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兰州百合多糖的免疫增强作用

Immune-enhancing effects of polysaccharides extracted from Lilium lancifolium Thunb.

机构信息

College of Life Sciences, Anhui Agricultural University, Hefei 230036, China.

College of Tea and Food Science and Technology, Anhui Agricultural University, Hefei 230036, China.

出版信息

Int Immunopharmacol. 2017 Nov;52:119-126. doi: 10.1016/j.intimp.2017.08.030. Epub 2017 Oct 12.

Abstract

Lilium lancifolium Thunb. is a Chinese traditional plant with various health benefits. In this study, we purified and characterized the water-soluble polysaccharide fraction (LLP-1A) of L. lancifolium. We also investigated the in vitro immune-enhancing activity of LLP-1A in macrophages and the underlying molecular mechanism. Results showed that LLP-1A was mainly composed of mannose and glucose at a molar ratio of 1.77:1, and its molecular weight was approximately 78.61kDa. The Fourier transform-infrared spectra of LLP-1A also revealed typical polysaccharide characteristics: the presence of uronic acid, pyranose rings and β-glycosidic bonds. With regard to its effects on macrophages, LLP-1A enhanced phagocytic activity and induced the NO production in a dose-dependent manner. Further, it induced expression of the cytokines interleukin-6, monocyte chemotactic protein 1, tumor necrosis factor-α and interleukin-1β. With regard to the molecular mechanism, LLP-1A increased protein expression of Toll-like receptor 4 and phosphorylation of the inhibitor of nuclear factor kappa-B kinase, inhibitor of NF-κB, and nuclear factor-kappa B in RAW 264.7 cells. Therefore, the data suggest that LLP-1A significantly upregulated the expression of immune reactive cytokines in RAW 264.7 macrophages through the TLR4-mediated NF-κB signal pathway. Thus, LLP-1A may have immunomodulatory functions that may prove beneficial for the treatment of immune-related diseases.

摘要

百合是一种具有多种健康益处的中国传统植物。在本研究中,我们从百合中分离纯化并鉴定了一种水溶性多糖(LLP-1A),研究了 LLP-1A 在巨噬细胞中的体外免疫增强活性及其潜在的分子机制。结果表明,LLP-1A 主要由甘露糖和葡萄糖组成,摩尔比为 1.77:1,分子量约为 78.61kDa。傅里叶变换红外光谱也显示 LLP-1A 具有典型的多糖特征:存在糖醛酸、吡喃环和β糖苷键。LLP-1A 能增强巨噬细胞的吞噬活性,诱导一氧化氮(NO)的产生,并呈剂量依赖性。此外,它还能诱导白细胞介素 6(IL-6)、单核细胞趋化蛋白 1(MCP-1)、肿瘤坏死因子-α(TNF-α)和白细胞介素 1β(IL-1β)等细胞因子的表达。在分子机制方面,LLP-1A 能增加 RAW 264.7 细胞中 Toll 样受体 4(TLR4)和核因子κB 激酶抑制剂(IKK)、核因子-κB(NF-κB)抑制蛋白的磷酸化。因此,数据表明 LLP-1A 通过 TLR4 介导的 NF-κB 信号通路显著上调 RAW 264.7 巨噬细胞中免疫反应性细胞因子的表达。因此,LLP-1A 可能具有免疫调节功能,有助于治疗与免疫相关的疾病。

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