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This study aimed to provide an updated critical review of the nutritional, therapeutic, biotechnological, and environmental aspects involved in the exploitation of Chenopodium quinoa Willd and its biowastes. Special attention was devoted to investigations of the therapeutic and nutritional properties of different parts and varieties of quinoa as well as of the use of the biowaste resulting from the processing of grain. Studies published from 2018 onward were prioritized. Extracts and fractions obtained from several Chenopodium quinoa matrices showed antioxidant, antidiabetic, immunoregulatory, neuroprotective, and antimicrobial effects in in vitro and in vivo models and some clinical studies. The activities were attributed to the presence of phytochemicals such as polyphenols, saponins, peptides, polysaccharides, and dietary fibers. Quinoa wastes are abundant and low-cost sources of bioactive molecules for the development of new drugs, natural antioxidants, preservatives, dyes, emulsifiers, and carriers for food and cosmetics applications. Among the demands to be fulfilled in the coming years are the following: (1) isolation of new bioactive phytochemicals from quinoa varieties that are still underexploited; (2) optimization of green approaches to the sustainable recovery of compounds of industrial interest from quinoa by-products; and (3) well-conducted clinical trials to attest safety and efficacy of extracts and compounds.
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Chenopodium quinoa , Chenopodium quinoa/química , Antioxidantes/farmacología , Antioxidantes/química , Polifenoles , Fibras de la Dieta/análisis , PolisacáridosRESUMEN
The beneficial effects of high-fat low-carbohydrate (HFLC) diets on glucose metabolism have been questioned and their effects on liver metabolism are not totally clear. The aim of this work was to investigate the effects of an HFLC diet under different energy conditions on glucose homeostasis, fatty liver development, and hepatic gluconeogenesis using the isolated perfused rat liver. HFLC diet (79% fat, 19% protein, and 2% carbohydrates in Kcal%) was administered to rats for 4 weeks under three conditions: ad libitum (hypercaloric), isocaloric, and hypocaloric (energy reduction of 20%). Fasting blood glucose levels and total fat in the liver were higher in all HFLC diet rats. Oral glucose tolerance was impaired in isocaloric and hypercaloric groups, although insulin sensitivity was not altered. HFLC diet also caused marked liver metabolic alterations: higher gluconeogenesis rate from lactate and a reduced capacity to metabolize alanine, the latter effect being more intense in the hypocaloric condition. Thus, even when HFLC diets are used for weight loss, our data imply that they can potentially cause harmful consequences for the liver.
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Grasas de la Dieta , Hígado Graso , Ratas , Animales , Gluconeogénesis , Carbohidratos de la Dieta/efectos adversos , Dieta Baja en Carbohidratos , Hígado/metabolismo , Dieta Alta en Grasa/efectos adversos , Hígado Graso/metabolismo , Glucemia/metabolismo , Homeostasis , Glucosa/metabolismoRESUMEN
The aim of this work was to compare the anti-inflammatory and antioxidant effects of three natural coumarins: 1,2-benzopyrone, umbelliferone and esculetin. The antioxidant capacity of coumarins was evaluated using both chemical and biological in vitro assays. Chemical assays included DPPH and ABTSâ+ radical scavenging as well as ferric ion reducing ability power (FRAP) assay. Inhibition of mitochondrial ROS generation and lipid peroxidation in brain homogenates were used as biological in vitro assays. The experimental method of carrageenan-induced pleurisy in rats was used for the in vivo investigation of the anti-inflammatory activity. In silico molecular docking analysis was undertaken to predict the affinity of COX-2 to the coumarins. Considering the antioxidant capacity, esculetin was the most efficient one as revealed by all employed assays. Particularly, the mitochondrial ROS generation was totally abolished by the compound at low concentrations (IC50 = 0.57 µM). As for the anti-inflammatory effects, the COX-2 enzyme presented good affinities to the three coumarins, as revealed by the molecular docking analyses. However, considering the in vivo anti-inflammatory effects, 1,2-benzopyrone was the most efficient one in counteracting pleural inflammation and it potentiated the anti-inflammatory actions of dexamethasone. Umbelliferone and esculetin treatments failed to reduce the volume of pleural exudate. Overall, therefore, our results support the notion that this class of plant secondary metabolites displays promising effects in the prevention and/or treatment of inflammation and other diseases associated with oxidative stress, although the singularities regarding the type of the inflammatory process and pharmacokinetics must be taken into account.
