RESUMEN

Obesity has become a major health issue worldwide and obese individuals possess higher levels of adipose tissue when compared with healthy individuals. Obesity is highly associated with the development of different chronic diseases, such as diabetes, cardiovascular diseases, hypertension, cancers, etc. Previous studies established that anthocyanin compounds play an important role in attenuating obesity-related consequences. Among various anthocyanin compounds, cyanidin-3-O-ß-glucoside (C3G) is the most important component and is widely distributed in various colored edible plant materials, especially berries, cherries, black rice, purple corn, etc. In recent decades, several studies have reported the therapeutical properties of C3G. C3G has various biological properties and health benefits, such as antioxidant, antimicrobial, anti-inflammatory, antidiabetic, anti-obesity, neuroprotective, anticancer, etc. In this review, we summarized the in vitro and in vivo studies in relation to the role of C3G in obesity-related complications. Several mechanistic studies demonstrated that C3G maintains the metabolism of glucose, fatty acids, and lipids by regulating different genes and signaling pathways. It could be concluded that the consumption of C3G protects healthy individuals from obesity-related issues by maintaining body weight and regulating their metabolism and energy balance. This review provides some important signaling pathways/targets of C3G to facilitate the prevention and treatment of obesity, leading to the development of important food supplements.

RESUMEN

Platelet chemokines play well-established roles in the atherosclerotic inflammation. Cyanidin-3-O-ß-glucoside (Cy-3-g) is one of the main bioactive compounds in anthocyanins, but its effects on chemokines during atherosclerosis have not been determined yet. In the present study, ApoE-/- mice were fed on the chow diet, high-fat diet (HFD), and HFD-supplemented Cy-3-g at 200, 400, and 800 mg/kg diet. After 16 weeks, Cy-3-g significantly alleviated the atherosclerotic lesion and inhibited platelet aggregation and activation. Moreover, Cy-3-g significantly reduced inflammatory chemokines CXCL4, CXCL7, CCL5, CXCL5, CXCL12, and CCL2 in plasma and downregulated CXCR4, CXCR7, and CCR5 on platelets and peripheral blood mononuclear cells. Besides, Cy-3-g decreased the mRNA of TNFα, IFNγ, ICAM-1, VCAM-1, CD68, MMP7, CCL5, CXCR4, and CCR5 in the aorta of mice. Therefore, it suggests that Cy-3-g plays important preventive roles in the process of atherosclerosis via attenuating chemokines and receptors in ApoE-/- mice.

Asunto(s)

Antocianinas , Aterosclerosis , Animales , Antocianinas/farmacología , Apolipoproteínas E/genética , Aterosclerosis/tratamiento farmacológico , Aterosclerosis/genética , Quimiocinas/genética , Glucósidos/farmacología , Inflamación , Leucocitos Mononucleares , Ratones , Ratones Endogámicos C57BL

RESUMEN

Atherosclerosis, a chronic multifactorial disease, is closely related to the development of cardiovascular diseases and is one of the predominant causes of death worldwide. Normal vascular endothelial cells play an important role in maintaining vascular homeostasis and inhibiting atherosclerosis by regulating vascular tension, preventing thrombosis and regulating inflammation. Currently, accumulating evidence has revealed that endothelial cell apoptosis is the first step of atherosclerosis. Excess apoptosis of endothelial cells induced by risk factors for atherosclerosis is a preliminary event in atherosclerosis development and might be a target for preventing and treating atherosclerosis. Interestingly, accumulating evidence shows that natural medicines have great potential to treat atherosclerosis by inhibiting endothelial cell apoptosis. Therefore, this paper reviewed current studies on the inhibitory effect of natural medicines on endothelial cell apoptosis and summarized the risk factors that may induce endothelial cell apoptosis, including oxidized low-density lipoprotein (ox-LDL), reactive oxygen species (ROS), angiotensin II (Ang II), tumor necrosis factor-α (TNF-α), homocysteine (Hcy) and lipopolysaccharide (LPS). We expect this review to highlight the importance of natural medicines, including extracts and monomers, in the treatment of atherosclerosis by inhibiting endothelial cell apoptosis and provide a foundation for the development of potential antiatherosclerotic drugs from natural medicines.

