| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
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 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. |
| 文献引用 | |
| 产品描述 | 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] References: |
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