RESUMO
Circadian rhythms (CRs) are 24-hour periodic oscillations governed by an endogenous circadian pacemaker located in the suprachiasmatic nucleus (SCN), which organizes the physiology and behavior of organisms. Circadian rhythm disruption (CRD) is also indicative of the aging process. In mammals, melatonin is primarily synthesized in the pineal gland and participates in a variety of multifaceted intracellular signaling networks and has been shown to synchronize CRs. Endogenous melatonin synthesis and its release tend to decrease progressively with advancing age. Older individuals experience frequent CR disruption, which hastens the process of aging. A profound understanding of the relationship between CRs and aging has the potential to improve existing treatments and facilitate development of novel chronotherapies that target age-related disorders. This review article aims to examine the circadian regulatory mechanisms in which melatonin plays a key role in signaling. We describe the basic architecture of the molecular circadian clock and its functional decline with age in detail. Furthermore, we discuss the role of melatonin in regulation of the circadian pacemaker and redox homeostasis during aging. Moreover, we also discuss the protective effect of exogenous melatonin supplementation in age-dependent CR disruption, which sheds light on this pleiotropic molecule and how it can be used as an effective chronotherapeutic medicine.
Assuntos
Relógios Circadianos , Melatonina , Humanos , Animais , Melatonina/farmacologia , Melatonina/fisiologia , Ritmo Circadiano/fisiologia , Relógios Circadianos/fisiologia , Núcleo Supraquiasmático/fisiologia , Envelhecimento/fisiologia , MamíferosRESUMO
Excessive dietary fat is mainly responsible for metabolic diseases including atherosclerosis and cardiovascular disease. We have evaluated the role of Vitamin C in an experimental hyperlipidemic model of rats (male Wistar rat 12-16 months). The hyperlipidemic model of the rat was created by treatment with an atherogenic suspension: cholesterol, cholic acid, and coconut oil, for 30 days once daily, and supplemented with Vitamin C (Ascorbic acid) doses of 0.5 g/kg body weight (orally) for the 30 days once daily. Bodyweight, fasting glucose, triglyceride, cholesterol, ROS (Reactive oxygen species), MDA (Malondialdehyde), FRAP (Ferric reducing the ability of plasma), GSH (Reduced glutathione), PCO (Protein carbonyl), PON-1(Paraoxonase-1), AGE (Advanced glycation end product), PMRS (Plasma membrane reduced system), and inflammatory cytokines (TNF-α and IL-6) were estimated in blood and plasma. Our result shows that oxidative stress, and inflammatory markers, were increased in the HFD-treated group of rats. Vitamin C supplementation protected against lipidemic and, oxidative stress. We conclude that Vitamin C may be useful in maintaining cellular redox balance and protecting against lipidemic stress.
RESUMO
An impaired redox homeostasis is an important hallmark of biological aging. Coenzyme Q10 is an endogenous lipophilic antioxidant that decreases with age and has been linked to oxidative stress. The purpose of this study was to evaluate the effect of CoQ10 supplementation on redox homeostasis and levels of inflammatory cytokines in young and old rats. Male Wistar rats (young and old) were randomly divided into four groups (n = 6). Group I: young control, Group II: young rats treated with CoQ10, Group III: old control, Group IV: old rats treated with CoQ10. CoQ10 (20 mg/kg) was administered daily to Group II and IV via oral gavage. After 28 days of treatment, rats were sacrificed and biomarkers of oxidative stress and inflammatory cytokines were evaluated. Results demonstrated a significant (p ≤ 0.05) increase in malondialdehyde, protein carbonyl oxidation, advanced oxidation protein products, inflammatory cytokines: CRP, IL-6, TNF-α, and a decline in levels of superoxide dismutase, catalase, reduced glutathione, ferric reducing antioxidant potential in plasma and plasma membrane redox system in old rats when compared to young rats. After treatment with CoQ10 significant decrease in the level of MDA, PCO, AOPP, CRP, IL-6, and TNF-α was observed. Also, significant up-regulation of SOD, CAT, GSH, FRAP, and PMRS was observed. The results show that supplementing rats with CoQ10 aids in the maintenance of redox equilibrium with replenishment of antioxidant reserves and down-regulation of inflammatory biomarkers. Thus CoQ10 supplementation could be a potential anti-aging therapy.
