ITT Cancer Research – Apoptosis – Oncology

Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

Oxymatrine (OMT) is the major quinolizidine alkaloid extracted from the root of Sophora flavescens Ait and has been shown to exhibit a diverse range of pharmacological properties. The aim of the present study was to investigate the role of OMT in diabetic brain injury in vivo and in vitro. Diabetic rats were induced by intraperitoneal injection of a single dose of 65 mg/kg streptozotocin (STZ) and fed a high-fat and high-cholesterol diet. Memory function was assessed using a Morris water maze test. A SH-SY5Y cell injury model was induced by incubation with glucose (30 mM/l) to simulate damage in vitro. The serum fasting blood glucose, insulin, serum S100B, malondialdehyde (MDA), and superoxide dismutase (SOD) levels were analyzed using commercial kits. Morphological changes were observed using Nissl staining and electron microscopy. Cell apoptosis was assessed using Hoechst staining and TUNEL staining. NADPH oxidase (NOX) and caspase-3 activities were determined.

The effects of NOX2 and NOX4 knockdown were assessed using small interfering RNA. The expression levels of NOX1, NOX2, and NOX4 were detected using reverse transcription-quantitative PCR and western blotting, and the levels of caspase-3 were detected using western blotting. The diabetic rats exhibited significantly increased plasma glucose, insulin, reactive oxygen species (ROS), S-100B, and MDA levels and decreased SOD levels. Memory function was determined by assessing the percentage of time spent in the target quadrant, the number of times the platform was crossed, escape latency, and mean path length and was found to be significantly reduced in the diabetic rats. Hyperglycemia resulted in notable brain injury, including histological changes and apoptosis in the cortex and hippocampus. The expression levels of NOX2 and NOX4 were significantly upregulated at the protein and mRNA levels, and NOX1 expression was not altered in the diabetic rats.

NOX and caspase-3 activities were increased, and caspase-3 expression was upregulated in the brain tissue of diabetic rats. OMT treatment dose-dependently reversed behavioral, biochemical, and molecular changes in the diabetic rats. In vitro, high glucose resulted in increases in reactive oxygen species (ROS), MDA levels, apoptosis, and the expressions of NOX2, NOX4, and caspase-3. siRNA-mediated knockdown of NOX2 and NOX4 decreased NOX2 and NOX4 expression levels, respectively, and reduced ROS levels and apoptosis. The results of the present study suggest that OMT alleviates diabetes-associated cognitive decline, oxidative stress, and apoptosis via NOX2 and NOX4 inhibition.

 

Activation of the Melanocortin-1 Receptor by NDP-MSH Attenuates Oxidative Stress and Neuronal Apoptosis through PI3K/Akt/Nrf2 Pathway after Intracerebral Hemorrhage in Mice

Oxidative stress and neuronal apoptosis play crucial roles in secondary brain injury (SBI) after intracerebral hemorrhage (ICH). Recently, Nle4-D-Phe7-α-melanocyte-stimulating hormone (NDP-MSH), a synthetic agonist of the melanocortin-1 receptor (Mc1r), has been proved to inhibit neuroinflammatory in several diseases. This study is aimed at exploring if NDP-MSH could reduce oxidative stress and neuronal apoptosis following ICH, as well as the potential mechanism. A mouse ICH model was induced by autologous blood injection. NDP-MSH was intraperitoneally injected at 1 h after ICH. Mc1r siRNA and PI3K inhibitor LY294002 were administrated to inhibit the expression of Mc1r and phosphorylation of PI3K, respectively.
Neurological test, brain water content, enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), immunofluorescence, and Western blot analysis were utilized in this study. The results exhibited that Mc1r was mainly expressed in neurons, and its level in the ipsilateral hemisphere was significantly elevated after ICH. NDP-MSH treatment significantly attenuated the neurological deficits and brain water content 24 hours after ICH, which was accompanied by the inhibition of oxidative stress and neuronal apoptosis. The administration of NDP-MSH after ICH significantly promoted the expression of Mc1r, p-PI3K, p-Akt, and p-Nrf2, followed by an increase of Bcl-2 and reduction of cleaved caspase-3.
Conversely, downregulating the expression of Mc1r and phosphorylation of PI3K aggravated the neurological deficits and brain edema at 24 hours after ICH, meanwhile, the effect of NDP-MSH on the expression of Mc1r, p-PI3K, p-Akt, p-Nrf2, Bcl-2, and cleaved caspase 3 was also abolished. In conclusion, our data suggest that the activation of Mc1r by NDP-MSH ameliorates oxidative stress and neuronal apoptosis through the PI3K/Akt/Nrf2 signaling pathway after ICH in mice.
 Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4
Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

