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目的探讨板蓝根抗内毒素活性部位F022对脂多糖(LPS)刺激鼠单核细胞释放炎性细胞因子的影响。方法取BALB/C小鼠腹腔内单核细胞,实验设计为6组。其中,实验组根据F022浓度分为1%、0.5%、0.25%、0.125%4组,分别加入板蓝根F022部位液后再加入LPS液;LPS阳性组仅加入LPS液;阴性组加入1%F022液。之后检测细胞培养上清液中3种炎性细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素6(IL-6)和一氧化氮(NO)水平。结果LPS可刺激鼠单核细胞过度释放炎性细胞因子TNF-α、IL-6和NO;与阳性组比较,实验组炎性细胞因子水平降低,且呈剂量依赖性。结论板蓝根抗内毒素活性部位F022对LPS刺激鼠单核细胞过度释放炎性细胞因子具有抑制作用。
Objective To investigate the effect of F022, an anti-endotoxic active site of Radix Isatidis, on the release of inflammatory cytokines by lipopolysaccharide (LPS)-stimulated murine monocytes. Methods The intraperitoneal mononuclear cells of BALB/C mice were used and the experimental groups were designed as six groups. Among them, the experimental group was divided into 1%, 0.5%, 0.25%, 0.125% 4 groups according to the concentration of F022, respectively, after adding Radix F022 site solution and then adding LPS solution; LPS positive group only added LPS solution; negative group added 1% F022 solution. . The levels of three inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO), were then measured in cell culture supernatants. Results LPS stimulated the release of inflammatory cytokines TNF-α, IL-6 and NO by monocytes. Compared with the positive group, the level of inflammatory cytokines in the experimental group was decreased in a dose-dependent manner. Conclusion F022, an anti-endotoxic activity site of Radix Isatidis, inhibited the excessive release of inflammatory cytokines from LPS-stimulated mouse monocytes.