Assuntos
Antioxidantes , Ubiquinona , Animais , Masculino , Ratos , Envelhecimento/metabolismo , Antioxidantes/farmacologia , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Interleucina-6 , Oxirredução , Ratos Wistar , Fator de Necrose Tumoral alfa/metabolismo , Ubiquinona/farmacologia , Ubiquinona/metabolismoRESUMO
CONTEXT: Fisetin as a caloric restriction mimetic (CRM) exerts numerous beneficial effects on different aging model systems. The effect of fisetin on erythrocyte membrane functions against induced aging is not very clear. OBJECTIVES: The potential role of fisetin in the modulation of erythrocytes membrane-bound transporters during natural and induced aging in rats was assessed. MATERIALS AND METHODS: Male Wistar rats were used for natural and D-galactose (D-gal) induced aging model. After supplementation with fisetin, the activities of different membrane transporters and biomarkers of oxidative stress were evaluated. RESULTS: Fisetin modulated membrane transporters such as calcium-ATPase, sodium potassium-ATPase and sodium hydrogen exchanger during senescence-induced as well as in natural aging. Fisetin also protected oxidative modifications in rat aging. DISCUSSION AND CONCLUSION: Fisetin supplementation improves the ionic homeostasis, a factor that is involved in the aetiology of several age-associated diseases, in naturally old as well as D-gal induced aged rats.
Assuntos
Restrição Calórica , Flavonóis , Animais , Homeostase , Masculino , Estresse Oxidativo , Ratos , Ratos WistarRESUMO
Circadian disruption due to artificial light affects cellular redox homeostasis and may lead to neurodegenerative diseases. The aim of the present study was to investigate the effect of continuous light exposure (CLE) and continuous dark exposure (CDE) along with melatonin supplementation on neuronal redox status, mitochondrial complexes, membrane bound transporters, inflammation, autophagy and neurodegeneration in chronodisrupted model of rat. In the study artificial light of white LED bulb with 500 lux intensity was used. Melatonin (10 mg/kg b.w., orally) was supplemented to control and CLE groups for 10 days. Standard protocols were employed to measure pro-oxidants, non-enzymatic antioxidants, and mitochondrial complexes in brain tissues. Membrane-bound ion transporter activities were evaluated in the crude synaptosomes. Gene expression analysis was performed to assess the expression of inflammatory, autophagy and neuronal marker genes. Histopathological changes in cerebral cortex and different hippocampus regions of the brain were studied. Melatonin exerted a significant normalization of redox status biomarkers in brain tissue. Further melatonin restored the activities of mitochondrial complexes and synaptosomal membrane bound ion transporters. RT-PCR data revealed that melatonin downregulated the expression of inflammatory (TNF-α, IL-6) autophagy (Atg-3, Beclin-1) and neurodegenerative genes (Ngb and NSE) in CLE group. Melatonin also preserved the histology architecture in cerebral cortex and hippocampus. Our results indicate that melatonin exerts a potent neuroprotective effect through reduction of oxidative stress, inflammation and autophagy. Melatonin supplementation might be a promising neurotherapeutic in the treatment neurodegenerative disorders caused by circadian disturbances.
