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#28034658   2016/12/30 Save this To Up

Rhizoma smilacis glabrae protects rats with gentamicin-induced kidney injury from oxidative stress-induced apoptosis by inhibiting caspase-3 activation.

Rhizoma smilacis glabrae (RSG), which is mild-natured and tastes sweet or bland, has pharmacological action of eliminating dampness, detoxifying, and ensuring that joints were healthy and supple in traditional Chinese medicine.

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Transcription factors: O Anti-AICDA(Activation-ind Anti AICDA(Activation ind Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon OXI TEK (Oxidative Stress Human Epstein-Barr Virus Active Human Caspase 310 Active Human Caspase 3100 Active Human Caspase 325

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#26453563   2015/10/10 Save this To Up

Huaiqihuang Granules () reduce proteinuria by enhancing nephrin expression and regulating necrosis factor κB signaling pathway in adriamycin-induced nephropathy.

To investigate the effects of Huaiqihuang Granules (, HQH), a mixture of Chinese herbs including Trametes robiniophila Murr, Fructus Lycii and Polygonatum sibiricum, on adriamycininduced nephropathy (ADRN) in rats and its underlying mechanisms.

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#22652377   2012/06/01 Save this To Up

Sulforaphane retards the growth of UM-UC-3 xenographs, induces apoptosis, and reduces survivin in athymic mice.

Sulforaphane (SFN), an isothiocyanate that exists exclusively in cruciferous vegetables, may be the most promising preventive agent for bladder cancer (BC) to date. We previously observed that SFN dramatically inhibits human BC T24 cells in vitro. Our hypothesis is that SFN may attenuate BC growth. To test our hypothesis, we investigated the effect of SFN on human BC UM-UC-3 cell xenografts implanted into athymic mice. Sulforaphane extract was routinely prepared in our laboratory, and its content was measured with high-performance liquid chromatography. Athymic mice were injected subcutaneously with a UM-UC-3 cell suspension (2.0×10(6) cells/200 μL per mouse) and randomly divided into 2 groups. The positive control group was orally gavaged with water, and the treatment group was orally administered SFN from broccoli sprout (12 mg/kg body weight) for 5 weeks. At the end of the experiment, tumor tissues were harvested and processed for hematoxylin and eosin staining and immunohistochemistry. The average tumor volume decreased from 4.1±1.67 cm(3) in the positive control mice to 1.5±0.72 cm(3) in the SFN-treated mice, evidencing an inhibitory rate of 63%. The SFN extract also reduced the appearance of tumors, including karyopyknosis and angiogenesis. Sulforaphane extract induced caspase 3 and cytochrome c expression but reduced the expression of survivin. Sulforaphane extract retards the growth of UM-UC-3 xenografts in vivo, confirming its future potential in BC therapy.

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FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Sterile filtered mouse s DNA (cytosine 5) methyltr Human Insulin-like Growth Human Interleukin-33 IL-3

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#15964118   2005/07/15 Save this To Up

Effects of anthocyanidin on the inhibition of proliferation and induction of apoptosis in human gastric adenocarcinoma cells.

Anthocyanins are naturally occurring reddish pigments that abundant in fruits and vegetables. To investigate the mechanistic basis for the anti-tumor properties of anthocyanins, five aglycone (cyanidin, delphinidin, malvidin, pelargonidin, and peonidin) and four glycosylated (cyanidin-3-glucoside, malvidin-3-glucoside, pelargonidin-3-glucoside and peonidin-3-glucoside) anthocyanins were used to examine their effects on cell cycle progression and induction of apoptosis in human gastric adenocarcinoma AGS cells. The data from cell viability assay showed that malvidin exhibited the most potent anti-proliferation effect on AGS cells in a time- and dose-dependent manner (P<0.05). This event is accompanied the arrest of AGS cells at the G0/G1 phase by malvidin at the tested concentrations of 0-200 microM. Cellular uptake of anthocyanin and anthocyanidin was confirmed by HPLC analysis and the intracellular accumulation of malvidin (24.9+/-1.1 microM/mg protein) was observed when treatment of AGS cells with malvidin for 12 h. In addition, an accumulation of AGS cells in sub-G1 phase (20% and 30% increase for 100 and 200 microM of malvidin, respectively) was observed as well as by the appearance of a fraction of cells with an aneudiploid DNA content. The occurrence of apoptosis induced by malvidin was confirmed by morphological and biochemical features, including apoptotic bodies formation, caspase-3 activation and poly(ADP-ribose) polymerase proteolysis. Furthermore, the mitochondrial membrane potential of apoptotic cells after treatment with malvidin was significantly lost and resulted in the elevation of Bax/Bcl-2 ratio for 1.6-fold against control for 100 microM treatment. In addition, the malvidin treatment significantly increased the p38 kinase expression and inhibited the ERK activity, and the effects of malvidin on caspase-3 activation were blocked, respectively, by the ERK and p38 inhibitors. These findings suggest that growth inhibition and cytotoxicity of AGS cells by malvidin is involved in the induction of apoptosis rather than necrosis.

