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#28927141   2017/09/20 Save this To Up

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway.

Catalpol is an effective active ingredient that functions as a diuretic and laxative, and exhibits blood sugar-lowering, liver protective, anti-aging and anticancer effects. In traditional Chinese medicine, catalpol is believed to be Yin nourishing. The anticancer effect of catalpol on human HCT116 colorectal cancer cells were investigated and the mechanism of action was evaluated. Cellular viability was detected using an MTT assay. Caspase-3 and caspase-9 activity, cellular apoptosis and nucleic morphology were analyzed using caspase-3 and caspase-9 activity assay kits, flow cytometric assays and DAPI staining assay, respectively. Western blot analysis was used to measure the protein expressions of phosphatidylinositol 3-kinase (PI3K), phosphorylated-protein kinase B (p-Akt) and Akt. Expression of microRNA-200 was detected using the reverse transcription-quantitative polymerase chain reaction. HCT116 cells were incubated with PI3K inhibitors in order to analyze the effect of catalpol on cell proliferation. Catalpol was able to inhibit HCT116 cell proliferation. Furthermore, catalpol induced apoptosis in HCT116 cells, which depended on the increased activities of caspase-3 and -9. In addition, catalpol reduced the expression of PI3K, p-Akt and Akt in HCT116 cells. However, downregulation of PI3K/Akt decreased the viability of HCT116 cells following treatment with catalpol and enhanced microRNA-200 expression. Catalpol promoted cellular apoptosis in human HCT116 colorectal cancer cells through upregulation of microRNA-200 expression, which depended on a downregulation of the phosphatase and tensin homolog/PI3K-Akt signaling pathway.

1083 related Products with: Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway.

AKT PKB Signaling Phospho Cancer Apoptosis Phospho- Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Mouse Anti-Human Insulin Rabbit Anti-Human Androge Rabbit Anti-Human Inhibin Macrophage Colony Stimula Macrophage Colony Stimula anti H inh human blood an anti CD7 All T cells Reco anti Transferrin receptor

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#28849509   2017/08/29 Save this To Up

Role of Taurine in BDE 209-Induced Oxidative Stress in PC12 Cells.

Polybrominated diphenyl ethers (PBDEs) are globally dispersed throughout the environment, and the levels of some PBDEs in the environment may still be increasing. Previous studies showed that BDE 209 exerted neurodevelopmental and neurobehavioral effects in humans and animals. Oxidative stress is a common mechanism reported in PBDEs-induced neurotoxicity. Taurine, as an antioxidant, whether it is effective in alleviating BDE 209-induced neurotoxicity is still unknown. PC12 cells were exposed to various concentrations of BDE 209 (6.25, 12.5, 25, 50, and 100 μM). 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was used to assess the cell viability. 2',7'-Dichlorofluorescin diacetate (DCFH-DA) detector was used to explore the production of ROS. Acridine orange was used to reflect the permeation of lysosomal membrane. Rhodamine 123 was used to reflect the permeation of mitochondrial membrane. Lactate dehydrogenase and catalase in PC12 cells exposed to BDE 209 were examined by kits. The results showed that taurine could significantly reverse the decreased viability, the serious oxidative stress and abnormal autophagy in PC12 cells exposed to BDE 209. Collectively, our results indicated that taurine could protect PC12 cells from BDE 209-induced neurotoxicity by alleviating oxidative stress.

2461 related Products with: Role of Taurine in BDE 209-Induced Oxidative Stress in PC12 Cells.

Anti beta3 AR Human, Poly Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu

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#28830513   2017/08/23 Save this To Up

Etlingera elatior Extract promotes cell death in B16 melanoma cells via down-regulation of ERK and Akt signaling pathways.

Torch ginger (Etlingera elatior, EE) is a ginger plant that found in Southeast Asia. Previous study showed its flowers and leaves composed of several flavonoids with anti-cancer activity. This study aims to investigate the mechanism of EE extract on cell death induction in melanoma cells.

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GLP 2 ELISA Kit, Rat Prog anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Macrophage Colony Stimula Macrophage Colony Stimula

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#28821565   2017/08/19 Save this To Up

Down-regulation of XIAP enhances the radiosensitivity of esophageal cancer cells in vivo and in vitro.

