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Lipopolysaccharides from Escherichia coli O111:B4
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
规格:98%
分子量:N/A
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议

产品介绍
Lipopolysaccharides (LPSs) are purified by gel-filtration chromatography.
货号:ajcx11604
CAS:N/A
分子式:N/A
分子量:N/A
溶解度:Soluble in water (5 mg/ml) or cell culture medium (1 mg/ml)
纯度:98%
存储:Store at -20°C
库存:现货

Background:

This product is extracted from E. coli serotype O111:B4 and purified by gel filtration. The source strain is from a private collection. This LPS serotype has been used to stimulate B-cells and induce NOS in human hepatocytes.

Lipopolysaccharides (LPSs) are characteristic components of the cell wall of Gram-negative bacteria. LPS and its lipid A moiety stimulate cells of the innate immune system by the Toll-like receptor 4 (TLR4), a member of the Toll-like receptor protein family, which recognizes common pathogen-associated molecular-patterns (PAMPs).

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]

参考文献:
[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.

Protocol:

Cell experiment [1]:

Cell lines

Human cancer cell line HT-29

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.

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%).

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]:

Animal models

Male Sprague-Dawley rats (200 – 250 g)

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.

Dosage form

30 mg/kg

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.

参考文献:

[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.