heart-health

Antioxidant synergism of green tea polyphenols with α-tocopherol and l-ascorbic acid in SDS micelles

Author: Fang Dai and Wei-Feng Chen and Bo Zhou

The synergistic antioxidant effect of polyphenols extracted from green tea, i.e. (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECG), (−)-epigallocatechin gallate (EGCG) and gallic acid (GA), with α-tocopherol (vitamin E) and l-ascorbic acid (vitamin C) against the peroxidation of linoleic acid has been studied in sodium dodecyl sulfate (SDS) micelles. The peroxidation was initiated thermally by a water-soluble azo initiator 2,2′-azobis(2-amidinopropane) hydrochloride (AAPH), and the reaction kinetics were studied by monitoring the formation of linoleic acid hydroperoxides and consumption of the antioxidants. It was found that the mixture of the green tea polyphenol, vitamin E and vitamin C could act synergistically to protect lipid peroxidation. Kinetic and mechanistic studies on the antioxidation process revealed that this antioxidant synergism was due to the regeneration of vitamin E by the green tea polyphenol and the regeneration of the latter by vitamin C.

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Author: Tae Il Kim and Yong Kyung Lee and Sang Gi Park and Im Seop Choi and Jung Ok Ban and Hyoung Kook Park and Sang-Yoon Nam and Young Won Yun and Sang Bae Han and Ki Wan Oh and Jin Tae Hong

Amyloid β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer disease (AD). In this study, we investigated the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Aβ1-42-induced neuronal cell death and memory impairment. Oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Aβ1-42 (2 μg/mouse, icv), significantly attenuated Aβ1-42-induced memory impairment. Furthermore, l-theanine reduced Aβ1-42 levels and the accompanying Aβ1-42-induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l-theanine inhibited Aβ1-42-induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor κB (NF-κB). l-Theanine also significantly reduced oxidative protein and lipid damage and the elevation of glutathione levels in the brain. These data suggest that the positive effects of l-theanine on memory may be mediated by suppression of ERK/p38 and NF-κB as well as the reduction of macromolecular oxidative damage. Thus, l-theanine may be useful in the prevention and treatment of AD.

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Author: Dongsun Park and Jeong Hee Jeon and Sunhee Shin and Seong Soo Joo and Dae-Hyuck Kang and Seol-Hee Moon and Min-Jung Jang and Yeoung Mi Cho and Jae Wook Kim and Hyeong-Jin Ji and Byeongwoo Ahn and Ki-Wan Oh and Yun-Bae Kim

The effects of green tea extract (GTE) on the fetal development and external, visceral and skeletal abnormalities induced by cyclophosphamide were investigated in rats. Pregnant rats were daily administered GTE (100 mg/kg) by gavage for 7 d, from the 6th to 12th day of gestation, and intraperitoneally administered with cyclophosphamide (11 mg/kg) 1 h after the final treatment. On the 20th day of gestation, maternal and fetal abnormalities were determined by Cesarian section. Cyclophosphamide was found to reduce fetal and placental weights without increasing resorption or death. In addition, it induced malformations in live fetuses; 94.6%, 41.5% and 100% of the external (skull and limb defects), visceral (cleft palate and ureteric dilatation) and skeletal (acrania, vertebral/costal malformations and delayed ossification) abnormalities. When pre-treated with GTE, cyclophosphamide-induced body weight loss and abnormalities of fetuses were remarkably aggravated. Moreover, repeated treatment with GTE greatly increased mRNA expression and activity of hepatic cytochrome P-450 (CYP) 2B, which metabolizes cyclophosphamide into teratogenic acrolein and cytotoxic phosphoramide mustard, while reducing CYP3A expression (a detoxifying enzyme). The results suggest that repeated intake of GTE may aggravate cyclophosphamide-induced body weight loss and malformations of fetuses by modulating CYP2B and CYP3A.