Asunto(s)

Apoptosis/efectos de los fármacos , Aterosclerosis/tratamiento farmacológico , Células Endoteliales/efectos de los fármacos , Extractos Vegetales/farmacología , Animales , Ensayos Clínicos como Asunto , Células Endoteliales/patología , Humanos , Lipoproteínas LDL/toxicidad , Extractos Vegetales/uso terapéutico , Especies Reactivas de Oxígeno/metabolismo , Factor de Necrosis Tumoral alfa/farmacología

RESUMEN

Alcoholic liver disease (ALD) is a major cause of liver disease worldwide. In patients with ALD, an increased level of hepatic inflammasome components was observed, together with an increased circulating pro-inflammatory cytokines. Cyanidin-3-O-ß-glucoside (Cy-3-G) is a bioactive compound belonging to the anthocyanin group, which widely exists in deep-colored fruits and vegetables. Consumption of Cy-3-G is associated with lower risks of non-alcoholic fatty liver disease (NAFLD), liver fibrosis, obesity, atherosclerosis, and inflammation. However, whether Cy-3-G has effects on inflammasome formation and activation thereby protects against alcohol-induced liver damage remain elusive. In this study, we identified that dietary provision of Cy-3-G remarkably attenuated liver damage caused by excess energy intake and alcohol consumption. Supplement with Cy-3-G mediated NAD+ homeostasis, which stimulated SirT1 activity, resulting in suppressed NF-κB acetylation. Interestingly, Cy-3-G treatment suppressed NF-κB acetylation when SirT1 action was blunted by selective antagonist, and subsequently suppressed NLRP3 inflammasome activation and proinflammatory cytokines release in hepatic cell lines. Our findings first demonstrate that Cy-3-G at a physiologically achievable dosage alleviates alcohol-induced hepatic inflammation via inactivation of NLRP3 inflammasome and deacetylation of NF-κB, suggesting a promising therapeutic approach to alleviate alcohol-induced liver damage.

Asunto(s)

Hígado Graso Alcohólico , Inflamasomas , Antocianinas/farmacología , Hígado Graso Alcohólico/tratamiento farmacológico , Humanos , FN-kappa B/genética , FN-kappa B/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Transducción de Señal , Sirtuina 1/genética

RESUMEN

Diabetic cataract is one of the most important causes of blindness worldwide. Cyanidin-3-O-glucoside (C3G) is found to exert beneficial effects on many diabetic complications. However, its effect on diabetic cataract is not well known. Herein, we investigated the effect of C3G on high glucose-induced lens epithelial cell (SRA01/04) apoptosis and cataract formation as well as the involved mechanisms. We found C3G (20 µM) could preserve cell viability in SRA01/04 cells exposed to high glucose (100 µM). Meanwhile, C3G inhibited SRA01/04 cell apoptosis and regulated the Bcl-2/Bax ratio. Additionally, C3G suppressed NF-κB activation and subsequent cyclooxygenases-2 (Cox-2) expression, which are associated with the protection against apoptosis. Moreover, C3G attenuated lens opacity and protein aggregation in lens culture exposed to high glucose. In conclusion, C3G protected against high glucose-induced SRA01/04 cell apoptosis and cataract formation, which indicated the potential protection of anthocyanins on diabetic cataract.

Asunto(s)

Antocianinas/administración & dosificación , Catarata/prevención & control , Ciclooxigenasa 2/metabolismo , Retinopatía Diabética/prevención & control , Glucosa/efectos adversos , FN-kappa B/metabolismo , Animales , Apoptosis/efectos de los fármacos , Catarata/metabolismo , Catarata/fisiopatología , Ciclooxigenasa 2/genética , Retinopatía Diabética/genética , Retinopatía Diabética/metabolismo , Retinopatía Diabética/fisiopatología , Células Epiteliales/citología , Células Epiteliales/efectos de los fármacos , Células Epiteliales/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Glucosa/metabolismo , Humanos , Cristalino/citología , Cristalino/efectos de los fármacos , Cristalino/metabolismo , FN-kappa B/genética , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Transducción de Señal/efectos de los fármacos

