E03L0268 Mouse Lipopolysaccharides ELISA kit
The Mouse Lipopolysaccharides ELISA kit can be used to identify samples from the mouse species. Lipopolysaccharides can also be called Lipoglycans, Lipooligosaccharide, Lipo-Oligosaccharide, Endotoxin, and LPS/LOS.
Product Information | |
Cat. No. | E03L0268 |
Product Name | Mouse Lipopolysaccharides ELISA kit |
Species | Mouse |
Product Size | 48 Tests / 96 Tests |
Concentration | 50-1000ng/mL |
Sensitivity | 1.0ng/mL |
Principal | Competitive ELISA |
Sample Volume | 100 ul |
Sample Type | Serum, plasma, cell culture supernatants, body fluid and tissue homogenate |
Assay Time | 90 minutes |
Platform | Microplate Reader |
Conjugate | HRP |
Detection Method | Colorimetric |
Storage | 2-8°C |
Kit Components | ||
MATERIALS | SPECIFICATION | QUANTITY |
MICROTITER PLATE | 96 wells | stripwell |
ENZYME CONJUGATE | 6.0 mL | 1 vial |
STANDARD A (0.5mL) | 0 ng/mL | 1 vial |
STANDARD B (0.5mL) | 50 ng/mL | 1 vial |
STANDARD C (0.5mL) | 100 ng/mL | 1 vial |
STANDARD D (0.5mL) | 250 ng/mL | 1 vial |
STANDARD E (0.5mL) | 500 ng/mL | 1 vial |
STANDARD F (0.5mL) | 1000 ng/mL | 1 vial |
SUBSTRATE A | 6 mL | 1 vial |
SUBSTRATE B | 6 mL | 1 vial |
STOP SOLUTION | 6 mL | 1 vial |
WASH SOLUTION (100 x) | 10 mL | 1 vial |
BALANCE SOLUTION | 3 mL | 1 vial |
Principle of the Assay |
LPS/LOS ELISA kit applies the competitive enzyme immunoassay technique utilizing an anti-LPS/LOS antibody and a LPS/LOS-HRP conjugate. The assay sample and buffer are incubated together with LPS/LOS-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the LPS/LOS concentration since LPS/LOS from samples and LPS/LOS-HRP conjugate compete for the anti-LPS/LOS antibody binding site. Since the number of sites is limited, as more sites are occupied by LPS/LOS from the sample, fewer sites are left to bind LPS/LOS-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The LPS/LOS concentration in each sample is interpolated from this standard curve. |
Coefficient of Variance | Intra Variation% ＜10% | |
Inter Variation% ＜12% | ||
Recovery | 95-102% | |
Linearity | Diluent Ratio | Range % |
1:2 | 93-105 | |
1:4 | 88-106 | |
1:8 | 86-108 | |
Specificity/Cross-reactivity | No significant cross-reactivity or interference between LPS/LOS and analogues was observed. | |
E03L0268 has been referenced in the below publications：
Bile acid is a significant host factor shaping the gut microbiome of diet-induced obese mice.
Distinctly altered gut microbiota in the progression of liver disease.
Chitin Oligosaccharide Modulates Gut Microbiota and Attenuates High-Fat-Diet-Induced Metabolic Syndrome in Mice.
Hepatic early inflammation induces downregulation of hepatic cytochrome P450 expression and metabolic activity in the dextran sulfate sodium-induced murine colitis.
Ulcerative colitis-induced hepatic damage in mice: Studies on inflammation, fibrosis, oxidative DNA damage and GST-P expression.
Melatonin Reduces Ulcerative Colitis-Associated Local and Systemic Damage in Mice: Investigation on Possible Mechanisms.
Mechanistic insight into beta-carotene-mediated protection against ulcerative colitis-associated local and systemic damage in mice.
Chitosan oligosaccharides improve the disturbance in glucose metabolism and reverse the dysbiosis of gut microbiota in diabetic mice.
Role of α-lipoic acid in dextran sulfate sodium-induced ulcerative colitis in mice: Studies on inflammation, oxidative stress, DNA damage and fibrosis.
The effects of neuroblastoma and chemotherapy on metabolism, fecal microbiome, volatile organic compounds, and gut barrier function in a murine model.
N-Acetylcysteine alleviates gut dysbiosis and glucose metabolic disorder in high-fat diet-fed mice.
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