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Author: Sara A. Khan and Shubha Priyamvada and Neelam Farooq and Sheeba Khan and Md Wasim Khan and Ahad N.K. Yusufi

Gentamicin (GM) is an effective aminoglycoside antibiotic against severe infections but nephrotoxicity and oxidative damage limits its long term clinical use. Various strategies were attempted to ameliorate GM nephropathy but were not found suitable for clinical practice. Green tea (GT) polyphenols have shown strong chemopreventive and chemotherapeutic effects against various pathologies. We hypothesized that GT prevents GM nephrotoxicity by virtue of its antioxidative properties. A nephrotoxic dose of GM was co-administered to control and GT-fed male Wistar rats. Serum parameters and enzymes of oxidative stress, brush border membrane (BBM), and carbohydrate metabolism were analyzed. GM increased serum creatinine, cholesterol, blood urea nitrogen (BUN), lipid peroxidation (LPO) and suppressed superoxide dismutase (SOD) and catalase activities in renal tissues. Activity of hexokinase, lactate dehydrogenase increased whereas malate dehydrogenase decreased. Gluconeogenic enzymes and glucose-6-phosphate dehydrogenase were differentially altered in the cortex and medulla. However, GT given to GM rats reduced nephrotoxicity parameters, enhanced antioxidant defense and energy metabolism. The activity of BBM enzymes and transport of Pi declined by GM whereas GT enhanced BBM enzymes and Pi transport. In conclusion, green tea ameliorates GM elicited nephrotoxicity and oxidative damage by improving antioxidant defense, tissue integrity and energy metabolism.

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Author: Doriane Richard and Kaouthar Kefi and Ullah Barbe and Andrea Poli and Pedro Bausero and Francesco Visioli

We investigated whether regular decaffeinated green tea intake could modulate body weight in an experimental model of obesity. Male leptin-deficient (ob/ob) mice and their C57BL/6J lean littermates (4 weeks of age; n 20/genotype) were assigned randomly to receive either decaffeinated green tea or vehicle, for 6 weeks. Body weights were recorded weekly and fluid intake was measured at each replacement. Blood was collected from the heart into collection tubes, with Li+-heparin as the anticoagulant. Administration of decaffeinated green tea to ob/ob mice significantly slowed their rate of weight gain, as compared with animals that were fed buffer alone. This effect is apparent after only 1 week of supplementation. No significant difference was recorded between C57BL/6J lean mice administrated decaffeinated green tea and those given buffer alone. Decaffeinated green tea consumption by ob/ob mice was also associated with significantly lower cholesterolemia, triglyceridemia, and adiponectin concentration. Fecal lipids did not change significantly throughout the experiment. In conclusion, administration of decaffeinated green tea might contribute to weight control and provides an opportunity for through-the-day consumption, without the excitatory effects of caffeine.

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Author: Sara A. Khan and Shubha Priyamvada and Wasim Khan and Sheeba Khan and Neelam Farooq and Ahad N.K. Yusufi

Cisplatin (CP) an anticancer drug is known to induce nephrotoxicity, which limits its long-term clinical use. Green tea (GT), consumed since ancient times is known for its numerous health benefits. It has been shown to improve kidney functions in animal models of acute renal failure. The present study was undertaken to see whether GT can prevent CP-induced nephrotoxic and other deleterious effects. A nephrotoxic dose of CP was co-administered to control and GT-fed male Wistar rats every fifth day for 25 days. The effect of GT was determined on CP-induced alterations in various serum parameters and on enzymes of carbohydrate metabolism, brush border membrane, and antioxidant defense system in renal cortex and medulla. CP nephrotoxicity was recorded by increased serum creatinine and blood urea nitrogen. CP increased the activities of lactate dehydrogenase and acid phosphatase whereas, the activities of malate dehydrogenase, glucose-6-phosphatase, superoxide dismutase, catalase, and 32Pi transport significantly decreased. GT consumption increased the activities of the enzymes of carbohydrate metabolism, brush border membrane, oxidative stress, and 32Pi transport. GT ameliorated CP-induced nephrotoxic and other deleterious effects due to its intrinsic biochemical/antioxidant properties.

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Author: Yuri Clement

Objective Habitual green tea consumption has long been associated with health benefits including chemoprevention and cardiovascular protection. This non-systematic literature review presents the clinical evidence to date. Method A literature review of peer-reviewed articles on observational and interventional studies was conducted to include green tea, its extract or its purified polyphenol (−)-epigallocatechin-3-gallate (EGCG). Electronic databases searched included PubMed (1966–2009) and the Cochrane Library (Issue 4, 2008). Results Observational studies are inconclusive on the benefits of habitual consumption of green tea in the prevention of most cancers. However, there are trends towards prevention in breast and prostate cancers. Interventional studies have demonstrated reduction in relapses following surgical resection in colorectal adenomas and increased survival rates in epithelial ovarian cancer. Observational studies indicate that green tea may provide protection against hypertension and reduce the risk for stroke, and interventional studies are providing biochemical and physiological evidence. Conclusion Although the overall clinical evidence is inconclusive, habitual green tea consumption may be providing some level of chemoprevention in prostate and breast cancer. Green tea may also attenuate the risk factors association with the development of atherosclerosis thus reducing the incidence of cardiovascular events and stoke.