Assuntos
Melatonina , Animais , Antioxidantes/metabolismo , Antioxidantes/farmacologia , Autofagia , Ritmo Circadiano , Melatonina/farmacologia , Neuroproteção , Estresse Oxidativo , RatosRESUMO
Circadian disruption due to artificial light at night (ALAN) is an alarming threat to modern society. In the present study we evaluated the protective effect of melatonin on age dependent redox insults and neurochemical deficits induced by ALAN in the brain of chronodisrupted rat model. Young (3 months) and old (22 months) male Wistar rats were exposed to ALAN along with melatonin supplementation (10 mg Kg-1, oral) for 10 days. Results demonstrated significant increment in the pro-oxidant biomarkers: reactive oxygen species, lipid hydroperoxidation, protein carbonyl, nitric oxide while suppression in the total thiol, ferric reducing antioxidant potential level, superoxide dismutase and catalase activities in the brain of ALAN exposed groups with higher amplitude in aged rats. Further these oxidative modifications were protected by subsequent administration of melatonin. Mitochondrial complexes (C-I to C-IV) activity was significantly altered in young and old ALAN exposed groups with melatonin showing protective effect. Histopathological analysis show dense cytosolic staining and neuronal degeneration in cerebral cortex and different hippocampus regions with greater extent in old ALAN rats effectively moderated by melatonin supplementation. RT-PCR data analysis revealed melatonin effectively downregulated neuroinflammatory (IL-6, TNF α) and neurodegenerative marker (Ngb) while upregulating the aging (Sirt 1) gene expression in both young and old melatonin supplemented ALAN exposed groups. Our results may help in understanding the degree of ALAN induced photo-oxidative damage in neuronal redox homeostasis during aging. We also show that melatonin supplementation might provide a basis for amelioration of oxidative disturbances to improve circadian entrainment in aged populations.
Assuntos
Melatonina , Animais , Ritmo Circadiano , Luz , Masculino , Melatonina/farmacologia , Oxirredução , Estresse Oxidativo , Ratos , Ratos WistarRESUMO
Circadian disruption or chronodisruption (CD) occurs when day-night cycles and other internal rhythms are not adjusted to environmental light-dark regimens and are unable to synchronize among each other. Artificial light-induced oxidative stress is a major concern as the circadian physiology of the cell is chronically altered due to suppression of the time-keeping hormone, melatonin. The relationship between age-related impaired redox status and disrupted circadian rhythms is still not fully understood. The present study evaluated the effect of artificial light at night (ALAN) with respect to aging and role of melatonin supplementation. This study was conducted on young (3 months) and old (24 months) male Wistar rats subdivided into four groups control (C), melatonin treated (MLT), artificial light at night (ALAN), and ALAN+MLT group. Pronounced changes were observed in the old compared to the young rats. Reactive oxygen species (ROS), malondialdehyde (MDA), plasma membrane redox system (PMRS), protein carbonyl (PCO), and sialic acid (SA) were significantly (p ≤ 0.05) increased, while ferric reducing ability of plasma (FRAP) and reduced glutathione (GSH) were significantly (p ≤ 0.05) suppressed in light-exposed young and old animals compared to their age-matched controls. Advanced oxidation protein products (AOPP) increased non-significantly in young rats of the ALAN group; however, significant (p ≤ 0.05) changes were observed in the old rats of the ALAN group compared to their respective controls. Advanced glycation end products (AGEs) increased and acetylcholinesterase (AChE) activity decreased, significantly (p ≤ 0.05) in young animals of the ALAN group, while nonsignificant changes of both parameters were recorded in the old animals of the ALAN groups compared with their age-matched controls. Melatonin supplementation resulted in maintenance of the normal redox homeostasis in both young and old animal groups. Our study suggests that aged rats are more susceptible to altered photoperiod as their circadian redox homeostasis is under stress subsequent to ALAN. Melatonin supplementation could be a promising means of alleviating age-related circadian disturbances, especially in light-polluted areas.