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Epidermal Growth Factor ( Epidermal Growth Factor ( Macrophage Colony Stimula Macrophage Colony Stimula Apoptosis (Human) Antibod Apoptosis (Human) Antibod Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Ofloxacin CAS Number [824 Rabbit Anti-Human Apoptos

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#11137483   2001/01/03 Save this To Up

Alcohol-induced sinusoidal endothelial cell dysfunction in the mouse is associated with exacerbated liver apoptosis and can be reversed by caspase inhibition.

The purpose of this study was to determine if a correlation exists between alcohol-induced liver sinusoidal endothelial cell (SEC) dysfunction and alcohol-induced augmented liver apoptosis in the mouse. Mice were fed an alcohol-containing liquid diet for 7 weeks. On the last day of feeding, the animals were treated with the pan-caspase inhibitor IDN1529 (N-[(indole-2-)-alaninyl]-3-amino-4-oxo-fluoropentanoic acid), killed, and plasma amino transferase activity, plasma hyaluronan, liver caspase-3 activity, the frequency of apoptotic nuclei in the liver, liver histology and electron microscopic appearance evaluated. Alcohol feeding significantly increased (2.5-fold) plasma hyaluronan levels, frequency of apoptotic nuclei (20-fold), and caspase-3 activity (1.7-fold), but did not affect plasma amino transferase activity. Transmission electron microscopy revealed that SEC was among the cell types undergoing apoptosis. Livers of alcohol-fed mice displayed marked fat accumulation without necrosis or fibrosis. Treatment of mice with IDN1529 reversed the alcohol effects on plasma hyaluronan levels, liver caspase-3 activity, and frequency of apoptotic nuclei. However, the inhibitor did not prevent fat accumulation in the liver. These data suggest that alcohol-induced exacerbation of apoptosis in the liver, which extends to the SEC, causes functional impairment of the sinusoidal lining and can be reversed by caspase inhibition.

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Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon Rabbit Anti-Cell death in Rabbit Anti-Cell death in Human Liver Sinusoidal Mi GFP Expressing Human Live RFP Expressing Human Live Mouse AntiT cell receptor Mouse Anti-Lipoprotein Li Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon HIV1 integrase antibody,

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#10874216   2000/08/18 Save this To Up

Human T cell leukemia cell death by apoptosis-inducing nucleosides from CD57(+) HLA-DR(bright) natural suppressor cell line.

Apoptosis-inducing nucleosides (AINs) released from CD57( +) HLA-DR(bright) natural suppressor (57.DR-NS) cell line, derived from human decidual tissue, were isolated from 57.DR-NS cell culture supernatant by the combination of thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). Apoptotic cell death was strongly induced in human T cell leukemia Molt4 cells treated with AINs, absolutely depending on DNA strand breaks, with activation of the caspase cascade, especially caspase-3. The administration of AINs to Molt4 tumor-bearing severe combined immunodeficiency (SCID) mice resulted in drastic suppression of tumor growth, with a decrease of tumor size and the appearance of apoptotic signals in tumor tissue. Thus, AINs are candidates for development as anticancer agents.

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CELLKINES Natural Human I Rabbit Anti-Cell death in Rabbit Anti-Cell death in anti SLAM anti CDw150 IgG TCGF (Natural T Cell Grow T-cell proliferation grad TCHI T cell proliferation TCHI T cell proliferation T-cell proliferation grad TCHII T cell proliferatio TCHII T cell proliferatio Cell Meter™ Caspase 3 7

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#10679236   2000/03/10 Save this To Up

Activation of caspase-3 in molt4 cells by apoptosis-inducing nucleosides from CD57(+)HLA-DR(bright) natural suppressor cell line.

Apoptosis-inducing nucleosides (AINs), which were released and isolated from CD57(+)HLA-DR(bright) natural suppressor (57.DR-NS) cell line derived from human decidual tissue, induced apoptosis in Molt4 cells. The addition of caspase-3 inhibitor into the reaction blocked the cleavage of caspase-3 and apoptosis in Molt4 cells treated with AINs, detected by flow cytometrical or spectrofluorometrical analysis and DNA fragmentation assay. Furthermore, by means of immunoblotting, the processing of caspase-3 was shown with the appearance of their catalytically active subunits of 20 and 11 kDa during the generation of apoptosis in Molt4 cells treated with AINs. This processing of caspase-3 into active subunits was also blocked by the addition of caspase-3 inhibitor. Thus, it was definitely revealed that the activation of caspase-3 was a key feature in the caspase cascade of AINs-induced apoptosis in Molt4 cells.

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