RESUMEN

Cyanidin-3-O-ß-glucoside (Cy-3-g), a typical and abundant monomer of anthocyanins, exhibits a variety of biological activities, such as anti-atherosclerosis, anti-obesity, and anticancer effects. However, to date little is known about its effects on asthma. This study aimed to investigate the efficacy of dietary Cy-3-g on allergic asthma in an animal model. BALB/c mice were sensitized and challenged with ovalbumin (OVA) to induce allergic asthma. The pathological changes of the lung tissues, type 2 helper (Th2)-associated cytokine production in bronchoalveolar lavage fluid (BALF), and the interleukin 4 receptor alpha (IL-4Rα)-signal transducer and activator of transcription 6 (STAT6) signaling pathway activities were assessed. We found that Cy-3-g significantly inhibited OVA-induced inflammatory cell infiltration and mucus hyper-production in lung tissues, reduced the production of interleukin 4 (IL-4), interleukin 5 (IL-5) and interleukin 13 (IL-13) in BALF. Furthermore, Cy-3-g effectively suppressed OVA-induced up-regulation of the IL-4Rα-STAT6 signaling pathway activity of the lung tissues. These results demonstrated that dietary Cy-3-g could attenuate allergic airway inflammation in a murine asthma model, and Cy-3-g might be used as an agent for asthma prevention and/or treatment in the future.

Asunto(s)

Antocianinas/uso terapéutico , Antiinflamatorios/uso terapéutico , Asma/tratamiento farmacológico , Glucósidos/uso terapéutico , Pulmón/inmunología , Hipersensibilidad Respiratoria/tratamiento farmacológico , Alérgenos/inmunología , Animales , Citocinas/metabolismo , Suplementos Dietéticos , Modelos Animales de Enfermedad , Femenino , Humanos , Pulmón/efectos de los fármacos , Ratones , Ratones Endogámicos BALB C , Ovalbúmina/inmunología , Receptores de Superficie Celular/metabolismo , Factor de Transcripción STAT6/metabolismo , Células Th2/inmunología

RESUMEN

This study investigated whether the anthocyanin cyanidin-3-O-ß-glucoside (Cy-3-g) could affect platelet apoptosis and proplatelet formation in vitro. Thrombin-stimulated or resting human platelets and Meg-01 megakaryocytes were incubated with Cy-3-g (0, 0.5, 5, or 50 µM). We found that the percentage of the platelet mitochondrial membrane potential treated with 5 and 50 µM Cy-3-g was significantly higher than control (15.50% ± 3.24% and 29.77% ± 4.06% versus 2.76% ± 1.33%, respectively; P < 0.05). Treatment with 5 and 50 µM Cy-3-g significantly increased phosphatidylserine exposure compared with control (40.56% ± 10.53% and 76.62% ± 8.28% versus 15.43% ± 3.93%, respectively; P < 0.05). Moreover, Cy-3-g significantly increased the expression of Bax, Bak, and cytochrome c while markedly decreasing Bcl-xL and Bcl-2 expression as well as stimulating caspase-3, caspase-9, caspase-8, Bid, and gelsolin cleavage in thrombin-activated platelets in a dose-dependent manner ( P < 0.05). However, no significant differences were observed in the apoptosis of resting platelets when treated with Cy-3-g ( P > 0.05). Furthermore, Cy-3-g significantly ( P < 0.05) enhanced cell viability (50 µM versus control, 1.34 ± 0.01 versus 0.35 ± 0.02), the number of colony-forming unit-megakaryocytes (50 µM versus control, 38 ± 3 versus 8 ± 3), CD41 expression (50 µM versus control, 96.80% ± 2.55% versus 25.57% ± 2.86%), DNA ploidy (16N) (50 µM versus control, 19.73% ± 2.34% versus 4.42% ± 1.96%), and proplatelet formation (50 µM versus control, 27.5% ± 3.77% versus 7.67% ± 2.25%) in Meg-01 cells. In conclusion, Cy-3-g promotes activated platelet apoptosis and enhances megakaryocyte proliferation, differentiation, and proplatelet formation in vitro.

