Lipopolysaccharides from Escherichia coli 055:B5
(Synonyms: LPS, 脂多糖) 目录号 : GC60995
脂多糖（Lipopolysaccharides from Escherichia coli 055:B5 LPS）对革兰氏阴性菌外膜的结构和功能完整性至关重要。
Sample solution is provided at 25 µL, 10mM.
Lipopolysaccharide (LPS) is vital to both the structural and functional integrity of the Gram-negative bacterial outer membrane. Ubiquitously expressed by all Gram-negative bacteria, and containing several well-conserved domains, lipopolysaccharide also serves as one of the primary targets of the innate arm of the mammalian immune system. The lipopolysaccharides have a profound effect on the mammalian immune system and are of great significance in the pathophysiology of many disease processes.[1]
In vitro study indicated that the bone resorption and the inhibition of collagen synthesis caused by lipopolysaccharide could be prevented by PB effectively. Lipopolysaccharide at a concentration of 10μg /ml inhibited bone collagen synthesis by 43% and PB reversed this inhibition in a dose-dependent manner. Even at concentrations as low as 5 μg/ml (PB: LPS =1:2) it reduced the bone-resorbing activity of the lipopolysaccharide by 85%. This effect was specific for resorption stimulated by lipopolysaccharide.[2]
Lipopolysaccharide preconditioning to mice obviously reduced coelenterazine-Induced fluorescent lesions of Colon26 cells at 7 and 14 days after the intraportal inoculation of Colon26 cells, which expressed Nano-lantern, in comparison to control mice. Moreover, lipopolysaccharide preconditioning significantly reduced the fluorescence intensity of tumors than that of the control mice at both 7 and 14 days after tumor inoculation as well as reduced the liver weight in comparison to control mice at 14 days. Results showed that tumor metastasis was exclusively found in the lungs but not liver. Lipopolysaccharide preconditioning also tended to reduce lung metastasis in vivo.[3]
脂多糖（LPS）是革兰氏阴性菌细胞外膜的结构和功能完整性所必需的。LPS由所有革兰氏阴性菌广泛表达，包含多个保守区域，同时也是哺乳动物先天免疫系统的主要靶标之一。脂多糖对哺乳动物免疫系统具有深远影响，在许多疾病过程的病理生理学中具有重要意义。[1]
体外研究表明，PB可以有效预防脂多糖引起的骨吸收和胶原合成抑制。浓度为10μg/ml的脂多糖抑制了43%的骨胶原合成，PB以剂量依赖的方式逆转了这种抑制。即使在浓度低至5μg/ml（PB：LPS = 1:2）时，它也将脂多糖引起的骨吸收活性降低了85%。这种效应是特异性的，只作用于脂多糖刺激引起的骨吸收。[2]
小鼠预处理脂多糖显著降低了Colon26细胞内注射后7天和14天共生物发光病变的发生率。与对照组相比，脂多糖预处理显著降低了肿瘤的荧光强度和14天后肝脏重量。结果显示，肿瘤转移仅发生在肺部而不是肝脏。脂多糖预处理还趋向于减少体内肺转移。[3]
References:
[1]. Erridge C, et al. Structure and function of lipopolysaccharides. Microbes Infect. 2002 Jul;4(8):837-51.
[2]. Harvey W, et al. In vitro inhibition of lipopolysaccharide-induced bone resorption by polymyxin B. Br J Exp Pathol. 1986 Oct;67(5):699-705.
[3]. Nishikawa M, et al. Lipopolysaccharide preconditioning reduces liver metastasis of Colon26 cells by enhancing antitumor activity of natural killer cells and natural killer T cells in murine liver. J Gastroenterol Hepatol. 2021 Jul;36(7):1889-1898.
| Cell experiment [1]: | |
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Cell lines |
Human cancer cell line HT-29 |
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Preparation Method |
HT-29 cells were incubated at 37℃ in a humidified atmosphere of 5% CO2 in low-D-glucose (16.67 mM) McCoy's 5a Medium Modified supplemented with 10% v/v heat-inactivated FBS, 2 mM L-glutamine, and 1% penicillin/streptomycin. |
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Reaction Conditions |
Prior to any treatment, cells were allowed to reach confluence in plate wells, and then monolayers were exposed to a range of concentrations of carrageenans (10, 50, and 100 μg x mL–1, final value), lipopolysaccharides (10 μg x mL–1, final value). Furthermore, stress model was induced by ethanol (10%). |
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Applications |
Mixtures of lipopolysaccharides and carrageenans exhibited a tendency toward the reference profile not exposed to ethanol, but at a rate less rapid than that of cells preincubated with the carrageenan alone. In the presence of lipopolysaccharides, κ/β-carrageenan remained active, whereas the other carrageenans had no activity. The differences. |
| Animal experiment [2]: | |
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Animal models |
Male Sprague-Dawley rats (200 – 250 g) |
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Preparation Method |
Animals were housed with free access to food and water. Lipopolysaccharide from Salmonella thyphosa (Sigma) dissolved in endotoxin-free saline was used for intraperitoneal injection. Animals were sacrificed after 2, 6, 12, and 24 h, and pancreas, liver, kidney, lung, brain, and intestine were processed. |
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Dosage form |
30 mg/kg |
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Applications |
Lipopolysaccharide treatment could induce p8 mRNA expression in the pancreas. Maximal induction (31fold) was observed after 12 h and expression remained significantly elevated after 24 h. p8 mRNA was also overexpressed after Lipopolysaccharide intraperitoneal injection in liver and kidney. Maximal p8 mRNA expression was obtained after 6 and 12 h of the LPS treatment in kidney and liver respectively. Induction was of 10 and 8fold in liver and kidney respectively. |
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References: [1]. Sokolova EV, et al. Effect of carrageenans alone and in combination with casein or lipopolysaccharide on human epithelial intestinal HT-29 cells. J Biomed Mater Res A. 2017 Oct;105(10):2843-2850. [2]. Jiang YF, et al. Lipopolysaccharides induce p8 mRNA expression in vivo and in vitro. Biochem Biophys Res Commun. 1999 Jul 14;260(3):686-90. |
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| Cas No. | SDF | ||
| 别名 | LPS, 脂多糖 | ||
| Canonical SMILES | [Lipopolysaccharides] | ||
| 分子式 | 分子量 | ||
| 溶解度 | 5mg/mL in water | 储存条件 | Store at -20°C |
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