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Antioxidantes , Cumarinas , Ratas , Animales , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Cumarinas/farmacología , Cumarinas/uso terapéutico , Especies Reactivas de Oxígeno , Ciclooxigenasa 2/metabolismo , Simulación del Acoplamiento Molecular , Umbeliferonas/farmacología , Umbeliferonas/uso terapéutico , Inflamación/inducido químicamente , Inflamación/tratamiento farmacológico , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéutico , Extractos Vegetales/farmacologíaRESUMEN
Conventional treatments for liver diseases are often burdened by side effects caused by chemicals. For minimizing this problem, the search for medicines based on natural products has increased. The objective of this review was to collect data on the potential hepatoprotective activity of plants of the Brazilian native flora. Special attention was given to the modes of extraction, activity indicators, and identification of the active compounds. The databases were Science direct, Pubmed, and Google Academic. Inclusion criteria were: (a) plants native to Brazil; (b) studies carried out during the last 15 years; (c) high-quality research. A fair number of communications met these criteria. Various parts of plants can be used, e.g., fruit peels, seeds, stem barks, and leaves. An outstanding characteristic of the active extracts is that they were mostly obtained from plant parts with low commercial potential, i.e., by-products or bio-residues. The hepatoprotective activities are exerted by constituents such as flavonoids, phenolic acids, vitamin C, phytosterols, and fructose poly- and oligosaccharides. Several Brazilian plants present excellent perspectives for the obtainment of hepatoprotective formulations. Very important is the economical perspective for the rural producers which may eventually increase their revenue by selling increasingly valued raw materials which otherwise would be wasted.
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Berberine is a plant alkaloid to which antihyperglycemic properties have been attributed. It is also known as an inhibitor of mitochondrial functions. In this work short-term translation of the latter effects on hepatic metabolism were investigated using the isolated perfused rat liver. Once-through perfusion with a buffered saline solution was done. At low portal concentrations berberine modified several metabolic pathways. It inhibited hepatic gluconeogenesis, increased glycolysis, inhibited ammonia detoxification, increased the cytosolic NADH/NAD+ ratio and diminished the ATP levels. Respiration of intact mitochondria was impaired as well as the mitochondrial pyruvate carboxylation activity. These results can be regarded as evidence that the direct inhibitory effects of berberine on gluconeogenesis, mediated by both energy metabolism and pyruvate carboxylation inhibition, represent most likely a significant contribution to its clinical efficacy as an antihyperglycemic agent. However, safety concerns also arise because all effects occur at similar concentrations and there is a narrow margin between the expected benefits and toxicity. Even mild inhibition of gluconeogenesis is accompanied by diminutions in oxygen uptake and ammonia detoxification and increases in the NADH/NAD+ ratio. All combined, desired and undesired effects could well in the end represent a deleterious combination of events leading to disruption of cellular homeostasis.
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Berberina , Amoníaco/metabolismo , Animales , Berberina/toxicidad , Gluconeogénesis , Hipoglucemiantes/farmacología , Hígado , Mitocondrias Hepáticas , NAD/metabolismo , Perfusión , Ácido Pirúvico/metabolismo , RatasRESUMEN
A practical approach to control glycemia in diabetes is to use plant natural products that delay hydrolysis of complex sugars and promote the diminution of the release of glucosyl units into the blood plasma. Polyphenolics have been described as being effective in inhibiting amylases and α-glucosidases. Grape pomace is an important sub product of the wine industry, still rich in many compounds such as polyphenolics. In this context, the purpose of this study was to search for possible effects of a grape pomace extract on salivary and pancreatic α-amylases and α-glucosidase, as well as on intestinal glucose absorption. The Merlot grape pomace extract (MGPE) was prepared using a hydroalcoholic mixture (40% ethanol + 60% water). In vitro inhibition was quantified using potato starch (for amylases) and maltose (for α-glucosidase) as substrates. In vivo inhibition was evaluated by running starch and maltose tolerance tests in rats with or without administration of MGPE. Ranking of the extract compounds for its affinity to the α-amylases was accomplished by computer simulations using three different programs. Both α-amylases, pancreatic and salivary, were inhibited by the MGPE. No inhibition on α-glucosidase, however, was detected. The IC50 values were 90 ± 10 µg/mL and 143 ± 15 µg/mL for salivary and pancreatic amylases, respectively. Kinetically this inhibition showed a complex pattern, with multiple binding of the extract constituents to the enzymes. Furthermore, the in silico docking simulations indicated that several phenolic substances, e.g., peonidin-3-O-acetylglucoside, quercetin-3-O-glucuronide and isorhamnetin-3-O-glucoside, besides catechin, were the most likely polyphenols responsible for the α-amylase inhibition caused by MGPE. The hyperglycemic burst, an usual phenomenon that follows starch administration, was substantially inhibited by the MGPE. Our results suggest that the MGPE can be adequate for maintaining normal blood levels after food ingestion.
