧化反应的抑制作用。

Inhibitory Effects of Decne. Extract on Inflammatory and Oxidative Responses in LPS-Treated Macrophages.

机构信息

Department of Biochemistry, Chonnam National University Medical School, Hwasun, Jeonnam-do 58128, Korea.

Combinatorial Tumor Immunotherapy Medical Research Center, Chonnam National University Medical School, Hwasun, Jeonnam-do 58128, Korea.

出版信息

Molecules. 2020 Mar 15;25(6):1336. doi: 10.3390/molecules25061336.

Abstract

Decne., known as "Mok-hyang" in Korea, has been used for the alleviation of abdominal pain, vomiting, diarrhea, and stress gastric ulcers in traditional oriental medicine. We investigated the anti-inflammatory and antioxidative effects of the ethanol extract of Decne. (ALDE) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. ALDE significantly inhibited the LPS-induced nitric oxide (NO) production and reduced inducible nitric oxide synthase (iNOS) expression in RAW 264.7 cells. The production of other proinflammatory mediators, including COX-2, interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α, was reduced by ALDE in LPS-stimulated RAW 264.7 cells. The mechanism underlying the anti-inflammatory effects of ALDE was elucidated to be the suppression of LPS-induced nuclear translocation of p65, followed by the degradation of IκB and the inhibition of the phosphorylation of mitogen-activated protein kinases (MAPK). In addition, ALDE showed enhanced radical scavenging activity. The antioxidant effect of ALDE was caused by the enhanced expression of heme oxygenase (HO-1) via stabilization of the expression of the nuclear transcription factor E2-related factor 2 (Nrf2) pathway. Collectively, these results indicated that ALDE not only exerts anti-inflammatory effects via the suppression of the NF-κB and MAPK pathways but also has an antioxidative effect through the activation of the Nrf2/HO-1 pathway.

摘要

Decne.,在韩国被称为“ Mok-hyang”,已被用于缓解传统东方医学中的腹痛,呕吐,腹泻和应激性胃溃疡。我们研究了 Decne.(ALDE)的乙醇提取物在脂多糖(LPS)刺激的 RAW 264.7 细胞中的抗炎和抗氧化作用。ALDE 可显著抑制 LPS 诱导的 RAW 264.7 细胞中一氧化氮(NO)的产生,并降低诱导型一氧化氮合酶(iNOS)的表达。ALDE 还可降低 LPS 刺激的 RAW 264.7 细胞中其他促炎介质(包括 COX-2,白细胞介素(IL)-6,IL-1β和肿瘤坏死因子(TNF)-α)的产生。 ALDE 抗炎作用的机制被阐明为抑制 LPS 诱导的 p65 核易位,随后降解 IκB 并抑制丝裂原激活的蛋白激酶(MAPK)的磷酸化。此外,ALDE 还显示出增强的自由基清除活性。 ALDE 的抗氧化作用是通过稳定核转录因子 E2 相关因子 2(Nrf2)途径来增强血红素加氧酶(HO-1)的表达而引起的。综上所述,这些结果表明,ALDE 不仅通过抑制 NF-κB 和 MAPK 途径发挥抗炎作用,而且还通过激活 Nrf2 / HO-1 途径发挥抗氧化作用。

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