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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.

1906 related Products with: Cell Cycle Arrest and Apoptosis Induced by Kinamycin F in Human Osteosarcoma Cells.

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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#28578345   2017/06/04 Save this To Up

Calcium Channel Opening Rather than the Release of ATP Causes the Apoptosis of Osteoblasts Induced by Overloaded Mechanical Stimulation.

Stress fracture is one of the most common overuse injuries in athletes. Overloaded mechanical stimulation is an important factor affecting stress fractures, but the mechanism is unclear.

1469 related Products with: Calcium Channel Opening Rather than the Release of ATP Causes the Apoptosis of Osteoblasts Induced by Overloaded Mechanical Stimulation.

BACTERIOLOGY BACTEROIDES TCP-1 theta antibody Sour voltage-dependent calcium Recombinant Thermostable Recombinant Thermostable Recombinant Thermostable Recombinant Human PKC the Recombinant Human PKC the Recombinant Human PKC the Single Strand DNA Ligase, Single Strand DNA Ligase, Thermostable TDG Enzyme &

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#27434554   2016/07/20 Save this To Up

[Effects of autophagy on lipopolysaccharide-induced vascular hyper-permeability].

To investigate the effects of autophagy on lipopolysaccharide (LPS)-induced vascular hyper-permeability.

2534 related Products with: [Effects of autophagy on lipopolysaccharide-induced vascular hyper-permeability].

Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein

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#27260571   2016/06/04 Save this To Up

The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells.

D-α-tocopherol succinate significantly reduced a cisplatin-induced hair cell loss in HEI-OC1 cell lines. These effects were mediated by its scavenging activity against reactive oxygen species (ROS) and inhibition of apoptosis.

2266 related Products with: The effects of the antioxidant α-tocopherol succinate on cisplatin-induced ototoxicity in HEI-OC1 auditory cells.

Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Multiple organ tumor tiss MultiGene Gradient therm Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon

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#27207282   2016/05/21 Save this To Up

Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.

Vascular endothelial apoptosis is significantly associated with atherosclerosis and cardiovascular diseases, for which oxidized low-density lipoprotein (ox-LDL) is a major risk factor. Allicin, the primary active ingredient of garlic, has been found to have cardiovascular protective effect by changing the fatty-acid composition, but its effect on ox-LDL-induced vascular endothelial injury remains unclear. We investigated the protective effect of allicin on cell viability, LDH release, apoptosis and apoptotic signaling in human umbilical vein endothelial cells (HUVECs).

2008 related Products with: Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.

Low Density Lipoprotein Low Density Lipoprotein Low Density Lipoprotein Primary antibody low den Lipoprotein, Human Plasma Mouse Anti-Human Low Dens CD31, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; CD34, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell;

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#26775664   2016/03/01 Save this To Up

Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.

Sulforaphane (SFN), a natural dietary isothiocyanate, is found to exert beneficial effects for cardiovascular diseases. This study aimed to investigate the mechanisms underlying the protective effects of SFN in a model of myocardial hypoxia/reoxygenation (H/R) injury in vitro.

1062 related Products with: Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.

Anti beta3 AR Human, Poly Sterile filtered rat ser Insulin 1 (Rat), syntheti anti FAS IgG1 (monoclonal anti CD20 monoclonal anti Goat Anti-Rat MARCH10, (i Goat Anti-Human ERN1 IRE1 Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN

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#26314451   2015/08/28 Save this To Up

[Protective Effect of Ulinastatin against Activation of Tourniquet-Induced Platelet Mitochondria Apoptotic Signaling].

To investigate the protective effect of ulinastatin against the activation of tourniquet-induced platelet mitochondria apoptotic signaling.

2970 related Products with: [Protective Effect of Ulinastatin against Activation of Tourniquet-Induced Platelet Mitochondria Apoptotic Signaling].

Ofloxacin CAS Number [824 Anti-AICDA(Activation-ind Anti AICDA(Activation ind Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon CELLKINES PLATELET DERIVE PLATELET DERIVED GROWTH F CELLKINES PLATELET DERIVE PLATELET DERIVED GROWTH F Human Platelet Derived Gr

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#26141531   2015/08/28 Save this To Up

Analysis of porcine granulosa cell death signaling pathways induced by vinclozolin.

Recent studies suggest that disturbing androgen-signaling pathways in porcine ovarian follicles may cause granulosa cell (GC) death. For this reason, we investigated which apoptotic pathway is initiated after GC exposure to an environmental antiandrogen, vinclozolin (Vnz), in vitro. Immunocytochemistry, Western blots, and fluorometric assays were used to quantify caspase-3 and -9 expression and activity. To elucidate the specific mechanism of Vnz action and toxicity, GCs were assessed for viability, cytotoxicity, and apoptotic activity using the ApoTox-Glo Triplex Assay. To further determine the mechanism of GC death induced by Vnz, we used the Apoptosis Antibody Array Kit. In response to Vnz stimulus, we found an increased level of caspase-3 protein expression (P ≤ 0.001) and an increase in caspase-3 proteolytic activity (P ≤ 0.001), confirming that Vnz is a potent proapoptotic factor. The strong immunoreaction of caspase-9 after Vnz treatment (P ≤ 0.001) suggests that intrinsic mitochondrial apoptosis pathway was activated during GC death. On the other hand, caspase-8, being a part of the extrinsic receptor pathway, was also activated (P ≤ 0.001). Therefore, it is possible that Vnz induces porcine granulosal apoptosis also through a parallel pathway. Activation of these two pathways was confirmed by the Apoptosis Antibody Array Kit. In conclusion, it is possible that the intrinsic signaling pathway may not act as an initial trigger for GC apoptosis but might contribute to the amplification and propagation of apoptotic cell death in the granulosa layer after treatment with this antiandrogen. Moreover, Vnz disturbs the physiological process of programmed cell death. Consequently, this could explain why atretic follicles are rapidly removed and suggests that normal function of the ovarian follicle may be destroyed.