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Diabetes Mellitus , Vitis , Animales , Simulación por Computador , Inhibidores de Glicósido Hidrolasas/farmacología , Extractos Vegetales/farmacología , Ratas , alfa-Amilasas , alfa-GlucosidasasRESUMEN
There are different varieties of mushrooms not yet studied spread all over the planet. The objective of this study was to evaluate biochemical properties and effects on mitochondrial respiration of eight Basidiomycete mushrooms: Flaviporus venustus EF30, Hydnopolyporus fimbriatus EF41 and EF44, Inonotus splitgerberi EF46, Oudemansiella canarii EF72, Perenniporia sp. EF79, Phellinus linteus EF81, and Pleurotus albidus EF84. Total phenols, ABTS, TEAC, FRAP, and ORAC were measured in order to determine the antioxidant capacity. Antimicrobial potential was studied by disc-diffusion and microdilution method. Cytotoxicity was determined in murine peritoneal macrophages. The bioenergetic aspects were evaluated by the uncoupling of the oxidative phosphorylation in mitochondrias. The H. fimbriatus mushroom was the one that presented the most significant results for the antioxidant assays. Three mushrooms presented antimicrobial activity, indicating a potential for formulation of drugs. The results suggest that I. spligerberi has an uncoupling activity, even at the lowest concentration tested, dissipating the mitochondrial electrochemical gradient. On the other hand, P. albidus has effect only on succinate-oxidase activity without influencing mitochondrial respiratory efficiency. Therefore, both interfere negatively in mitochondrial respiration. In relation with the cytotoxicity in peritoneal macrophages, O. canarii and F. venustus were cytotoxic in this type of cells.
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Basidiomycota/química , Mitocondrias/efectos de los fármacos , Fenoles/química , Animales , Antibacterianos/química , Antibacterianos/farmacología , Antioxidantes/química , Antioxidantes/metabolismo , Basidiomycota/metabolismo , Macrófagos Peritoneales/citología , Macrófagos Peritoneales/efectos de los fármacos , Macrófagos Peritoneales/metabolismo , Mitocondrias/metabolismo , Oxidación-Reducción , Fosforilación Oxidativa/efectos de los fármacos , Consumo de Oxígeno/efectos de los fármacos , Fenoles/aislamiento & purificación , Fenoles/farmacología , Staphylococcus aureus/efectos de los fármacos , Ácido Succínico/químicaRESUMEN
Carvacrol presents action in Salmonella Typhimurium biofilms, however the antibiofilm mechanism of this compound has not been fully established yet. In the present study, the aim was to evaluate protein profile changes in S. Typhimurium biofilm treated with carvacrol. Proteomic analysis of treated versus untreated biofilm showed several changes in proteins involved with S. Typhimurium biofilm and antioxidant activity. The proteins DsbA (thiol: disulfide interchange protein DsbA), LuxS (S-ribosylhomocysteine lyase), DksA (RNA polymerase binding transcription factor DksA), and SODs (superoxide dismutases) A, B and C had their synthesis decreased after treatment with carvacrol. These proteins play a key role in S. Typhimurium biofilm formation, demonstrating the dynamic antibiofilm action of carvacrol. The differentially expressed proteins identified provide possible action targets for future studies in order to gain more insight into the mechanism of action of carvacrol on S. Typhimurium biofilm.
