anthraquinone/hypoxia

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Ruthenium(II) anthraquinone complexes as two-photon luminescent probes for cycling hypoxia imaging in vivo.

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Recently, cycling hypoxia, with cycles of hypoxia followed by reoxygenation, was found to induce the up-regulation of HIF-1 activity in tumor cells and reduce the success rate of radiotherapy or chemotherapy. Thus, the ability to visualize cycling hypoxia in cells and in vivo is of great

Iridium(III) Anthraquinone Complexes as Two-Photon Phosphorescence Probes for Mitochondria Imaging and Tracking under Hypoxia.

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In the present study, four mitochondria-specific and two-photon phosphorescence iridium(III) complexes, Ir1-Ir4, were developed for mitochondria imaging in hypoxic tumor cells. The iridium(III) complex has two anthraquinone groups that are hypoxia-sensitive moieties. The phosphorescence of the

Involvement of human cytochromes P450 (CYP) in the reductive metabolism of AQ4N, a hypoxia activated anthraquinone di-N-oxide prodrug.

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OBJECTIVE To establish the role of the human cytochromes P450 (CYPs) in the reductive metabolism of the novel anthraquinone di-N-oxide prodrug AQ4N. METHODS Metabolism of AQ4N was conducted in a panel of 17 human phenotyped liver microsomes. AQ4N and metabolites were detected by reverse phase

Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.

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Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study

Inhibiting AKT phosphorylation employing non-cytotoxic anthraquinones ameliorates TH2 mediated allergic airways disease and rhinovirus exacerbation.

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BACKGROUND Severe asthma is associated with T helper (TH) 2 and 17 cell activation, airway neutrophilia and phosphoinositide-3-kinase (PI3K) activation. Asthma exacerbations are commonly caused by rhinovirus (RV) and also associated with PI3K-driven inflammation. Anthraquinone derivatives have been

Rhein protects the myocardiac cells against hypoxia/reoxygention-induced injury by suppressing GSK3β activity.

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BACKGROUND Rhein, an anthraquinone compound isolated from rhubarb, has been shown to protect the pancreatic β cells from hyperglycemia induced apoptosis in our previous studies. OBJECTIVE In the present study, we examined whether rhein can protect myocardial cells against ischemia reperfusion

Hypoxia-dependent retinal toxicity of bioreductive anticancer prodrugs in mice.

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The bioreductive anticancer prodrug CI-1010 ((2R)-1-[(2-bromoethyl)amino]-3-(2-nitro-1H-imidazol-1-yl)-2-propanol hydrobromide) is an alkylating nitroimidazole which shows selective toxicity against hypoxic cells in murine tumors, but causes extensive apoptosis in the outer retina in rodents and

Kanglexin, a novel anthraquinone compound, protects against myocardial ischemic injury in mice by suppressing NLRP3 and pyroptosis.

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Pyroptosis is a form of inflammatory cell death that could be driven by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation following myocardial infarction (MI). Emerging evidence suggests the therapeutic potential for

Cyclometalated Ruthenium(II) Anthraquinone Complexes Exhibit Strong Anticancer Activity in Hypoxic Tumor Cells.

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Hypoxia is the critical feature of the tumor microenvironment that is known to lead to resistance to many chemotherapeutic drugs. Six novel ruthenium(II) anthraquinone complexes were designed and synthesized; they exhibit similar or superior cytotoxicity compared to cisplatin in hypoxic HeLa, A549,

Chrysophanol Suppresses Hypoxia-Induced Epithelial-Mesenchymal Transition in Colorectal Cancer Cells.

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Colorectal cancer (CRC) is a common human malignancy, accounting for 600,000 death cases annually worldwide. Chrysophanol is a naturally occurring anthraquinone compound and exhibits anti-neoplastic activities. This study aims to explore the biological effects of chrysophanol on CRC metastasis and

Rationale for the use of aliphatic N-oxides of cytotoxic anthraquinones as prodrug DNA binding agents: a new class of bioreductive agent.

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NAD(P)H dependent cytochrome P450's and other haemoproteins under hypoxia, mediate two-electron reduction of a wide range of structurally dissimilar N-oxides to their respective tertiary amines. Metabolic reduction can be utilised, in acute and chronic hypoxia, to convert N-oxides of DNA affinic

Emodin prevents ethanol-induced developmental anomalies in cultured mouse fetus through multiple activities.

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BACKGROUND Maternal alcohol ingestion on pregnant period causes fetal alcohol syndrome including psychological and behavioral problems, and developmental abnormality. In this study, we investigated the effect of emodin, an active anthraquinone component found in the roots and bark of the genus

Emodin inhibits proinflammatory responses and inactivates histone deacetylase 1 in hypoxic rheumatoid synoviocytes.

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Chronic inflammation of rheumatoid arthritis (RA) is promoted by proinflammatory cytokines and closely linked to angiogenesis. In the present study, we investigated the anti-inflammatory effects of emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) isolated from the root of Rheum palmatum L. in

Anti-fatigue effects of active ingredients from traditional Chinese medicine: a review.

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Fatigue, a phenomenon which is believed to be caused by body exercise, can lead to the failure of predetermined exercise intensity maintenance and sport ability declination. The usage of traditional Chinese medicine (TCM) in the treatment of fatigue has long been practiced in clinical and showed

Rhein, a novel Histone Deacetylase (HDAC) inhibitor with antifibrotic potency in human myocardial fibrosis.

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Although fibrosis depicts a reparative mechanism, maladaptation of the heart due to excessive production of extracellular matrix accelerates cardiac dysfunction. The anthraquinone Rhein was examined for its anti-fibrotic potency to mitigate cardiac fibroblast-to-myofibroblast transition (FMT).

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