1211 related Products with: Analysis of porcine granulosa cell death signaling pathways induced by vinclozolin.

T-cell proliferation grad TCPI T cell proliferation TCPI T cell proliferation Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu T-cell proliferation grad TCPII T cell proliferatio TCPII T cell proliferatio AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF

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#25760023   2015/05/07 Save this To Up

Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells.

Recent studies have revealed that an intrinsic apoptotic signaling cascade is involved in vascular hyperpermeability and endothelial barrier dysfunction. Propofol (2,6-diisopropylphenol) has also been reported to inhibit apoptotic signaling by regulating mitochondrial permeability transition pore (mPTP) opening and caspase-3 activation. Here, we investigated whether propofol could alleviate burn serum-induced endothelial hyperpermeability through the inhibition of the intrinsic apoptotic signaling cascade. Rat lung microvascular endothelial cells (RLMVECs) were pretreated with propofol at various concentrations, followed by stimulation with burn serum, obtained from burn-injury rats. Monolayer permeability was determined by transendothelial electrical resistance. Mitochondrial release of cytochrome C was measured by ELISA. Bax and Bcl-2 expression and mitochondrial release of second mitochondrial-derived activator of caspases (smac) were detected by Western blotting. Caspase-3 activity was assessed by fluorometric assay; mitochondrial membrane potential (Δψm) was determined with JC-1 (a potential-sensitive fluorescent dye). Intracellular ATP content was assayed using a commercial kit, and reactive oxygen species (ROS) were measured by dichlorodihydrofluorescein diacetate (DCFH-DA). Burn serum significantly increased monolayer permeability (P<0.05), and this effect could be inhibited by propofol (P<0.05). Compared with a sham treatment group, intrinsic apoptotic signaling activation - indicated by Bax overexpression, Bcl-2 downregulation, Δψm reduction, decreased intracellular ATP level, increased cytosolic cytochrome C and smac, and caspase-3 activation - was observed in the vehicle group. Propofol not only attenuated these alterations (P<0.05 for all), but also significantly decreased burn-induced ROS production (P<0.05). Propofol attenuated burn-induced RLMVEC monolayer hyperpermeability by regulating the intrinsic apoptotic signaling pathway.

1481 related Products with: Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells.

Signal transduction antib AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp ErbB Her Signaling Phosph ERK Signaling Phospho-Spe GPCR Signaling to MAPK ER IGF-1R Signaling Phospho- mTOR Signalign Phospho-Sp NF-kB II Phospho-Specific p53 Signaling Phospho-Spe T-Cell Receptor Signaling TGF-Beta Signaling Phosph

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#25550770   2014/12/31 Save this To Up

Ulinastatin inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling.

Oxidants are important signaling molecules known to increase endothelial permeability. Studies implicate reactive oxygen species (ROS) and the intrinsic apoptotic signaling cascades as mediators of vascular hyperpermeability. Here we report the protective effects of ulinastatin, a serine protease inhibitor with antiapoptotic properties, against oxidant-induced endothelial monolayer hyperpermeability. HUVECs were respectively pretreated with 10,000 and 50,000 u/l ulinastatin, followed by stimulation of 0.6 mM H₂O₂. Monolayer permeability was determined by transendothelial electrical resistance (TER); Mitochondrial release of cytochrome c was determined by enzyme-linked immunosorbent assay; Caspase-3 activity was measured by fluorometric assay; Adherens junction protein β-catenin was detected by immunofluorescense staining; Ratio of cell apoptosis was evaluated by Annexin-V/PI double stain assay; Mitochondrial membrane potential (Δψm) was determined with JC-1; Intracellular ATP content was assayed by a commercial kit; Bax and Bcl-2 expression were estimated by western blotting; Intracellular reactive oxygen species (ROS) level was measured by DCFH-DA. H₂O₂ exposure resulted in endothelial hyperpermeability and ROS formation (P < 0.05). The activation of mitochondrial intrinsic apoptotic signaling pathway was evidenced from BAX up-regulation, Bcl-2 down-regulation, mitochondrial depolarization, an increase in cytochrome c release, and activation of caspase-3 (P < 0.05). UTI (50,000 u/l) attenuated endothelial hyperpermeability, ROS formation, mitochondrial dysfunction, cytochrome c release, activation of caspase-3, and disruption of cell adherens junctions (P < 0.05). Together, these results demonstrate that UTI provides protection against vascular hyperpermeability by modulating the intrinsic apoptotic signaling.

2476 related Products with: Ulinastatin inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling.

CD31, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; CD34, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Endocrine Gland Vas Human Vascular Endothelia

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