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Proteómica , Salmonella typhimurium , Biopelículas , Cimenos/farmacología , Salmonella typhimurium/genéticaRESUMEN
ETHNOPHARMACOLOGICAL RELEVANCE: Trichilia catigua A. Juss (Meliaceae) preparations have been used in folk medicine to alleviate fatigue, stress, and improve memory. Antinociceptive, antiinflammatory, and in vitro neuroprotective effects have been observed in animals. Cerebral ischemia/reperfusion (I/R) leads to severe neuropsychological deficits that are largely associated with oxidative stress, inflammation and neurodegeneration. We reported previously that an ethyl-acetate fraction (EAF) of T. catigua reduced brain ischemia-induced learning and memory impairments in the absence of histological protection. AIM OF THE STUDY: Continuing those studies, here we aimed to investigate the antioxidant and antiinflammatory properties of T. catigua in an in vivo model of I/R. MATERIAL AND METHODS: Rats were subjected to 15â¯min of brain ischemia (4-VO model) followed by up to 15 days of reperfusion. Vehicle was given by gavage 30â¯min before ischemia and at 1â¯h of reperfusion. In a first experiment, brain ischemia-induced changes in oxidative stress markers, i.e., reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and protein carbonyl groups (PCGs) were measured on days 1, 3, and 5 post-ischemia. Similar time course analysis was done for neuroinflammation markers, i.e., microglia (OX42 immunorreactivity) and astrocytes (GFAP immunorreactivity), in the hippocampus. In a second experiment, the time points at which these markers of oxidative stress and neuroinflammation peaked were used to test the effects of T. catigua (400â¯mg/kg, p.o.). RESULTS: Oxidative stress markers peaked on day 1 post-ischemia. GSH decreased (-23.2%) while GSSG increased (+ 71.1%), which yielded a significant reduction in the GSH/GSSG ratio (-39.1%). The activity of CAT was largely reduced by ischemia (-54.6% to -65.1%), while the concentration of PCG almost doubled in the brain of ischemic rats (+99.10%) in comparison to sham. Treatment with the EAF of T. catigua normalized these changes in oxidative markers to the control levels (GSH: +27.5%; GSSG: -23.8%; GSH/GSSG: +44.6%; PCG: -80.3%). In the hippocampus, neuroinflammation markers peaked on day 5 post-ischemia, with microglial and astrocytic responses increasing to 54.8% and 37.1%, respectively. The elevation in glial cells response was completely prevented by EAF. CONCLUSION: These results demonstrate that T. catigua has both antioxidant and antiinflammatory activities after transient global cerebral ischemia in rats, which may contribute to the previously reported memory protective effect of T. catigua.
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Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Isquemia Encefálica/tratamiento farmacológico , Meliaceae , Fármacos Neuroprotectores/uso terapéutico , Extractos Vegetales/uso terapéutico , Daño por Reperfusión/tratamiento farmacológico , Acetatos/química , Animales , Antiinflamatorios/farmacología , Antioxidantes/farmacología , Isquemia Encefálica/metabolismo , Antígeno CD11b/metabolismo , Catalasa/metabolismo , Proteína Ácida Fibrilar de la Glía/metabolismo , Glutatión/metabolismo , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Masculino , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Fitoterapia , Extractos Vegetales/farmacología , Tallos de la Planta/química , Ratas Wistar , Daño por Reperfusión/metabolismo , Solventes/química , Superóxido Dismutasa/metabolismoRESUMEN
We originally reported that an ethyl-acetate fraction (EAF) of Trichilia catigua prevented the impairment of water maze learning and hippocampal neurodegeneration after transient global cerebral (TGCI) in mice. We extended that previous study by evaluating whether T. catigua (i) prevents the loss of long-term retrograde memory assessed in the aversive radial maze (AvRM), (ii) confers hippocampal and cortical neuroprotection, and (iii) mitigates oxidative stress and neuroinflammation in rats that are subjected to the four vessel occlusion (4-VO) model of TGCI. In the first experiment, naive rats were trained in the AvRM and then subjected to TGCI. The EAF was administered orally 30min before and 1h after TGCI, and administration continued once per day for 7days post-ischemia. In the second experiment, the EAF was administered 30min before and 1h after TGCI, and protein carbonylation and myeloperoxidase (MPO) activity were assayed 24h and 5days later, respectively. Retrograde memory performance was assessed 8, 15, and 21days post-ischemia. Ischemia caused persistent retrograde amnesia, and this effect was prevented by T. catigua. This memory protection (or preservation) persisted even after the treatment was discontinued, despite the absence of histological neuroprotection. Protein carbonyl group content and MPO activity increased around 43% and 100%, respectively, after TGCI, which were abolished by the EAF of T. catigua. The administration of EAF did not coincide with the days of memory testing. The data indicate that antioxidant and/or antiinflammatory actions in the early phase of ischemia/reperfusion contribute to the long-term antiamnesic effect of T. catigua.