The study investigated the effects of X-chromosome-linked inhibitor of apoptosis (XIAP) gene silencing on the radiosensitivity of esophageal cancer (EC) cells. Western blotting was used to select EC cell lines with XIAP overexpression. Selected EC9706 and KYSE30 cell lines were both divided into four groups: the blank control group, the negative control (NC) group (transfected with pBSHH1), the siRNA-enhanced group (transfected with pBSHH1-XIAP1-siRNA), and the siRNA-decreased group (transfected with pBSHH1-XIAP2-siRNA). Expressions of XIAP were measured by reverse-transcription quantitative PCR (RT-qPCR) and Western blotting, cell survival and viability by MTT assay and colony formation assay, and cell apoptosis by flow cytometry, respectively. Caspase-3 and caspase-9 activity were detected using caspase-3 and caspase-9 activity detection kits. A nude mice model of EC9706 cell line was established to measure tumorigenesis ability. Compared with the NC group, XIAP mRNA and protein expressions were decreased, caspase-3 and caspase-9 activity and apoptosis were up-regulated, and cell survival rate and colony-forming efficiency were lower in the siRNA-enhanced and siRNA-decreased groups in both the cell lines; while the opposite trends were found in the siRNA-decreased group compared with the siRNA-enhanced group. Tumor weight and volume of nude mice were decreased in the siRNA-enhanced and siRNA-decreased groups than those in the NC group, and were elevated in the siRNA-decreased group compared with the siRNA-enhanced group. These results indicate that XIAP gene silencing would strengthen the radiosensitivity of EC9706 cells, which provides a novel target for the treatment of EC.

2837 related Products with: Down-regulation of XIAP enhances the radiosensitivity of esophageal cancer cells in vivo and in vitro.

GLP 2 ELISA Kit, Rat Prog Esophageal cancer tissue Esophageal cancer tissue High density esophageal c Esophageal cancer tissue Esophageal cancer and adj Esophageal cancer and adj Esophageal cancer tissue Middle advanced stage eso Esophageal cancer and nor Esophageal cancer tissue GI cancer (esophageal, ga

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#28805483   2017/08/14 Save this To Up

Tet1-mediated DNA demethylation involves in neuron damage induced by bilirubin in vitro.

The aim of this study is to identify the role of Tet1-mediated DNA demethylation in the neurotoxicity caused by unconjugated bilirubin (UCB) in vitro. Primary neuronal cells after cultured for 72 h were exposed to UCB (0-100 μmol/L) for 24 h. Following exposure to UCB cytotoxicity was determined with the methyl tetrazolium (MTT) assay, reactive oxygen species (ROS) and caspase-3 activity in neuron cells were measured with the corresponding assay kits. The expression of Tet1 and Klotho was determined with RT-PCR at mRNA level and western blot at protein level. Our results showed that UCB can cause time-dependent and dose-dependent reduction of cell viability of neuronal cells, induce oxidative stress through increasing the production of ROS and increase caspase-3 activity. Quantitative real-time PCR and western blot analysis showed that UCB can inhibit Tet1 and Klotho expression in cultured neuronal cells at both the mRNA and protein level, respectively. These results are first to suggest UCB may, in part, exert its neurotoxicity through alteration of the neuronal antioxidant status and inhibition of Klotho and Tet1 gene expression. The elevation of DNA methylation in global genome through inhibition of Tet1 gene expression may, in part, play an important role in the neurotoxicity caused by UCB in vitro.

2941 related Products with: Tet1-mediated DNA demethylation involves in neuron damage induced by bilirubin in vitro.

OxiSelect™ Cellular UV- removed without changing Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon DNA (cytosine 5) methyltr Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu

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#28739694   2017/07/25 Save this To Up

Cell Cycle Arrest and Apoptosis Induced by Kinamycin F in Human Osteosarcoma Cells.

Kinamycin F is a bacterial metabolite which contains an unusual and potentially reactive diazo group that is known for its ability to inhibit cell growth. In this study, the potential anti-tumor activity of kinamycin F was investigated in three human osteosarcoma cell lines, MG-63, U-2 OS and HOS as an antitumor agent with a potentially novel target.

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Macrophage Colony Stimula Macrophage Colony Stimula Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Anti C Reactive Protein A Epidermal Growth Factor ( Epidermal Growth Factor ( TGF beta induced factor 2 GLP 2 ELISA Kit, Rat Prog Leptin ELISA Kit, Rat Lep

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#28736364   2017/07/24 Save this To Up

[Angiotensin-(1-7) protects cardiac myocytes against high glucose-induced injury by inhibiting ClC-3 chloride channels].