Assuntos
Ritmo Circadiano , Homeostase , Melatonina , Envelhecimento , Animais , Luz , Masculino , Melatonina/farmacologia , Oxirredução , Ratos , Ratos WistarRESUMO
Aging is associated with decreased cellular cysteine uptake, which acts as a precursor for glutathione biosynthesis. Whey protein, a liquid aspect of milk, is an effective cysteine delivery system. The study was undertaken to evaluate the potential role of whey protein concentrate (WPC) on the redox biomarkers during aging. Male Wistar rats were divided into following four groups: young control (4 months old); young treated with WPC (300 mg/kg b.w./day orally); old (24 months old) control; old treated with WPC for 28 days. After treatment, changes in body weight, lipid profile and levels of redox biomarkers were determined. A marked decrease in prooxidants such as reactive oxygen species, lipid peroxidation and protein carbonyl and significant (p ≤ 0.05) increase in antioxidants such as reduced glutathione and GST levels were observed after WPC supplementation in old age rats. We also found marked decrease in the level of sialic acid and AGEs after WPC supplementation. In conclusion, WPC provides protection against age-dependent redox imbalance which might be attributed to its antioxidant activity.
Assuntos
Envelhecimento/efeitos dos fármacos , Eritrócitos/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Proteínas do Soro do Leite/uso terapêutico , Envelhecimento/metabolismo , Animais , Biomarcadores/metabolismo , Cisteína/metabolismo , Avaliação Pré-Clínica de Medicamentos , Eritrócitos/metabolismo , Produtos Finais de Glicação Avançada/metabolismo , Metabolismo dos Lipídeos/efeitos dos fármacos , Masculino , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Triptofano/sangue , Tirosina/análogos & derivados , Tirosina/sangue , Proteínas do Soro do Leite/farmacologiaRESUMO
Continuous light or dark photoperiods are the leading cause of disruption in the circadian rhythm of day-night cycle. The purpose of this study was to understand the cellular redox balance in a model of circadian disrupted rat model and determine the effect of melatonin supplementation. Young male Wistar rats were randomly divided into five groups (nâ¯=â¯4). Group (I): normal day-night (12â¯h:12â¯h) cycle, Group (II): normal rats treated with melatonin, Group (III): rats subjected to continuous light exposure (CLE), Group (IV): CLE rats treated with melatonin, and Group (V) Rats subjected to continuous dark. Melatonin (10â¯mg/kg) was administered orally at dusk to the Group (II) & (IV). Rats were sacrificed after 10â¯days of treatment and biomarkers of oxidative stress were evaluated. Results demonstrated significant (pâ¯<â¯0.05) increase of malondialdehyde (MDA), plasma membrane redox system (PMRS), protein carbonyl oxidation (PCO), advanced oxidation protein products (AOPPs), and advanced glycation end products (AGEs) during CLE. A significantly (pâ¯<â¯0.05) decreased level of reduced glutathione (GSH) and ferric reducing antioxidant potential in plasma (FRAP) was also observed during CLE. Treatment with melatonin in CLE rats showed reduced level of MDA, PMRS, PCO, AOPPs and AGEs while GSH and FRAP activity were increased. During continuous dark exposure (CDE) the biomarkers of oxidative stress were attenuated compared to control. Supplementation of melatonin could be a promising strategy to maintain redox homeostasis during prolonged condition of light exposure and other conditions of redox imbalance.