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Amnesia Retrógrada/tratamiento farmacológico , Amnesia Retrógrada/etiología , Isquemia Encefálica/complicaciones , Inflamación/tratamiento farmacológico , Inflamación/etiología , Meliaceae/química , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/uso terapéutico , Animales , Biomarcadores/metabolismo , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/metabolismo , Modelos Animales de Enfermedad , Hipocampo/metabolismo , Aprendizaje por Laberinto/efectos de los fármacos , Extractos Vegetales/química , RatasRESUMEN
p-Synephrine is one of the main active components of the fruit of Citrus aurantium (bitter orange). Extracts of the bitter orange and other preparations containing p-synephrine have been used worldwide to promote weight loss and for sports performance. The purpose of the study was to measure the action of p-synephrine on hepatic enzyme activities linked to carbohydrate and energy metabolism and the levels of adenine mononucleotides. Enzymes and adenine mononucleotides were measured in the isolated perfused rat liver and in vivo after oral administration of the drug (50 and 300 mg/kg) by using standard techniques. p-Synephrine increased the activity of glycogen phosphorylase in vivo and in the perfused liver. It decreased, however, the activities of pyruvate kinase and pyruvate dehydrogenase also in vivo and in the perfused liver. p-Synephrine increased the hepatic pools of adenosine diphosphate and adenosine triphosphate. Stimulation of glycogen phosphorylase is consistent with the reported increased glycogenolysis in the perfused liver and increased glycemia in rats. The decrease in the pyruvate dehydrogenase activity indicates that p-synephrine is potentially capable of inhibiting the transformation of carbohydrates into lipids. The capability of increasing the adenosine triphosphate-adenosine diphosphate pool indicates a beneficial effect of p-synephrine on the cellular energetics.
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Adenosina Trifosfato/metabolismo , Metabolismo de los Hidratos de Carbono/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/enzimología , Sinefrina/farmacología , Administración Oral , Animales , Citrus/química , Glucógeno Fosforilasa/metabolismo , Hígado/irrigación sanguínea , Hígado/cirugía , Masculino , Complejo Piruvato Deshidrogenasa/antagonistas & inhibidores , Complejo Piruvato Deshidrogenasa/metabolismo , Piruvato Quinasa/antagonistas & inhibidores , Piruvato Quinasa/metabolismo , Ratas , Ratas Wistar , Sinefrina/administración & dosificación , Sinefrina/químicaRESUMEN
Dinoseb is a highly toxic pesticide of the dinitrophenol group. Its use has been restricted, but it can still be found in soils and waters in addition to being a component of related pesticides that, after ingestion by humans or animals, can originate the compound by enzymatic hydrolysis. As most dinitrophenols, dinoseb uncouples oxidative phosphorylation. In this study, distribution, lipid bilayer affinity and kinetics of the metabolic effects of dinoseb were investigated, using mainly the isolated perfused rat liver, but also isolated mitochondria and molecular dynamics simulations. Dinoseb presented high affinity for the hydrophobic region of the lipid bilayers, with a partition coefficient of 3.75×104 between the hydrophobic and hydrophilic phases. Due to this high affinity for the cellular membranes dinoseb underwent flow-limited distribution in the liver. Transformation was slow but uptake into the liver space was very pronounced. For an extracellular concentration of 10µM, the equilibrium intracellular concentration was equal to 438.7µM. In general dinoseb stimulated catabolism and inhibited anabolism. Half-maximal stimulation of oxygen uptake in the whole liver occurred at concentrations (2.8-5.8µM) at least ten times above those in isolated mitochondria (0.28µM). Gluconeogenesis and ureagenesis were half-maximally inhibited at concentrations between 3.04 and 5.97µM. The ATP levels were diminished, but differently in livers from fed and fasted rats. Dinoseb disrupts metabolism in a complex way at concentrations well above its uncoupling action in isolated mitochondria, but still at concentrations that are low enough to be dangerous to animals and humans even at sub-lethal doses.