To explore whether angiotensin-(1-7) [Ang-(1-7)] protects cardiac myocytes against high glucose (HG)-induced injury by inhibiting ClC-3 chloride channels.

2955 related Products with: [Angiotensin-(1-7) protects cardiac myocytes against high glucose-induced injury by inhibiting ClC-3 chloride channels].

Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu 5-Acetamidonaphthalene-1- Acetylcholine Chloride C7 Acetylcholine-d9 Chloride Asoxime Chloride C14H16Cl 2-Azido-2-deoxy-D-glucose Insulin Glucose Phospho-S Cytokine (Mouse) Antibody Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A

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#28735483   2017/07/23 Save this To Up

AMLprofiler: A Diagnostic and Prognostic Microarray for Acute Myeloid Leukemia.

Acute myeloid leukemia is characterized by the proliferation and accumulation of immature hematopoietic cells of the myeloid lineage in the bone marrow. The disease is typified by diverse genetic abnormalities and marked heterogeneity both with regard to response to treatment and survival. The AMLprofiler is a qualitative in vitro diagnostic microarray developed by SkylineDx for use with Affymetrix technology. The AMLprofiler makes use of RNA chemistry and incorporates seven separate assays based on three different technologies-cytogenetics, mutation, and expression analysis-to predict post-therapy survival rates in patients with acute myeloid leukemia. The assay has been validated for processing of bone marrow samples from which RNA is isolated within 48 h. The samples are subsequently processed using Affymetrix GeneChip reagent kits and analyzed on the Affymetrix GeneChip 3000Dx v2 system. The scanned AMLprofiler data is sent to a centralized server of SkylineDx via a secured Internet connection, and a diagnostic report is generated within 15 min. We have performed several AMLprofiler assays in our laboratory and found the data generated via this assay to be consistent with standard modalities.

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#28713974   2017/07/17 Save this To Up

miRNA-125b regulates apoptosis of human non-small cell lung cancer via the PI3K/Akt/GSK3β signaling pathway.

The present investigation demonstrated that regulation of microRNA (miR)-125b affected the apoptosis of human non-small cell lung cancer (NSCLC) through targeting of the PI3K/Akt and Wnt/β-catenin signaling pathways. The expression of miR-125b was assessed in patients with NSCLC, which demonstrated that miR-125b expression in NSCLC tissue was higher than that in para-carcinoma tissue. Furthermore, survival analysis of patients with NSCLC over 3 years indicated that the overall survival (OS) and disease-free survival (DFS) rates of patients with low miR-125b expression were higher than those of patients with high miR-125b expression. Proliferation and apoptosis assays were subsequently conducted in the human NSCLC cell line A549 using MTT assay and Annexin V-FITC/PI kits, respectively. Caspase-3 activity ELISA and western blot analysis were also used to assess caspase-3 activity and the protein expression of Bax, Akt, phosphorylated (p)-Akt, p-GSK3β, Wnt and β-catenin. It was observed that downregulation of miR-125b inhibited the proliferation and induced the apoptosis of A549 cells. Downregulation of miR-125b also suppressed the protein expression of p-Akt, Wnt and β-catenin, and increased caspase-3 activity and Bax protein expression in A549 cells. In addition, downregulation of miR-125b combined with the PI3K inhibitor LY294002 enhanced cell growth inhibition, suppression of p-GSK3β, Wnt and β-catenin protein expression and promotion of caspase-3 activity in A549 cells. These results revealed that the downregulation of miR-125b regulates apoptosis in human NSCLC through the suppression of the PI3K/Akt/GSK3β and Wnt/β-catenin signaling pathways.

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#28662498   2017/06/29 Save this To Up

Modulation of Oxidative Stress by 17 β-Estradiol and Genistein in Human Hepatic Cell Lines In Vitro.

estrogens and phytoestrogens exert hepatoprotection through mechanisms not clearly examined yet. Here, we investigated the protective effects exerted by 17β-estradiol and genistein against oxidative stress in hepatocytes and hepatic stellate cells (HSCs) and the involvement of specific receptors and the intracellular signalling.

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