Peng Qiang, Liu Huajing, Shi Shihui, Li Ming
College of Food Science and Engineering, Northwest A&F University, Yangling 712100, China.
College of Resources and Environmental Science, Northeast Agricultural University, Harbin 150030, China.
Int J Biol Macromol. 2014 Jun;67:330-5. doi: 10.1016/j.ijbiomac.2014.03.023. Epub 2014 Mar 25.
Polysaccharide has been reported to possess diverse biological activities, however, the inflammatory activity of polysaccharide isolated from Lycium ruthenicum remains unknown so far. In the present study, we investigated the effects of L. ruthenicum polysaccharide (LRGP3) on inflammatory reaction induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells and some potential underlying mechanisms. Our results showed that LRGP3 treatment significantly inhibited the LPS-induced NO production and the mRNA expression of iNOS, as well as the level of Toll-like receptor 4 (TLR4). Furthermore, LRGP3 treatment prevented the IκBα degradation and reduced phospho-NF-κB p65 protein expression in LPS-stimulated RAW264.7 cells. Meanwhile, the levels of pro-inflammatory cytokines, such as interleukin (IL)-α, IL-6, tumor necrosis factor (TNF)-α were suppressed by LRGP3 in LPS-stimulated RAW264.7 cells. Taken together, our results suggested that LRGP3 attenuated LPS-induced inflammation via inhibiting TLR4/NF-κB signaling pathway.
据报道，多糖具有多种生物活性，然而，迄今为止，从黑果枸杞中分离得到的多糖的炎症活性尚不清楚。在本研究中，我们研究了黑果枸杞多糖（LRGP3）对小鼠巨噬细胞RAW264.7细胞中脂多糖（LPS）诱导的炎症反应的影响以及一些潜在的作用机制。我们的结果表明，LRGP3处理显著抑制了LPS诱导的NO产生、iNOS的mRNA表达以及Toll样受体4（TLR4）的水平。此外，LRGP3处理可防止LPS刺激的RAW264.7细胞中IκBα的降解，并降低磷酸化NF-κB p65蛋白的表达。同时，LRGP3在LPS刺激的RAW264.7细胞中抑制了促炎细胞因子如白细胞介素（IL）-α、IL-6、肿瘤坏死因子（TNF）-α的水平。综上所述，我们的结果表明，LRGP3通过抑制TLR4/NF-κB信号通路减轻了LPS诱导的炎症。