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2,4-Dinitrofenol/análogos & derivados , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Metabolismo Energético/efectos de los fármacos , Hígado/efectos de los fármacos , Plaguicidas/toxicidad , 2,4-Dinitrofenol/química , 2,4-Dinitrofenol/toxicidad , Adenosina Trifosfato/metabolismo , Animales , Transporte Biológico , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Fructosa/metabolismo , Gluconeogénesis/efectos de los fármacos , Glucógeno/metabolismo , Interacciones Hidrofóbicas e Hidrofílicas , Técnicas In Vitro , Cinética , Ácido Láctico/metabolismo , Membrana Dobles de Lípidos , Hígado/metabolismo , Hígado/patología , Masculino , Lípidos de la Membrana/química , Lípidos de la Membrana/metabolismo , Mitocondrias Hepáticas/efectos de los fármacos , Mitocondrias Hepáticas/metabolismo , Modelos Biológicos , Simulación de Dinámica Molecular , Fosforilación Oxidativa/efectos de los fármacos , Plaguicidas/química , Ratas Wistar , Medición de Riesgo , Urea/metabolismoRESUMEN
The aim of the present study was to compare the in vitro inhibitory effects on the salivary and pancreatic α-amylases and the in vivo hypoglycemic actions of the hydrolysable tannin from Chinese natural gall and the condensed tannin from Acacia mearnsii. The human salivary α-amylase was more strongly inhibited by the hydrolysable than by the condensed tannin, with the concentrations for 50% inhibition (IC50) being 47.0 and 285.4 µM, respectively. The inhibitory capacities of both tannins on the pancreatic α-amylase were also different, with IC50 values being 141.1 µM for the hydrolysable tannin and 248.1 µM for the condensed tannin. The kinetics of the inhibition presented complex patterns in that for both inhibitors more than one molecule can bind simultaneously to either the free enzyme of the substrate-complexed enzyme (parabolic mixed inhibition). Both tannins were able to inhibit the intestinal starch absorption. Inhibition by the hydrolysable tannin was concentration-dependent, with 53% inhibition at the dose of 58.8 µmol/kg and 88% inhibition at the dose of 294 µmol/kg. For the condensed tannin, inhibition was not substantially different for doses between 124.4 µmol/kg (49%) and 620 µmol/kg (57%). It can be concluded that both tannins, but especially the hydrolysable one, could be useful in controlling the postprandial glycemic levels in diabetes.
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The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of adjuvant-induced arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The adjuvant-induced arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the adjuvant-induced arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by arthritis than that reported for the former tissues. Even so, the modifications caused by arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the arthritis disease.
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Artritis Experimental/metabolismo , Miocardio/metabolismo , Estrés Oxidativo , Especies Reactivas de Oxígeno/metabolismo , Animales , Citosol/metabolismo , Complejo IV de Transporte de Electrones/metabolismo , Glutamato Deshidrogenasa/metabolismo , Glutatión/metabolismo , Humanos , Isocitrato Deshidrogenasa/metabolismo , Peroxidación de Lípido , Masculino , Mitocondrias Cardíacas/metabolismo , Oxidación-Reducción , Carbonilación Proteica , Ratas , Succinato Deshidrogenasa/metabolismoRESUMEN
Pleurotus pulmonarius was cultivated on a corncob-based substrate for producing of mushrooms and for assessing the transformation of the lignocellulosics during the development of fungal biomass. Associated events, such as the release of relevant enzymes and the H2O2 generation, were also monitored. The peaks of laccase and catalase activities occurred at the 5th day and that of Mn peroxidase at the 30th day, simultaneously with a high activity of superoxide dismutase. Increase in the endocellulase and xylanase activities was observed after 10 days, with maximal activities achieved during the 20-30-day period. Maximal values of H2O2 were found after 10 days of cultivation. Electron microscopy and Fourier transform infrared (FTIR) spectroscopy showed strong alterations in the lignocellulosic fibers. The uncultivated and the cultivated substrates at different times were hydrolyzed with commercial cellulase and ß-glucosidase. The highest values of reducing sugars (110.5 ± 5.6 µmol/mL), being 65 % glucose, were obtained using the 20-day cultivated substrate. After the fruiting stage (first flush), enzymatic hydrolysis of the spent mushroom substrate (SMS) yielded 53.0 ± 2.8 and 77.5 ± 4.0 µmol/mL of glucose and total reducing sugars, respectively. Although the release of reducing sugars of the P. pulmonarius SMS was lower than that obtained after 20 days of cultivation, it was still 50 % higher than that obtained using the uncultured substrate. This observation, combined with the fact that SMS constitutes a residue generated as a by-product of the depletion of an agro-industrial residue, allows to conclude that this material offers an interesting economic perspective for the obtainment of cellulosic ethanol.