Assuntos
Ritmo Circadiano/fisiologia , Suplementos Nutricionais , Homeostase , Melatonina/farmacologia , Animais , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Proteínas Sanguíneas/metabolismo , Peso Corporal/efeitos dos fármacos , Membrana Celular/efeitos dos fármacos , Membrana Celular/metabolismo , Eritrócitos/efeitos dos fármacos , Eritrócitos/metabolismo , Glutationa/metabolismo , Homeostase/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Malondialdeído/metabolismo , Melatonina/administração & dosagem , Modelos Animais , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismoRESUMO
N-acetyl-l-cysteine (NAC) is a precursor of cysteine, which is known to increase the level of glutathione (GSH) in the brain. Several neurodegenerative changes linked to oxidative stress take place in the aging brain. This study aimed to assess the neuroprotective effect of NAC supplementation on age-dependent neurodegeneration in the rat brain. Young (4 months) and old (24 months) Wistar rats (n = 6 rats/group) were supplemented with NAC (100 mg/kg b.w. orally) for 14 days. Enzymatic and nonenzymatic antioxidants such as superoxide dismutase and catalase, and GSH and total thiol respectively, prooxidants such as protein carbonyl, advanced oxidation protein products, reactive oxygen species, and malondialdehyde were assessed in the brain homogenates. Furthermore, nitric oxide level, acetylcholinesterase activity, and Na+/K+-ATPase activity were measured and gene expression studies were also performed. The results indicated that NAC augmented the level of enzymatic and nonenzymatic antioxidants with a significant reduction in prooxidant levels in old rats. NAC supplementation also downregulated the expression of inflammatory markers (TNF-α, IL-1ß, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats. The present findings support a neuroprotective role of NAC which has therapeutic implication in controlling age-related neurological disorders.
Assuntos
Acetilcisteína/farmacologia , Envelhecimento/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Doenças Neurodegenerativas/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Acetilcolinesterase/metabolismo , Envelhecimento/metabolismo , Animais , Antioxidantes/farmacologia , Biomarcadores/metabolismo , Encéfalo/metabolismo , Modelos Animais de Doenças , Regulação para Baixo/efeitos dos fármacos , Inflamação/metabolismo , Masculino , Doenças Neurodegenerativas/metabolismo , Óxido Nítrico/metabolismo , Ratos , Ratos Wistar , ATPase Trocadora de Sódio-Potássio/metabolismo , Regulação para Cima/efeitos dos fármacosRESUMO
Whey protein concentrate (WPC) is a rich source of sulfur-containing amino acids and is consumed as a functional food, incorporating a wide range of nutritional attributes. The purpose of this study is to evaluate the neuroprotective effect of WPC on rat brain during aging. Young (4 months) and old (24 months) male Wistar rats were supplemented with WPC (300 mg/kg body weight) for 28 days. Biomarkers of oxidative stress and antioxidant capacity in terms of ferric reducing antioxidant potential (FRAP), lipid hydroperoxide (LHP), total thiol (T-SH), protein carbonyl (PC), reactive oxygen species (ROS), nitric oxide (NO), and acetylcholinesterase (AChE) activity were measured in brain of control and experimental (WPC supplemented) groups. In addition, gene expression and histopathological studies were also performed. The results indicate that WPC augmented the level of FRAP, T-SH, and AChE in old rats as compared with the old control. Furthermore, WPC-treated groups exhibited significant reduction in LHP, PC, ROS, and NO levels in aged rats. WPC supplementation also downregulated the expression of inflammatory markers (tumor necrosis factor alpha, interleukin (IL)-1ß, IL-6), and upregulated the expression of marker genes associated with autophagy (Atg3, Beclin-1, LC3B) and neurodegeneration (neuron specific enolase, Synapsin-I, MBP-2). The findings suggested WPC to be a potential functional nutritional food supplement that prevents the progression of age-related oxidative damage in Wistar rats.
