Human Toll-like receptor 4 ELISA Kit

Name: Human Toll-like receptor 4 ELISA Kit
SKU: DEIA4321
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Serum, plasma, tissue homogenates and other biological fluids

Species Reactivity

Human

Detection Method

sELISA

Intended Use

TLR4 ELISA Kit allows for the in vitro quantitative determination of TLR4 concentrations in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

E001 ELISA Microplate(Dismountable) , 8×12, 2-8°C/-20°C
E002 Lyophilized Standard, 2vial, 2-8°C/-20°C
E039 Sample/Standard Dilution Buffer, 20ml, 2-8°C
E003 Biotin-labeled Antibody(Concentrated), 120ul, 2-8°C(Avoid Direct Light)
E040 Antibody Dilution Buffer, 10ml, 2-8°C
E034 HRP-Streptavidin Conjugate(SABC), 120ul, 2-8°C(Avoid Direct Light)
E049 SABC Dilution Buffer, 10ml, 2-8°C
E024 TMB Substrate, 10ml, 2-8°C(Avoid Direct Light)
E026 Stop Solution, 10ml, 2-8°C
E038 Wash Buffer(25X), 30ml, 2-8°C
E006 Plate Sealer, 5pieces
E007 Product Description 1copy

Storage

2-8°C for 6 months

Precision

Intra-Assay: CV<8%; Inter-Assay: CV<10%

Detection Range

0.313-20ng/ml

Sensitivity

0.188ng/ml

Standard Curve

Results of a typical standard operation of a TLR4 ELISA Kit are listed below. This standard curve was generated at our lab for demonstration purpose only. Users shall obtain standard curve as per experiment by themselves. (N/A=not applicable)

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Adverse reproductive function induced by maternal BPA exposure is associated with abnormal autophagy and activating inflamation via mTOR and TLR4/NF-kappa B signaling pathways in female offspring rats

REPRODUCTIVE TOXICOLOGY

Authors: Meng, Yuan; Zhao, Yannan; Lin, Ren; Sun, Qi; Wei, Wei; Jia, Lihong

Abstract

Bisphenol A (BPA) can affect reproductive function, but its mechanism of reproductive toxicity is unclear, and the effect of BPA on the onset of puberty was inconsistent. The main purpose of this study is to investigate the effects of perinatal exposure to BPA on the onset of puberty and reproductive function, and its mechanism from the aspect of autophagy and inflammation in ovarian and uterus tissues of female offspring. Twenty-one pregnant SD rats were randomly divided into three groups: Control group, 1 mu g/mL BPA (LBPA) and 10 mu g/mL BPA group (HBPA) via drinking water from gestational day 6 to the end of lactation. After weaning, female offspring rats were fed a normal diet and drinking water for 5 weeks. The levels of E2, LH, FSH, T, and IL-6 and TNF-alpha, and the onset of puberty, and morphological changes in ovarian and uterine were determined in female offspring at 8 weeks. The levels of TLR4, NF-kappa B, PI3K/Akt/mTOR and autophagy related protein in uterine tissue were also detected. Our results indicated that perinatal exposure to BPA advanced puberty, which was associated with increased serum E2, LH and FSH levels. There was a significantly thin endometrium epithelium in HBPA group compared with control group, which may affect reproductive function. The adverse effect of perinatal BPA exposure on reproductive function maybe was associated with the activation of inflammation and abnormal autophagy via TLR4/NF-kappa B and mTOR signaling pathways respectively in female offspring.

MicroRNA-27 attenuates pressure overload-Induced cardiac hypertrophy and dysfunction by targeting galectin-3

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

Authors: Zhang, Meiqi; Cheng, Kang; Chen, Huan; Tu, Jianfeng; Shen, Ye; Pang, Lingxiao; Wu, Weihua

Abstract

Cardiac hypertrophy is an adaptive response to hemodynamic stress to compensate for cardiac dysfunction. MicroRNAs can regulate cardiac function and play a vital role in the regulation of cardiac hypertrophy. In the current study, in vivo and vitro hypertrophy models are established to explore the role of miR-27b and to elucidate the underlying mechanism in cardiac hypertrophy. Expression of miR-27b was down-regulated in mice with cardiac hypertrophy. The cardiac function of the mice with cardiac hypertrophy could be restored with the overexpression of miR-27b, this is observed in terms of decreasing LVEDd, LVESd, and increasing LVFS, LVEF. This study also predicted and confirmed that galectin-3 is a target gene of miR-27b. Depletion of galectin-3 significantly attenuated hypertrophy of hearts in both in vitro and in vivo tests. In conclusion, MiR-27b be used to exert a protective role against cardiac dysfunction and hypertrophy by decreasing the expression level of galectin-3. The methodology suggested in this study provides a novel therapeutic strategy against cardiac hypertrophy.