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Lignina/análisis , Pleurotus/crecimiento & desarrollo , Pleurotus/metabolismo , Zea mays/química , Zea mays/microbiología , Enzimas/análisis , Peróxido de Hidrógeno/análisis , Microscopía Electrónica , Espectroscopía Infrarroja por Transformada de Fourier , Zea mays/ultraestructuraRESUMEN
The purpose of the study was to evaluate the possible effects of the administration of a green tea extract on the oxidative state of the liver and brain of adjuvant-induced arthritic rats, a model for human rheumatoid arthritis. Daily doses of 250 mg kg(-1) (59.8 mg catechins per kg) for 23 days were administered. This treatment produced significant diminutions in protein and lipid damage in liver, brain and plasma. It also diminished the tissue ROS contents and increased the antioxidant capacity of the plasma. The antioxidant defenses, which are diminished by arthritis, were improved by the green tea treatment, as revealed by the restoration of the GSH and protein thiol levels and by the strong tendency for normalizing the activities of the antioxidant enzymes. The activity of glucose 6-phosphate dehydrogenase, which is increased by arthritis in the liver, was also almost normalized by the treatment. In conclusion, it can be said that green tea consumption is possibly beneficial for the liver and brain of patients suffering from rheumatoid arthritis because it attenuates the pronounced oxidative stress that accompanies the disease and, thus, diminishes the injury to lipids and proteins in both liver and brain. There are also indications that, in the liver, the green tea can contribute to normalize the metabolic functions that are substantially modified by arthritis. For example, the green tea normalized the activity of glucose 6-phosphate dehydrogenase, a key enzyme of an important metabolic route (pentose monophosphate pathway). It is expected that the green tea treatment is equally able to normalize the activity of other enzymes (e.g., glucokinase and glucose 6-phosphatase), a hypothesis to be tested by future work.
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Artritis Experimental/tratamiento farmacológico , Encéfalo/efectos de los fármacos , Camellia sinensis/química , Hígado/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/administración & dosificación , Animales , Artritis Experimental/metabolismo , Encéfalo/metabolismo , Humanos , Hígado/metabolismo , Masculino , Ratas , Ratas Sprague-Dawley , Té/químicaRESUMEN
BACKGROUND: Intestinal ischemia/reperfusion injury can be caused by surgical procedures and inflammatory bowel disease. It is normally associated with the increased production of free radicals and changes in the enteric nervous system. AIMS: Given the antioxidant and neuroprotective properties of resveratrol, the present study assessed its influence on oxidative stress in the intestinal wall and the morphology of myenteric neurons in the ileum of rats subjected to ischemia/reperfusion. METHODS: Resveratrol was orally administered daily at a dose of 10 mg/kg for 5 days. Changes in the ileum response to ischemia after 45 min were investigated followed by 3 h reperfusion. Lipoperoxide and carbonylated protein levels, and the activity of the antioxidant enzymes glutathione reductase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase were measured following ischemia/reperfusion injury. RESULTS: The density and morphometry of the general neuronal population, nitrergic neurons and glial cells, and morphometry of VIP varicosities in the ileum were also studied. Lipoperoxide and carbonylated protein levels were 171 and 40% higher during the ischemia/reperfusion, respectively, compared to control cohorts, and resveratrol attenuated these values. The glutathione ratio was 64% lower during ischemia/reperfusion, compared to control cohorts. Resveratrol increased the reduced/oxidized glutathione ratio, attenuated the changes in the activity of the antioxidant enzymes and the detrimental morphologic changes caused by ischemia/reperfusion in the general neuronal population and nitrergic neurons. CONCLUSIONS: Oral treatment with resveratrol reduced the oxidative stress in the ileum and attenuated the morphologic changes that occurred in the myenteric plexus of the ileum in rats subjected to ischemia/reperfusion.
Asunto(s)
Antioxidantes/farmacología , Enfermedades del Íleon/tratamiento farmacológico , Íleon/efectos de los fármacos , Plexo Mientérico/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Daño por Reperfusión/tratamiento farmacológico , Estilbenos/farmacología , Administración Oral , Animales , Antioxidantes/administración & dosificación , Modelos Animales de Enfermedad , Glucosafosfato Deshidrogenasa/metabolismo , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Glutatión Reductasa/metabolismo , Enfermedades del Íleon/metabolismo , Enfermedades del Íleon/patología , Íleon/inervación , Íleon/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Plexo Mientérico/metabolismo , Plexo Mientérico/patología , Fármacos Neuroprotectores/administración & dosificación , Neuronas Nitrérgicas/efectos de los fármacos , Neuronas Nitrérgicas/metabolismo , Neuronas Nitrérgicas/patología , Carbonilación Proteica/efectos de los fármacos , Ratas Wistar , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Resveratrol , Estilbenos/administración & dosificaciónRESUMEN
The purpose of the present study was to evaluate the oxidative status of the brain of arthritic rats, based mainly on the observation that arthritis induces a pronounced oxidative stress in the liver of arthritis rats and that morphological alterations have been reported to occur in patients with rheumatoid arthritis. Rats with adjuvant-induced arthritis were used. These animals presented higher levels of reactive oxygen species (ROS) in the total brain homogenate (25% higher) and in the mitochondria (+55%) when compared to healthy rats. The nitrite plus nitrate contents, nitric oxide (NO) markers, were also increased in both mitochondria (+27%) and cytosol (+14%). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (+43%), mitochondria (+69%) and cytosol (+145%). Arthritis caused a diminution of oxygen consumption in isolated brain mitochondria only when ascorbate was the electron donor. The disease diminished the mitochondrial cytochrome c oxidase activity by 55%, but increased the transmembrane potential by 16%. The pro-oxidant enzyme xanthine oxidase was 150%, 110% and 283% higher, respectively, in the brain homogenate, mitochondria and cytosol of arthritic animals. The same occurred with the calcium-independent NO-synthase activity that was higher in the brain homogenate (90%) and cytosol (122%) of arthritic rats. The catalase activity, on the other hand, was diminished by arthritis in all cellular fractions (between 30 and 40%). It is apparent that the brain of rats with adjuvant-induced arthritis presents a pronounced oxidative stress and a significant injury to lipids and proteins, a situation that possibly contributes to the brain symptoms of the arthritis disease.