Assuntos
Envelhecimento/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Doenças Neurodegenerativas/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Proteínas do Soro do Leite/farmacologia , Acetilcolinesterase/metabolismo , Animais , Autofagia/efeitos dos fármacos , Proteínas Relacionadas à Autofagia/genética , Proteínas Relacionadas à Autofagia/metabolismo , Proteína Beclina-1/genética , Proteína Beclina-1/metabolismo , Biomarcadores/sangue , Encéfalo/metabolismo , Suplementos Nutricionais , Regulação da Expressão Gênica , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/metabolismo , Óxido Nítrico/metabolismo , Peptídeo Sintases/genética , Peptídeo Sintases/metabolismo , Carbonilação Proteica , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Compostos de Sulfidrila/metabolismo , Sinapsinas/genética , Sinapsinas/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Present study was conducted to evaluate the effect of oral supplementation of composite extract of leaves (CLE) of four medicinal plants; Aegle marmelos, Ocimum sanctum, Murraya koenigii and Azadirachta indica on markers of oxidative stress in brain tissues of alloxan-induced diabetic rats in vivo. Enhanced lipid peroxidation, protein oxidation and reduced antioxidative defence systems were measured in brain tissues of diabetic rats. Supplementation of CLE, once in a day for 35 days significantly (p < .05) protected the peroxidation of lipid, oxidation of protein and ameliorated the antioxidant defence in brain tissue of diabetic rats. It was observed that the insulin-like effect of CLE was dose dependent; higher effect at higher doses. The results of the study suggest that supplementation CLE may provide an overall homeostasis and significant neuro-protection through rescuing brain cells from oxidative abuse and accelerating brain antioxidative defence during advanced stage of hyperglycaemia.
Assuntos
Antioxidantes/uso terapêutico , Diabetes Mellitus Experimental/dietoterapia , Suplementos Nutricionais , Estresse Oxidativo , Extratos Vegetais/uso terapêutico , Folhas de Planta/química , Plantas Medicinais/química , Animais , Antioxidantes/administração & dosagem , Biomarcadores/sangue , Biomarcadores/metabolismo , Encéfalo/efeitos dos fármacos , Encéfalo/enzimologia , Encéfalo/metabolismo , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/metabolismo , Hiperglicemia/prevenção & controle , Hipoglicemiantes/administração & dosagem , Hipoglicemiantes/uso terapêutico , Índia , Insulina Isófana Humana/uso terapêutico , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Proteínas do Tecido Nervoso/química , Proteínas do Tecido Nervoso/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/enzimologia , Neurônios/metabolismo , Fármacos Neuroprotetores/administração & dosagem , Fármacos Neuroprotetores/uso terapêutico , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Oxirredutases/metabolismo , Extratos Vegetais/administração & dosagem , Folhas de Planta/crescimento & desenvolvimento , Plantas Medicinais/crescimento & desenvolvimento , Ratos WistarRESUMO
Several health beneficial effects have been attributed to tea consumption, most of the effects are due to the strong antioxidant property of tea catechins. The present study evaluates the effect of black tea extract (BTE) supplementation on the redox balance of rats at different stages in their life span. We have evaluated erythrocyte and plasma redox status in young (4 months), middle-aged (12 months) and old-aged (24 months) male Wistar rats, by quantifying an array of parameters linked to redox status. Our results show that BTE augments redox status, measured in terms of intracellular reduced glutathione (GSH), malondialdehyde (MDA), advanced oxidation protein products (AOPPs), plasma membrane redox system (PMRS) and ferric reducing antioxidant potential (FRAP) of plasma, in rats from three different age groups. This study provides experimental evidence of a strong antioxidant property of black tea on rats in different stages of their lifespan.