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Author: Dong Wook Shin and Su Nam Kim and Sang Min Lee and Woojung Lee and Min Jeong Song and Sun Mi Park and Tae Ryong Lee and Joo-Hyun Baik and Han Kon Kim and Jeong-Ho Hong and Minsoo Noh

Green tea intake has been shown to confer various health benefits to patients suffering from metabolic disorders. Here, we studied the effect of several major green tea polyphenols on adipocyte differentiation in human bone marrow mesenchymal stem cells (hBM-MSCs) and compared it to the effect of representative antidiabetic drugs. (−)-Catechin was the most potent of the eight green tea polyphenols evaluated in promoting adipocyte differentiation in hBM-MSCs, and this effect was dose-dependent. (−)-Catechin increased the mRNA levels of various adipogenic markers, such as adiponectin, peroxisome proliferator-activated receptor gamma (PPARγ), FABP4, and LPL, as measured during adipocyte differentiation in hBM-MSCs. In addition, (−)-catechin upregulated the secretion of adiponectin in hBM-MSC culture. Using a reporter gene assay and a competitive ligand binding study, (−)-catechin also significantly activated PPARγ in a dose-dependent fashion; however, (+)-catechin, the enantiomer of (−)-catechin, was not effective as a PPARγ agonist, which seems to imply that the effect of (−)-catechin on PPARγ is stereospecific. In conclusion, our data suggest that (−)-catechin promotes adipocyte differentiation and increased sensitivity to insulin in part by direct activation of PPARγ, which could be at the basis of the observed pharmacological benefits of green tea intake in reducing the risk of type 2 diabetes.

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Author: T. Malik and D.J. Haleem

Haloperidol (HAL) a conventional antipsychotic is known to induce oxidative stress-related anxiety. Parkinsonism and Tardive Dyskinesia (TD) in patients treated with drug. Antioxidative agents may suppress the neuroleptic induced anxiety and TD. The constituents of green tea have found antioxidative. In a view of antioxidative properties of green tea, the present study was designed to monitor a possible suppression of anxiety and Tardive Vacuous Chewing Movement (tVCM) by green tea in rat model of TD and anxiety. Associated changes of Dopamine (DA) and Serotonin (5-hydroxytryptamine; 5-HT) metabolism were also monitored in the dorsal (dStr) and ventral striatum (vStr). Rats on HAL for 8 weeks exhibited tVCMs and anxiety. Green tea Extract (GTE) alone as a sole source of water did not produce tVCMs and anxiety but HAL induced significant anxiety and tVCMs were 100% (two fold) greater than water treated group. The metabolism of DA as indicated by Homovanellic acid (HVA) concentration increased in the dStr of HAL plus GTE treated animals. HAL plus GTE treated group exhibited smaller increase of HVA. The mteabolism of 5-HT as indicated by 5-hydroxyindoleacetic acid (5-HIAA) concentration also increased in the dStr of HAL but not GTE treated animals. Groups of co-treated with HAL and GTE exhibited a large increase 5 HIAA in the dStr. The results suggested that interaction of HAL with some constituents of GTE may exacerbated HAL induced  anxiety and TD by producing an imbalance of DA/5-HT control over anxiety and motor impairment.

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Author: Vadivel Senthil Kumaran and Karpagavinayagam Arulmathi and Periandavan Kalaiselvi

Objective The activities and capacities of antioxidant systems of tissue cells are declined during aging, leading to the gradual loss of pro-oxidant/antioxidant balance and accumulation of oxidative damage. Hence, the present study evaluated the role of green tea extract (GTE), rich in polyphenols, in combating age-associated macromolecular damage in rat cardiac tissue. Methods The antioxidant defense system, lipid peroxidation, protein oxidation, and redox status in heart tissue were studied using young and aged rats. Results Significant increases in lipid peroxidation, protein carbonyls, and marked decreases in glutathione redox status, protein thiols, and activities of enzymatic and non-enzymatic antioxidants were observed in aged rats compared with young rats. Supplementation of GTE (100 mg/kg of body weight per day) orally for 30 days ameliorated these changes significantly. Conclusion This study accredits GTE's antioxidant rejuvenating potency and its role in the amelioration of senescence-mediated redox imbalance in aged rat cardiac tissue.

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