Nimbolide induces cell death in T lymphoma cells: Implication of altered apoptosis and glucose metabolism

Nimbolide is a tetranortriterpenoid derived from the leaves and flowers of Azadirachta indica (Neem). It exhibits anticancer activity against a variety of cancers by modulating various crucial features, including cell proliferation, apoptosis, and invasion and metastasis. More importantly, the cytotoxic effect of nimbolide has also been observed against T cell lymphoma, but the underlying mechanisms are still unexplored. So far, no study has been conducted to observe the effect of nimbolide on cancer cell metabolism. Therefore, the present investigation was designed to explore the molecular mechanisms of the antitumor potential of nimbolide against T cell lymphoma, a neoplastic disorder of thymic origin.
In addition, we also unraveled the anti-glycolytic activity of nimbolide against T lymphoma cells with possible molecular mechanisms. Our results showed the cytotoxic action of nimbolide against three different cell lines of T cell lymphoma, namely Dalton’s lymphoma, HuT-78, and J6. Nimbolide-induced apoptosis in T lymphoma cells by altering the level of reactive oxygen species, p53, Bcl2, Bax, and cytochrome c, with subsequent cleavage of caspase 3. Remarkably, nimbolide inhibited the expression of hypoxia-inducible factor-1α, glucose transporter 3, hexokinase II, and pyruvate dehydrogenase kinase 1, which led to the suppression of glycolysis with concomitant activation of oxidative phosphorylation.

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Goat IgG-PE conjugate (isotype control)

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Rat IgG-Biotin conjugate (isotype control) (Isotype control)

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Rat IgG-FITC conjugate (isotype control) (Isotype control)

20005-F 100 ug
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Rat IgG-HRP conjugate (isotype control) (Isotype control)

20005-HP 100 ug
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Rat IgG-PE conjugate (isotype control) (Isotype control)

20005-PE 25 tests
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Description: Armenian Hamster monoclonal IgG Isotype Control antibody

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Rat IgG, purified (Isotype control)

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Rabbit IgG-biotinylated (isotype control)

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IgG Isotype Control antibody (FITC)

61R-1136 50 ug
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61R-1337 200 ug
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Description: Armenian Hamster monoclonal IgG Isotype Control antibody (PE)

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IgG Isotype Control antibody (biotin)

61R-1586 50 ug
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Description: Armenian Hamster monoclonal IgG Isotype Control antibody (biotin)

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Description: Syrian Hamster monoclonal IgG Isotype Control antibody (biotin)

IgG Isotype Control antibody (allophycocyanin)

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Description: Armenian Hamster monoclonal IgG Isotype Control antibody (allophycocyanin)

IgG Isotype Control antibody (allophycocyanin)

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Description: Syrian Hamster monoclonal IgG Isotype Control antibody (allophycocyanin)

IgG Isotype Control antibody (FITC)

61R-1800 25 ug
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Description: Rabbit polyclonal IgG Isotype Control antibody (FITC)

FITC Rabbit IgG - Isotype control

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Syrian Hamster IgG Isotype Control

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Syrian Hamster IgG Isotype Control

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Donkey IgG (Control, non-immune, isotype control)

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Goat IgG control

31R-AG001 1 mg
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Description: Goat Immunoglobulins Goat IgG control

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Hamster IgG, purified (Syrian, isotype control)

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Hamster IgG, purified (Armenian, Isotype control)

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Mouse IgG-Biotin conjugate (isotype control)

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Mouse IgG-FITC conjugate (isotype control)

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Mouse IgG-HRP conjugate (isotype control)

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Mouse IgG-PE conjugate (isotype control)

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Rabbit IgG-FITC conjugate (isotype control)

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Rabbit IgG-HRP conjugate (isotype control)

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Rabbit IgG-PE conjugate (isotype control)

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Rabbit IgG Isotype Control APC Conjugate

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Rabbit IgG Isotype Control RPE Conjugate

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Donkey IgG (non-immune, isotype control) IgG, purified