Assuntos
Envelhecimento/efeitos dos fármacos , Envelhecimento/fisiologia , Antioxidantes/farmacologia , Suplementos Nutricionais , Estresse Oxidativo/efeitos dos fármacos , Chá/química , Produtos da Oxidação Avançada de Proteínas/metabolismo , Animais , Eritrócitos/efeitos dos fármacos , Glutationa/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Malondialdeído/metabolismo , Oxirredução , Ratos , Ratos WistarRESUMO
Metformin, a biguanide, is a widely used antidiabetic drug, which inhibits gluconeogenesis and is used to treat hyperglycemia in type 2 diabetes. Through activation of AMPK (AMP-activated protein kinase) pathway, metformin also mimics caloric restriction health benefits. Aging causes substantial molecular to morphological changes in brain, the brain cells being more susceptible toward oxidative stress mediated damages due to the presence of high lipid content and higher oxygen consumption. Wistar rats (naturally aged and d-galactose induced rat model) were supplemented with metformin (300 mg/kg b.w. orally) for 6 weeks. The biomarkers of oxidative stress such as antioxidant capacity (ferric reducing antioxidant potential [FRAP]), malondialdehyde (MDA), reduced glutathione (GSH), protein carbonyl (PCO), reactive oxygen species (ROS), acetylcholinesterase (AChE) activity, and nitric oxide (NO) were measured in brain tissues of control and experimental groups. The results indicate that metformin treatment augmented the levels of FRAP and GSH in naturally aged, and d-gal induced aging model groups compared to the respective controls. In contrast, metformin treated groups exhibited significant reduction in MDA, PCO, ROS, and NO levels and a significant increase in AChE activity in induced aging rats. The administration of d-galactose upregulated the expression of sirtuin-2, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) and downregulated the expression of Beclin-1. Metformin supplementation downregulated the d-galactose induced expressions of sirtuin-2, IL-6, and TNF-α expression, whereas upregulated the Beclin-1 expression. Our data confirm that metformin restores the antioxidant status and improves healthy brain aging through the activation of autophagy and reduction in inflammation.
Assuntos
Envelhecimento/fisiologia , Encéfalo/fisiologia , Metformina/farmacologia , Modelos Biológicos , Acetilcolinesterase/metabolismo , Animais , Antioxidantes/metabolismo , Autofagia/efeitos dos fármacos , Biomarcadores/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Ferro/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Óxido Nítrico/metabolismo , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Carbonilação Proteica/efeitos dos fármacos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismoRESUMO
Wound, burn and tissue related diseases are the most common and devastating forms of trauma worldwide and thousands are still dying each year when they are left untreated. The traditional treatments for wound infection using medicinal plant extracts in hydrogels and ointment formulations have several disadvantages, delicate shape and dry up quickly upon exposure to air. Indeed, there is need for the development of an alternative form of dressing material for wound healing applications. Because the medicinal plant products are economical, researchers have adopted a novel approach of complexing the active components of plants with various groups of polymers to develop biodegradable fabrications. Moreover, fabricated constructs are very extremely useful as scaffold in tissue regeneration with known successes in wound healing/ dressing applications that the fabricated substitutes mimic the extracellular matrix of tissue. In this review, we give an extensive overview on scientifically evaluated bioactive molecules of medicinal plants as well as plant extract blended polymeric constructs for the possible treatment of various skin injuries. In addition, the technological challenges and future trends for recent developments of the treatments of wound infections are extensively summarized. Copyright © 2016 John Wiley & Sons, Ltd.
Assuntos
Regeneração Tecidual Guiada/métodos , Extratos Vegetais/uso terapêutico , Plantas Medicinais , Cicatrização/efeitos dos fármacosRESUMO
Increased oxidative stress has been shown to play an important role in the etiology and pathogenesis of diabetes and its complications. Abelmoschus esculentus (Okra) has been reported to possess many important biological properties. We undertook in vivo studies on male Wistar rats to examine the antioxidative potential of okra in normal and alloxan-treated diabetic rats. Okra extract was administered to control and diabetic rats for 35 consecutive days. Erythrocyte plasma membrane redox system (PMRS) activity (p < 0.05), erythrocytes lipid peroxidation (MDA) (p < 0.01), and advanced oxidation protein products (AOPP) (p < 0.001), increased by 153%, 31%, and 290%, respectively, in response to alloxan treatment, while intracellular reduced glutathione (p < 0.001) and total antioxidant potential of plasma in terms of Ferric reducing ability (FRAP) (p < 0.01) decreased by 75% and 22%, respectively, on alloxan treatment. Okra supplementation provided protection to the rats against alloxan-induced changes. Based on the present results, we hypothesize that okra has strong antioxidative potential and may be used as a dietary supplementation in diabetes for prevention of oxidative stress-mediated complications.
