stilbene/hypoxia

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Protective effect of piceatannol and bioactive stilbene derivatives against hypoxia-induced toxicity in H9c2 cardiomyocytes and structural elucidation as 5-LOX inhibitors.

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Stilbenes with well-known antioxidant and antiradical properties are beneficial in different pathologies including cardiovascular diseases. The present research was performed to investigate the potential protective effect of resveratrol (1) and piceatannol (2), against hypoxia-induced oxidative

Polyacetal-stilbene conjugates - The first examples of polymer therapeutics for the inhibition of HIF-1 in the treatment of solid tumours.

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We report here the first examples of Polymer Therapeutics synthesised with the intention of inhibiting Hypoxia Inducible Factor-1 (HIF-1), a transcription factor heavily involved in numerous cell processes under a low oxygen environment. Four compounds were selected for use in these systems;

Synthesis of novel imine stilbene analogues exhibiting potent anticancer activity.

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BACKGROUND Resveratrol (RV) and its analogues Aza-stilbenes were found effective in exhibiting anticancer activity. OBJECTIVE The present study mainly focused on the green synthesis of novel imine stilbene analogues and evaluation of their anticancer activity besides their influence on

Hypoxia-inducible factor 1alpha- mediated resistance to phenolic anticancer.

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BACKGROUND Phenolic compounds EGCG [(-)-epigallocatechin-3-gallate], resveratrol (3,4',5-trihydroxy-trans-stilbene) and capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) are worth investigating for clinical application in cancer prevention and chemotherapy. Hypoxia-induced drug resistance is a

Resveratrol reduces the hypoxia-induced resistance to doxorubicin in breast cancer cells.

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Resveratrol (3,4',5-trihydroxy-trans-stilbene) is known to enhance the cytotoxicity of the anticancer drug doxorubicin. On the other hand, breast cancer MCF-7 cells acquire resistance to doxorubicin under hypoxic conditions. In this study, we investigated the effect of resveratrol on hypoxia-induced

Resveratrol inhibits hypoxia-inducible factor-1α-mediated androgen receptor signaling and represses tumor progression in castration-resistant prostate cancer.

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Androgen-dependent prostate cancer inevitably progresses to incurable castration-resistant prostate cancer (CRPC) after androgen deprivation therapy. Because castration-induced hypoxia-inducible factor (HIF)-1α enhances the transcriptional activity of androgen receptor (AR) at low androgen levels

Reactive oxygen species released from mitochondria during brief hypoxia induce preconditioning in cardiomyocytes.

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Reactive oxygen species (ROS) have been proposed to participate in the induction of cardiac preconditioning. However, their source and mechanism of induction are unclear. We tested whether brief hypoxia induces preconditioning by augmenting mitochondrial generation of ROS in chick cardiomyocytes.

Evidence for resveratrol-induced preservation of brain mitochondria functions after hypoxia-reoxygenation.

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We have previously shown, as have other authors, that trans-resveratrol (E-resveratrol, 3,4,5-trihydroxy-E-stilbene) reduces reactive oxygen species (ROS) generation of mitochondria freshly isolated from healthy rat brains and that it also counteracts the effect of uncouplers (CCCP) on mitochondrial

Redox regulation of p53 during hypoxia.

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The transcription factor p53 can induce growth arrest or death in cells. Tumor cells that develop mutations in p53 demonstrate a diminished apoptotic potential, which may contribute to growth and tumor metastasis. Cellular levels of p53 are stabilized during hypoxia. The present study tested the

Involvement of anion exchange in the hypoxia/reoxygenation-induced changes in pH(i) and.

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The involvement of Cl(-)/HCO(3)(-) exchange in hypoxia/reoxygenation-induced changes in pH(i) and Ca(2+) concentration ([Ca(2+)](i)) was examined in rat ventricular myocytes. During 10-min hypoxia, the initial pH(i) (7.21+/-0.04) fell to below 6.8. Subsequent reperfusion with reoxygenated buffer

Increase in chloride-dependent L-glutamate transport activity in synaptic membrane after in vitro ischemic treatment.

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The effect of energy failure on Cl(-)-dependent L-glutamate (L-Glu) transport was examined with an in vitro preparation. Rat brain slices were incubated in low oxygen and glucose-deprived medium (in vitro ischemia), and a synaptic membrane fraction was prepared from the slices. Cl(-)-dependent

Baicalein preconditioning protects cardiomyocytes from ischemia-reperfusion injury via mitochondrial oxidant signaling.

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Previous studies suggest baicalein, in addition to its antioxidant effects, protects against hypoxia/reoxygenation injury via its pro-oxidant properties. We hypothesize that a brief period of baicalein treatment prior to ischemia/reperfusion (I/R) may trigger preconditioning protection via a

Mechanism of luminal alkalinization by bullfrog fundic mucosa.

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Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 mueq.cm-2.h-1.OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3(-)-free nutrient solution. In Na+ solutions, increasing

Inhibition of bicarbonate transport protects embryonic heart against reoxygenation-induced dysfunction.

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It has not been well established whether the mechanisms participating in pH regulation in the anoxic-reoxygenated developing myocardium resemble those operating in the adult. We have specially examined the importance of Na+/H+ exchange (NHE) and HCO3-dependent transports in cardiac activity after

Sources for superoxide release: lessons from blockade of electron transport, NADPH oxidase, and anion channels in diaphragm.

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Isolated diaphragm releases low levels of superoxide (O2*-) at rest and much higher levels during heat stress. The molecular source is unknown. The hypothesis was tested that heat stress stimulates mitochondrial complex activity or NADPH oxidases, resulting in increased O2*- release. The

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