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Llama IgG (Control, non-immune, isotype control, ELISA grade)

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Camel IgG (Control, non-immune, isotype control, ELISA grade)

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G. Pig IgG-FITC conjugate (isotype control)

20004-F 100 ug
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Rat IgG Fab fragment, purified (isotype control)

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Rat IgG (Fc) fragment, purified (isotype control)

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Chimpanzee IgG (non-immune, isotype control), purified

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Donkey IgG (non-immune, isotype control), purified

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Dog IgG (isotype control, non-immune), purified

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Baboon IgG (non-immune, isotype control), purified

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Baboon IgG (non-immune, isotype control), purified

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Description: Syrian Hamster monoclonal IgG Isotype Control Fc fusion protein (FITC)

Mouse IgG Isotype control; Ready-To-Use

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Rat IgG, purified (Whole, non-immune) (isotype control)

20005-1 1 mg
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Rat IgG (Fc)-Biotin Conjuagte (isotype control), purified

20005-1-FC-B 0.1 mg
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Rat IgG (Fc)-FITC Conjuagte (isotype control), purified

20005-1-FC-F 0.1 mg
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Rat IgG (Fc)-HRP Conjuagte (isotype control), purified

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Rat IgG, purified (Whole, non-immune) (isotype control)

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Human IgG, purified (serum, non-immune, isotype control)

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Human IgG, purified (serum, non-immune, isotype control)

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Human IgG, purified (serum, non-immune, isotype control)

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Human IgG, purified (serum, non-immune, isotype control)

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Mouse IgG, purified (serum non-immune, isotype control)

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Mouse IgG, purified (serum non-immune, isotype control)

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Mouse IgG, purified (serum non-immune, isotype control)

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Mouse IgG F(c)-FITC conjugate (isotype control)

20008-Fc-F 100 ug
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Mouse IgG-R-PE-Cy5 conjugate (isotype control)

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Rabbit IgG, purified (serum non-immune, isotype control)

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Rabbit IgG, purified (serum non-immune, isotype control)

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Rabbit IgG, purified (serum non-immune, isotype control)

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Rabbit IgG F(c)-biotin conjugate, isotype control

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Rabbit IgG F(c)-FITC conjugate, isotype control

20009-Fc-F 100 ug
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Rabbit IgG F(c)-HRP conjugate, isotype control

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EUR 164

Chicken IgG unlabeled (isotype control, non-immune), purified

20010-1 1 mg
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Monkey IgG (Rhesus, non-immune, isotype control), purified

20012-1 1 mg
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Squirrel Monkey IgG (non-immune, isotype control), purified

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EUR 164

Monkey IgG (Rhesus, non-immune, isotype control), purified

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Pig IgG (swine non-immune, isotype control), purified

20017-1 1 mg
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Monkey IgG (Cynomolgous, non-immune, isotype control), purified

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Monkey IgG (Cynomolgous, non-immune, isotype control), purified

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Ferret IgG/IgM/IgA, semi-purified (isotype control)

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Turkey IgG, purified (non-immune, isotype control) Serum

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Turkey IgG, purified (non-immune, isotype control) Serum

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Cat IgG, unlabeled (non-immune, isotype control) purified

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Armenian Hamster IgG Isotype Control (PIP), APC-100ug

QAB69-APC-100ug 100ug
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Ferret IgG (Control, non-immune, isotype control), semi-pure for ELISA

20021-1 100 ug
EUR 225

Elk IgG, semi-pure for ELISA (Control, non-immune, isotype control)

20024-1 100 ug
EUR 225

Deer IgG, semi-pure for ELISA (Control, non-immune, isotype control)

20024-2 100 ug
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Bison IgG, semi-pure for ELISA (Control, non-immune, isotype control)

20025-1 100 ug
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Raccoon IgG, semi-pure for ELISA (Control, non-immune, isotype control)

20026-1 100 ug
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Skunk IgG, semi-pure for ELISA (Control, non-immune, isotype control)

20027-1 100 ug
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Positive control tissue section for each antibody; Based on availability INQUIRE

Control-Slides Set of 5
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Hence, the results of the present investigation demonstrate that nimbolide exerts tumoricidal activity against T lymphoma cells via augmentation of apoptosis and reversal of altered cell metabolism. Thus, the present study provides a new insight for the therapeutic utilization of nimbolide against T cell lymphoma.

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