In this study, we investigated the anti-inflammatory effects and mechanisms of Hizikia fusiformis (HF) extracts in lipopolysaccharide (LPS)-induced RAW 264.7 cells. We extracted HF using solvent and sub-critical water techniques. In results, HF extracts inhibited nitric oxide (NO) production in cell-free and LPS-stimulated RAW 264.7 cells. HF210 (extract prepared with sub critical water at 210oC) was most effective. The HF210 extract dose-dependently inhibited inducible nitric oxide synthase expression (iNOS) and nuclear factor kappa (NF-B) p65 translocation from cytosol to the nucleus. Furthermore, HF210 extract dose-dependently inhibited the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), Jun N-terminal kinase (JNK), and signal transducers and activators of transcription (STAT)-1in LPS-induced RAW 264.7 cells. Thus, our results suggest that anti-inflammatory effects of HF210 extract showed a noticeable distinction by regulation of multiple signaling pathways in LPS-induced RAW 264.7 cells.

译文

在这项研究中,我们研究了梭状冬青 (HF) 提取物在脂多糖 (LPS) 诱导的原始264.7细胞中的抗炎作用和机制。我们使用溶剂和亚临界水技术提取HF。结果,HF提取物抑制无细胞和LPS刺激的原始264.7细胞中一氧化氮 (NO) 的产生。HF210 (在210oC下用亚临界水制备的提取物) 最有效。HF210提取物剂量依赖性地抑制诱导型一氧化氮合酶 (iNOS) 表达和核因子 κ (NF-B) p65从细胞质到细胞核的转运。此外,HF210提取物在LPS诱导的原始264.7细胞中剂量依赖性地抑制p38丝裂原活化蛋白激酶 (p38mapk) 、6月N端激酶 (JNK) 和信号转导子和转录激活子 (STAT)-1的磷酸化。因此,我们的结果表明,HF210提取物的抗炎作用通过调节LPS诱导的原始264.7细胞中的多种信号通路显示出明显的区别。

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