Epicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB

Mohamed, Rasha H.; Karam, Rehab A.; Amer, Mona G.

doi:10.1016/j.brainresbull.2011.07.001

Cited by 82 publications

(46 citation statements)

References 39 publications

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“…Doxorubicin (DOX; Adriamycin) is an anthracycline antibiotic commonly used as chemotherapy of solid tumors, especially for treating breast and esophageal carcinomas . However, it has been noted that long‐term use of DOX tends to induce neurotoxicity and may cause neuropsychiatric diseases including depression and impaired cognition function .…”

Section: Introductionmentioning

confidence: 99%

Prophylactic effects of ellagic acid and rosmarinic acid on doxorubicin‐induced neurotoxicity in rats

Rizk

Masoud

Maher

2017

J Biochem & Molecular Tox

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Doxorubicin (DOX) is a chemotherapeutic agent widely used in human malignancies. Its long-term use cause neurobiological side effects. The aim of the present study was to investigate the prophylactic effect exerted by daily administration of ellagic acid (EA) and rosmarinic acid (RA) on DOX-induced neurotoxicity in rats. Our data showed that DOX-induced significant elevation of brain malondialdehyde, tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), caspase-3, and cholinesterase associated with significant reduction in reduced glutathione, monoamines namely serotonin, dopamine, as well as norepinephrine. Concomitant administration of EA (10 mg/kg/day, p.o. for 14 days) and/or RA (75 mg/kg/day, p.o. for 14 days) with DOX significantly mitigated the neural changes induced by DOX. Meanwhile, treatment ameliorated pro-inflammatory cytokines as TNF-α, iNOS, and attenuated oxidative stress biomarkers as well as brain monoamines. In conclusion, EA and RA can effectively protect against DOX-induced neurotoxicity, and the mechanisms underlying the neuroprotective effect are potentially associated with its antioxidant, anti-inflammatory, and antiapoptotic properties.

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Section: Introductionmentioning

confidence: 99%

Prophylactic effects of ellagic acid and rosmarinic acid on doxorubicin‐induced neurotoxicity in rats

Rizk

Masoud

Maher

2017

J Biochem & Molecular Tox

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“…8 Additionally, no toxicity has been reported for EPI and, in fact, it has been used as an attenuator for the effects of other toxic agents. 9 Interesting results have been found in studies involving the effects of dark chocolate, 10 flavonoid-rich foods or extracts, 11 and other purified flavanols 12 on postprandial metabolism. However, the possible use of EPI as a modulator of postprandial metabolism has not been explored…”

Section: Introductionmentioning

confidence: 99%

Acute effects of an oral supplement of (−)-epicatechin on postprandial fat and carbohydrate metabolism in normal and overweight subjects

et al. 2014

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Postprandial hyperglycemia, in particular when accompanied by excessive hypertriglyceridemia, is associated with increased cardiovascular risk, mainly in overweight or obese subjects, as it favors oxidative stress, systemic inflammation and endothelial dysfunction. Thus, treatments that favorably modulate metabolism by reducing steep increases in postprandial serum glucose and triglycerides, are of considerable interest. Evidence suggests that (−)-epicatechin (EPI) is responsible for reductions in cardiometabolic risk associated with chocolate consumption these effects may be associated with favorable effects of EPI on postprandial metabolism. The aims of this study were to assess the effects of EPI on postprandial metabolism in normal-weight and overweight/obese subjects. Twenty adult volunteers (normal and overweight) underwent oral metabolic tolerance tests in the absence and presence of oral EPI (1 mg/kg). Metabolic responses were examined using indirect calorimetry and determining blood glucose and triglycerides at 0, 2 and 4 hours after metabolic load ingestion. Results show that EPI increased postprandial lipid catabolism, as evidenced by a significant decrease in the respiratory quotient, which implies an increase in fat oxidation. The effect was associated with significantly lower postprandial plasma glucose and triglycerides concentrations. The effects were more prominent in overweight subjects. In conclusion, EPI modulates postprandial metabolism by enhancing lipid oxidation accompanied by reductions in glycemia and triglyceridemia.

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“…The ability of catechins to attenuate DOX toxicity was frequently described. In rat, individual catechins and/or green tea extract exhibited protective effects against DOX-induced cardiovascular abnormalities (16), cardiomyocyte injury (17, 18), brain toxicity (19), and spermatogenic disorders (20). Moreover, catechins are able to inhibit carbonyl reductase 1, the main DOX deactivation enzyme (21), and in this way they enhanced DOX efficacy in tumor-bearing mice (22).…”

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confidence: 99%

Effect of selected catechins on doxorubicin antiproliferative efficacy and hepatotoxicity in vitro

et al. 2014

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Catechins may influence both desirable and undesirable effects of many drugs. In this study, the in vitro effect of (+)-catechin, (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate, and (-)-epigallocatechin gallate (EGCG) on the efficacy of anticancer drug doxorubicin (DOX) was studied in HCT-8 cancer cells. Rat hepatocytes were used to study the influence of EGCG on DOX hepatotoxicity. Cell proliferation and viability were studied by 3-[4,5-dimethylthiazol- 2-yl]-2,5-diphenyl tetrazolium bromide and neutral red uptake test assays. Formation of reactive oxygen species (ROS) was determined using the dichlorofluorescein assay. All of the studied catechins (1-25 μmol L-1) had no effect on the proliferation of intestinal cancer cells and did not affect the antiproliferative effect of DOX (1-8 μmol L-1) in these cells. Moreover, EGCG at 25 μmol L-1 increased the viability of isolated hepatocytes and significantly protected these cells against DOX-induced toxicity and ROS production. Consumption of EGCG during DOX therapy seems to be safe and beneficial, since EGCG does not decrease DOX anticancer efficacy and could ameliorate DOX hepatotoxicity

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Epicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB

Cited by 82 publications

References 39 publications

Prophylactic effects of ellagic acid and rosmarinic acid on doxorubicin‐induced neurotoxicity in rats

Prophylactic effects of ellagic acid and rosmarinic acid on doxorubicin‐induced neurotoxicity in rats

Acute effects of an oral supplement of (−)-epicatechin on postprandial fat and carbohydrate metabolism in normal and overweight subjects

Effect of selected catechins on doxorubicin antiproliferative efficacy and hepatotoxicity in vitro

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