Assuntos
Abelmoschus/química , Diabetes Mellitus Experimental/prevenção & controle , Extratos Vegetais/administração & dosagem , Produtos da Oxidação Avançada de Proteínas/sangue , Animais , Antioxidantes , Glicemia/análise , Membrana Eritrocítica/química , Frutas/química , Glutationa/sangue , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Fitoterapia , Ratos , Ratos WistarRESUMO
The incidence of diabetes mellitus continue to rise annually all over the world with India and Nigeria having recorded cases of 65.1 and 3.9 million respectively in 2013 and expected to increase by a large amount in 2035. Hyperglycemia is a pre-condition for the development of diabetic complications and is accompanied by an increase in the production of free radicals. The present available treatment option for diabetes like sulfonylurea, metformin and alpha-glucosidase are restricted by their limited actions, secondary failure rates, and side-effects; and unaffordable to the majority of the population. Hence, the need to screen for more medicinal plants with antidiabetic ability due to the fact that plants are; biodegradable, safe and cheap with fewer side-effects. In this review article, we have presented the current status of diabetes in India and Nigeria and the role of some less commonly used medicinal plants from both countries that have antidiabetic potential.
RESUMO
OBJECTIVE: The purpose of this study was to investigate the in vivo anti-oxidant effect of black tea extract (BTE) supplemented to normal and alloxan-induced diabetic rats. METHODS: Black tea extract (BTE) was fed to control and experimental diabetic rats by gavage technique at a dose of 1 ml/100 g body weight/day. Markers of oxidative stress in blood were determined. RESULT: Results show a significant (P < 0.01) decrease (73%) in plasma anti-oxidant potential, increase in activity of plasma membrane redox system (122%), protein oxidation and lipid peroxidation in diabetic rats, BTE supplemented diabetic rats had improved anti-oxidant profile and lower protein and lipid peroxidation levels. Diabetic rats displayed lower intracellular glutathione (GSH), BTE supplementation improved GSH levels. CONCLUSION: Results of this study suggest that the 2.5% aqueous extract of black tea is effective to ameliorate diabetes associated oxidative stress parameters in experimental model of diabetes.
Assuntos
Antioxidantes/administração & dosagem , Camellia sinensis/química , Diabetes Mellitus Experimental/dietoterapia , Eritrócitos/efeitos dos fármacos , Chá/química , Administração Oral , Produtos da Oxidação Avançada de Proteínas/sangue , Aloxano , Animais , Antioxidantes/química , Biomarcadores/sangue , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/induzido quimicamente , Diabetes Mellitus Experimental/patologia , Eritrócitos/química , Eritrócitos/metabolismo , Glutationa/sangue , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Estresse Oxidativo , Ratos , Ratos Wistar , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Triglicerídeos/sangueRESUMO
BACKGROUND: Paraoxonase 1 (PON1) protects the oxidative modification of low-density lipoprotein (LDL) and is a major anti-atherosclerotic protein component of high-density lipoprotein. We explored the effect of onion extract and flavonoids (quercetin and catechin) in the regulation of PON1 expression and correlating with oxidised LDL levels in male Wistar rats subjected to mercuric chloride (HgCl2) induced oxidative insult. Rats were divided into eight groups: Control, Experimental (HgCl2), Experimental + onion/catechin/quercetin, Positive control (Normal + onion/catechin/quercetin). Treatment continued for 4 weeks. RESULTS: PON1 activity and radical scavenging activity decreased in the Experimental group (P < 0.001) with increased susceptibility of LDL for oxidation and plasma malondialdehyde levels (P < 0.001). Onion extract significantly attenuated the adverse effects of HgCl2 by up-regulating PON1 activity (P < 0.05), radical scavenging activity (P < 0.01), and protected against LDL oxidation (P < 0.001) and lipid peroxidation (P < 0.01). Similar effects were observed with quercetin and to a lesser extent with catechin. CONCLUSIONS: The findings may explain the anti-atherosclerotic effect of onion and also foods containing quercetin and catechins.