Asunto(s)

Antocianinas/química , Plaquetas/metabolismo , Glucósidos/química , Megacariocitos/efectos de los fármacos , Activación Plaquetaria/efectos de los fármacos , Polifenoles/química , Adulto , Antocianinas/uso terapéutico , Apoptosis/efectos de los fármacos , Caspasa 3 , Caspasa 9 , Diferenciación Celular , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Glucósidos/uso terapéutico , Humanos , Potencial de la Membrana Mitocondrial , Polifenoles/uso terapéutico

RESUMEN

AIM: Cyanidin-3-O-ß-glucoside (Cy-3-G) the most abundant monomer of anthocyanins has multiple protective effects on many diseases. To date, whether Cy-3-G could regulate the function of brown adipose tissue (BAT) is still unclear and whether this regulation could influence the secretion of adipokines from BAT to prevent non-alcoholic fatty liver disease (NAFLD) indirectly remains to be explored. In this study we investigated the effect of Cy-3-G on BAT and the potential role of Cy-3-G to prevent fatty liver through regulating the secretion of BAT. METHODS: Male C57BL/6 J mice were fed with a high fat high cholesterol (HFC) diet with or without 200 mg/kg B.W Cy-3-G for 8 weeks. In in vitro experiments, the differentiated brown adipocytes (BAC) and C3H10T1/2 clone8 cells were treated with 0.2 mM palmitate with or without Cy-3-G for 72 or 96 h. Then the culture media of C3H10T1/2 clone8 cells were collected for measuring the adipokines secretion by immunoblot assay and were applied to culture HepG2 cells or LO2 cells for 24 h. Lipid accumulation in HepG2 cells or LO2 cells were evaluated by oil red O staining. RESULTS: Here we found that Cy-3-G regulated the activation of BAT and the expression of adipokines in BAT which were disrupted by HFC diet and alleviated diet induced fatty liver in mice. In in vitro experiments, Cy-3-G inhibited the release of adipokines including extracellular nicotinamide phosphoribosyltransferase (eNAMPT) and fibroblast growth factor 21 (FGF21) from differentiated C3H10T1/2 clone8 cells induced by palmitate, which was accompanied by a reduction of lipid accumulation in HepG2 cells and LO2 cells cultured by the corresponding collected media of C3H10T1/2 clone8 cells. CONCLUSIONS: These results indicate that Cy-3-G can regulate the thermogenic and secretory functions of BAT. Furthermore, our data suggest that the protective effect of Cy-3-G on hepatic lipid accumulation is probably via regulating the secretion of adipokines from BAT.

Asunto(s)

Adipoquinas/metabolismo , Tejido Adiposo Pardo/metabolismo , Antocianinas/farmacología , Dieta Alta en Grasa/efectos adversos , Glucósidos/farmacología , Enfermedad del Hígado Graso no Alcohólico/prevención & control , Sustancias Protectoras/farmacología , Adipocitos/efectos de los fármacos , Adipocitos/metabolismo , Animales , Antocianinas/uso terapéutico , Diferenciación Celular/efectos de los fármacos , Modelos Animales de Enfermedad , Glucósidos/uso terapéutico , Células Hep G2 , Humanos , Masculino , Ratones Endogámicos C57BL , Enfermedad del Hígado Graso no Alcohólico/etiología , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Sustancias Protectoras/uso terapéutico

RESUMEN

This study investigated whether cyanidin-3-O-ß-glucoside (Cy-3-G), a predominant anthocyanin, could exert a protective role on liver injury and its further mechanisms of the anti-fibrosis actions in mice. The results demonstrated that the treatment of Cy-3-G (800 mg/kg diet) for 8 weeks significantly attenuated hepatotoxicity and fibrosis in carbon tetrachloride (CCl4) administered mice. Cy-3-G strongly down-regulated the expression of α-smooth muscle actin (α-SMA), desmin, and matrix metalloproteinase (MMPs), which showed its suppression effect on the activation of hepatic stellate cells (HSCs). In addition, Cy-3-G favorably regulated oxidative stress and apoptosis in liver. Furthermore, Cy-3-G ameliorated the infiltration of inflammatory cells such as neutrophils and leukocytes and meanwhile suppressed the production of pro-inflammatory cytokines and growth factors. In conclusion, daily intake of Cy-3-G could prevent liver fibrosis progression in mice induced by CCl4 through inhibiting HSC activation, which provides a basis for clinical practice of liver fibrosis prevention.