Asunto(s)
Artritis Experimental/metabolismo , Encéfalo/metabolismo , Estrés Oxidativo , Animales , Metabolismo de los Lípidos , Masculino , Mitocondrias/metabolismo , Óxido Nítrico Sintasa/metabolismo , Ratas , Especies Reactivas de Oxígeno/metabolismo , Xantina Oxidasa/metabolismoRESUMEN
Citrus aurantium extracts, which contain large amounts of p-synephrine, are widely used for weight loss purposes and as appetite suppressants. In the liver, C. aurantium (bitter orange) extracts affect hemodynamics, carbohydrate metabolism, and oxygen uptake. The purpose of the present work was to quantify the action of p-synephrine and also to obtain indications about its mechanism of action, a task that would be difficult to accomplish with C. aurantium extracts due to their rather complex composition. The experimental system was the isolated perfused rat liver. p-Synephrine significantly stimulated glycogenolysis, glycolysis, gluconeogenesis, and oxygen uptake. The compound also increased the portal perfusion pressure and the redox state of the cytosolic NAD(+)/NADH couple. A Ca(2+)-dependency for both the hemodynamic and the metabolic effects of p-synephrine was found. p-Synephrine stimulated both cAMP overflow and the initial Ca(2+) release from the cellular stores previously labeled with (45)Ca(2+). The metabolic and hemodynamic actions of p-synephrine were strongly inhibited by α-adrenergic antagonists and moderately affected by ß-adrenergic antagonists. The results allow to conclude that p-synephrine presents important metabolic and hemodynamic effects in the liver. These effects can be considered as both catabolic (glycogenolysis) and anabolic (gluconeogenesis), they are mediated by both α- and ß-adrenergic signaling, require the simultaneous participation of both Ca(2+) and cAMP, and could be contributing to the overall stimulation of metabolism that usually occurs during weight loss periods.
Asunto(s)
Metabolismo de los Hidratos de Carbono/efectos de los fármacos , Hígado/metabolismo , Consumo de Oxígeno/efectos de los fármacos , Sinefrina/farmacología , Antagonistas de Receptores Adrenérgicos alfa 1/farmacología , Antagonistas de Receptores Adrenérgicos alfa 2/farmacología , Antagonistas de Receptores Adrenérgicos beta 3/farmacología , Animales , Calcio/metabolismo , Citrus/metabolismo , AMP Cíclico/biosíntesis , Gluconeogénesis/efectos de los fármacos , Glucogenólisis/efectos de los fármacos , Glucólisis/efectos de los fármacos , Masculino , Oxidación-Reducción/efectos de los fármacos , Extractos Vegetales/farmacología , Prazosina/farmacología , Propanolaminas/farmacología , Propranolol/farmacología , Ácido Pirúvico/metabolismo , Ratas , Ratas Wistar , Transducción de Señal , Yohimbina/farmacologíaRESUMEN
The particular characteristics of growth and development of mushrooms in nature result in the accumulation of a variety of secondary metabolites such as phenolic compounds, terpenes and steroids and essential cell wall components such as polysaccharides, b-glucans and proteins, several of them with biological activities. The present article outlines and discusses the available information about the protective effects of mushroom extracts against liver damage induced by exogenous compounds. Among mushrooms, Ganoderma lucidum is indubitably the most widely studied species. In this review, however, emphasis was given to studies using other mushrooms, especially those presenting efforts of attributing hepatoprotective activities to specific chemical components usually present in the mushroom extracts.