Human Cytochrome P450 2E1 ELISA kit

Name: Human Cytochrome P450 2E1 ELISA kit
SKU: DEIA-BJ31
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, cell culture supernatant and other biological samples

Species Reactivity

Human

Detection Method

sELISA

Intended Use

In vitro quantitative determination of Cyp2e1 concentrations in cell lysates, tissue homogenates and other biological samples.

Contents of Kit

1. ELISA Microplate (Dismountable): 8×12, 2-8°C/-20°C. Put the rest strips into a sealed foil bag with the desiccant. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C.
2. Lyophilized Standard: 2 vials, 2-8°C/-20°C. Put the rest standards into a desiccant bag. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C
3. Sample Dilution Buffer: 20 ml, 2-8°C
4. Biotin-labeled Antibody (Concentrated): 120 μl, 2-8°C (Avoid Direct Light)
5. Antibody Dilution Buffer: 10 ml, 2-8°C
6. HRP-Streptavidin Conjugate (SABC, 100×): 120 μl, 2-8°C (Avoid Direct Light)
7. SABC Dilution Buffer: 10 ml, 2-8°C
8. TMB Substrate: 10 ml, 2-8°C (Avoid Direct Light)
9. Stop Solution: 10 ml, 2-8°C
10. Wash Buffer (25X): 30 ml, 2-8°C
11. Plate Sealer: 5 pieces
12. Product Description: 1 copy

Storage

2-8°C and -20°C

Precision

Intra-assay Precision:samples with low,medium and high concentration are tested 20 times on same plate.
Inter-assay Precision:samples with low,medium and high concentration are tested 20 times on three different plates.

Detection Range

0.156-10 ng/ml

Sensitivity

0.094 ng/ml

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Hepatic PGC-1 alpha is not essential for fasting-induced cytochrome p450 regulation in mouse liver

BIOCHEMICAL PHARMACOLOGY

Authors: Thogersen, Rebekka; Kristensen, Caroline Maag; Olsen, Mette Algot; Bertram, Hanne Christine; Pilegaard, Henriette; Rasmussen, Martin Kroyer

Abstract

Fasting has been shown to regulate the expression of the cytochrome p450 (CYP) enzyme system in the liver. However, the exact mechanism behind the fasting-induced regulation of the CYP's remains unknown. In the present study we tested the hypothesis that the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha), which is a key-regulator of energy metabolism, is responsible for the fasting-induced regulation of the CYP's. Lox/lox and liver specific PGC-1 alpha (LKO) mice of both sexes, fasted for 18 h and the content of the CYP's as well as the hepatic metabolome was assessed. Fasting increased the mRNA content of Cyp2a4, Cyp2e1, Cyp3a11 and Cyp4a10. The fasting-induced response in Cyp4a10 mRNA content was different between lox/lox and LKO mice, while the absence of PGC-1 alpha had no effect on the fasting-induced response for the other Cyp's. Moreover, the fasting-induced response in mRNA content of Sirtinus 1 and Perilipin 2 was different between lox/lox and LKO mice. Only the CYP1A isoform showed a fasting-induced response at the protein level. Absence of hepatic PGC-1 alpha had no effect on the apparent metabolome, where fasting vs fed was the only discriminate in the following multivariate analysis. In conclusion, hepatic PGC-1 alpha is not essential for the fasting-induced regulation of hepatic CYP's.

Cisplatin and farnesol co-encapsulated PLGA nano-particles demonstrate enhanced anti-cancer potential against hepatocellular carcinoma cells in vitro

MOLECULAR BIOLOGY REPORTS

Authors: Mondal, Jesmin; Khuda-Bukhsh, Anisur Rahman

Abstract

Cisplatin (CDDP) is a potent chemotherapeutic drug, but its severe side-effects often prohibit its use. Combined treatment with CDDP plus Farnesol (FAR) and their co-encapsulated nano form were investigated in in vitro to examine if synergistic cytotoxicity of this combination could reduce unwanted side-effects of CDDP chemotherapy and potentiate CDDP anticancer activity against hepatocellular carcinoma (HCC) cells. After finding combination therapy of CDDP and FAR successfully combat HCC we formulated co-encapsulation of CDDP and FAR within poly(lactic-co-glycolic acid) copolymer (NCDDPFAR) by following the standardized solvent displacement method. NCDDPFAR treatment caused faster drug mobility, sustained particle release, site-specific action and higher percentage of apoptotic death compared with single drug treatment even at relatively low concentrations. Co-encapsulation of two drugs exhibited additive effects against HCC; FAR reduced CDDP-induced glutathione level by increasing expression of CYP2E1 while CDDP directly interacted with DNA; FAR up-regulated the expression of TopII, thereby promoting DNA breaks and escaping DNA repair machinery. Expression pattern of apoptotic genes like p53, Bax, cytochrome c and caspase-3 suggested that NCDDPFAR induced HCC cell death through mitochondrial intrinsic pathway. Administration of NCDDPFAR had better ability of drug carriage and enhanced anticancer potentials against HCC cells.