Asunto(s)

Antocianinas/administración & dosificación , Glucósidos/administración & dosificación , Células Estrelladas Hepáticas/efectos de los fármacos , Cirrosis Hepática/tratamiento farmacológico , Oryza/química , Extractos Vegetales/administración & dosificación , Sustancias Protectoras/administración & dosificación , Animales , Antocianinas/aislamiento & purificación , Tetracloruro de Carbono/efectos adversos , Citocinas/metabolismo , Modelos Animales de Enfermedad , Glucósidos/aislamiento & purificación , Células Estrelladas Hepáticas/citología , Células Estrelladas Hepáticas/metabolismo , Humanos , Cirrosis Hepática/inducido químicamente , Cirrosis Hepática/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales/aislamiento & purificación , Sustancias Protectoras/aislamiento & purificación

RESUMEN

Apoptosis is an early event of steatohepatitis in non-alcoholic fatty liver disease (NAFLD), and an increase in oxidative stress induced by hyperglycemia has been linked to an acceleration of apoptosis in hepatocytes. Cyanidin-3-O-ß-glucoside (C3G), a classic anthocyanin, has been reported to reduce oxidative stress and attenuate non-alcoholic steatohepatitis in mice. In this study, we evaluated the toxicity of high glucose in primary hepatocytes of mice fed with a high fat diet and amelioration of this toxicity by C3G. Incubation of hepatocytes with 35mM glucose for 12h resulted in a significant decrease in cell viability and increase in apoptotic cell death. Furthermore, hyperglycemia-induced mitochondrial depolarization was accompanied by the release of cytochrome c and altered expression of Bax and Bcl-2, suggesting a mitochondria-mediated apoptotic mode of cell death. Pre-incubation with 50µM C3G induced changes associated with better cell survival and function, including a reduction in reactive species generation, improvement of mitochondrial membrane potential, inactivation of caspase-3 and -9, and down-regulation of the pro-apoptotic Bax protein. We further investigated the role of the phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen-activated protein kinases (MAPKs) pathways with respect to the anti-apoptotic action of C3G, and our results showed that C3G could activate Akt. Additionally, C3G inactivated c-Jun N-terminal protein kinase (JNK), but not extracellular signal-regulated kinase or p38 MAPK, in glucose-stressed cells. Interestingly, JNK inhibitor enhanced the protective effect of C3G on cell survival. Our results suggest that anthocyanin C3G may exhibit hepatoprotective potential against NAFLD by promoting functional integrity and survival of hepatocytes.

Asunto(s)

Antocianinas/farmacología , Hígado Graso/patología , Glucosa/metabolismo , Glucósidos/farmacología , Hepatocitos/efectos de los fármacos , Mitocondrias/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Citocromos c/metabolismo , Dieta Alta en Grasa , Grasas de la Dieta/administración & dosificación , Hígado Graso/inducido químicamente , Hígado Graso/genética , Regulación de la Expresión Génica , Glucosa/farmacología , Hepatocitos/metabolismo , Hepatocitos/patología , Proteínas Quinasas JNK Activadas por Mitógenos/genética , Proteínas Quinasas JNK Activadas por Mitógenos/metabolismo , Masculino , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Ratones , Mitocondrias/metabolismo , Mitocondrias/patología , Enfermedad del Hígado Graso no Alcohólico , Fosfatidilinositol 3-Quinasa/genética , Fosfatidilinositol 3-Quinasa/metabolismo , Cultivo Primario de Células , Inhibidores de Proteínas Quinasas/farmacología , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Proteína Destructora del Antagonista Homólogo bcl-2/genética , Proteína Destructora del Antagonista Homólogo bcl-2/metabolismo , Proteína X Asociada a bcl-2/genética , Proteína X Asociada a bcl-2/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/genética , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo

RESUMEN

Cyanidin-3-O-ß-glucoside (C3G), a typical anthocyanin pigment that exists in the human diet, has been reported to have anti-inflammatory properties. The aim of this study was to detect the effect of C3G on LPS-induced acute lung injury and to investigate the molecular mechanisms. Acute lung injury was induced by intratracheal administration of LPS in mice. Alveolar macrophages from mice were stimulated with LPS and were treated with C3G. Our results showed that C3G attenuated lung histopathologic changes, myeloperoxidase (MPO) activity, TNF-α, IL-1ß and IL-6 production in LPS-induced acute lung injury model. In vitro, C3G dose-dependently inhibited TNF-α, IL-1ß, IL-6, IL-10 and IFN-ß production, as well as NF-κB and IRF3 activation in LPS-stimulated alveolar macrophages. Furthermore, C3G disrupted the formation of lipid rafts by depleting cholesterol and inhibited TLR4 translocation into lipid rafts. Moreover, C3G activated LXRα-ABCG1-dependent cholesterol efflux. Knockout of LXRα abrogated the anti-inflammatory effects of C3G. In conclusion, C3G has a protective effect on LPS-induced acute lung injury. The promising anti-inflammatory mechanisms of C3G is associated with up-regulation of the LXRα-ABCG1 pathway which result in disrupting lipid rafts by depleting cholesterol and reducing translocation of TLR4 to lipid rafts, thereby suppressing TLR4 mediated inflammatory response.

Asunto(s)

Lesión Pulmonar Aguda/tratamiento farmacológico , Antocianinas/farmacología , Glucósidos/farmacología , Lipopolisacáridos/farmacología , Macrófagos Alveolares/efectos de los fármacos , Receptores Nucleares Huérfanos/genética , Receptor Toll-Like 4/genética , Transportador de Casetes de Unión a ATP, Subfamilia G, Miembro 1 , Transportadoras de Casetes de Unión a ATP/genética , Transportadoras de Casetes de Unión a ATP/inmunología , Lesión Pulmonar Aguda/genética , Lesión Pulmonar Aguda/patología , Animales , Transporte Biológico , Células Cultivadas , Colesterol , Regulación de la Expresión Génica , Factor 3 Regulador del Interferón/genética , Factor 3 Regulador del Interferón/inmunología , Interferón beta/genética , Interferón beta/inmunología , Interleucina-10/genética , Interleucina-10/inmunología , Interleucina-1beta/genética , Interleucina-1beta/inmunología , Interleucina-6/genética , Interleucina-6/inmunología , Intubación Intratraqueal , Lipoproteínas/genética , Lipoproteínas/inmunología , Receptores X del Hígado , Macrófagos Alveolares/inmunología , Macrófagos Alveolares/patología , Masculino , Microdominios de Membrana , Ratones , FN-kappa B/genética , FN-kappa B/inmunología , Receptores Nucleares Huérfanos/antagonistas & inhibidores , Receptores Nucleares Huérfanos/inmunología , Peroxidasa/genética , Peroxidasa/inmunología , Transducción de Señal , Receptor Toll-Like 4/inmunología , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/inmunología

RESUMEN

The aim of the present study was to evaluate the effect of long-term cyanidin 3-O-ß-D-glucoside (C3G) and/or Ochratoxin A (OTA)-exposure on dimethylarginine dimethylamino hydrolase/nitric oxide synthase (DDAH/NOS) pathway in rats. The experiments were performed in rats supplemented with C3G (1 g/kg feed), OTA (200 ppb), and OTA + C3G. After 4 weeks of daily treatment, liver and kidneys were processed for eNOS, iNOS and DDAH-1 Western blotting, nitrite levels evaluation and DDAH activity determination. Results show that OTA is able to induce iNOS both in kidney and liver, whereas OTA is able to induce eNOS and DDAH-1 overexpression and DDAH activation only in kidney, resulting in increased nitrite levels. In kidney of OTA + C3G fed rats, iNOS, eNOS and DDAH-1 expression were less pronounced compared with those observed in the OTA-treated group. Coherent with the decreased iNOS, eNOS and DDAH-1 expression a decrease in nitrite levels and DDAH activity was observed in the OTA + C3G group. Results demonstrate that C3G is able to counteract the deleterious effects of chronic consumption of OTA and also suggest a possible involvement of iNOS-eNOS-DDAH impairment in OTA nephrocarcinogenity.

Asunto(s)

Antocianinas/farmacología , Carcinógenos/toxicidad , Glucósidos/farmacología , Ocratoxinas/toxicidad , Sustancias Protectoras/farmacología , Amidohidrolasas/metabolismo , Animales , Riñón/efectos de los fármacos , Riñón/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Nitratos/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Óxido Nítrico Sintasa de Tipo III/metabolismo , Nitritos/metabolismo , Ratas , Ratas Sprague-Dawley