Centre for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Research and Development Centre for Natural Health Products, Hong Kong Baptist University Shenzhen Research Institute and Continuing Education, Shenzhen 518057, China.
J Tradit Chin Med. 2019 Oct;39(5):624-631.
To investigate the effect of Young Yum pill (YYP) on inflammatory mediators in cultured RAW 264.7 cells and elucidate the nuclear factor-kappa B (NF-κB)-related mechanism behind the action.
YYP was extracted with 95% ethanol Lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages were used to evaluate the effect of YYP on inflammatory mediators. Production of nitric oxide (NO) and prostaglandin E2 (PGE2) were measured by Griess test and enzyme-linked immunosorbent assay, respectively. The levels of genes and proteins involved in the generation of inflammatory mediators were examined using real-time polymerase chain reaction and Western blotting, respectively.
YYP dose-dependently suppressed LPS-induced production of NO, PGE2 and tumor necrosis factor-α (TNF-α), and elevation of mRNA and protein levels of inducible NO synthase and cyclooxygenase-2 in RAW 264.7 macrophages. These observations were associated with decreased NF-κB p65 phosphorylation and nuclear localization, enhanced Akt (protein kinase B) phosphorylation, as well as reduced inhibitor of κB (IκB) α degradation and IκB kinase α/β phosphorylation.
The present study demonstrated an inhibitory effect of YYP on the NF-κB-regulated inflammatory mediators NO, PGE2 and TNF-α in LPS-stimulated RAW 264.7 macrophages, providing a pharmacological basis for the use of YYP in treating inflammatory disorders.
研究 Young Yum 丸(YYP)对培养的 RAW 264.7 细胞中炎症介质的影响,并阐明其作用的核因子-κB(NF-κB)相关机制。
用 95%乙醇提取 YYP,用脂多糖(LPS)刺激 RAW 264.7 巨噬细胞,以评估 YYP 对炎症介质的影响。通过格里斯试验测量一氧化氮(NO)和前列腺素 E2(PGE2)的产生,分别通过酶联免疫吸附试验和实时聚合酶链反应检测参与炎症介质生成的基因和蛋白质的水平。
YYP 呈剂量依赖性抑制 LPS 诱导的 RAW 264.7 巨噬细胞中 NO、PGE2 和肿瘤坏死因子-α(TNF-α)的产生,以及诱导型一氧化氮合酶和环氧化酶-2 的 mRNA 和蛋白水平的升高。这些观察结果与 NF-κB p65 磷酸化和核定位减少、Akt(蛋白激酶 B)磷酸化增强以及 IκBα降解和 IκB 激酶α/β磷酸化减少有关。
本研究表明 YYP 对 LPS 刺激的 RAW 264.7 巨噬细胞中 NF-κB 调节的炎症介质 NO、PGE2 和 TNF-α具有抑制作用,为 YYP 治疗炎症性疾病提供了药理学基础。