RESUMO
Recently, peptidic antioxidants have attracted much attention due to their promising applications in the production of valuable functional food and nutraceuticals with health-promoting properties [...].
RESUMO
Recently, there has been an increased demand for functional foods, to reduce the risk of age-related cognitive impairment, dementia, and Alzheimer's disease. Among them, plant-derived bioactive compounds, such as phytochemicals and peptides, have notable potential in improving memory and cognitive functions. Many studies have provided potential data concerning the characteristics and structure-activity relationships of memory-enhancing peptides. When considering the proof of efficacy of these plant-based peptides in humans as neurological treatment options, it is necessary to accumulate evidence concerning their bioavailability and permeability through blood-brain barrier (BBB). This review focuses on the memory-enhancing effects of peptides derived from plant proteins and presents a current perspective on their structure-activity relationships and BBB permeability.
Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Cognição/efeitos dos fármacos , Memória/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Fragmentos de Peptídeos/farmacologia , Proteínas de Plantas/metabolismo , Animais , Barreira Hematoencefálica/metabolismo , HumanosRESUMO
The microbiota-gut-brain axis has attracted increasing attention in the last decade. Here, we investigated whether okara, a soybean by-product rich in dietary fiber, can attenuate cognitive impairment in senescence-accelerated mouse prone 8 (SAMP8) mice by altering gut microbial composition. Mice were fed either a standard diet, or a diet containing okara (7.5% or 15%, w/w) for 26 weeks. In the memory test, the 7.5% okara-fed mice showed a longer step-through latency and the 15% okara-fed mice had a short escape latency compared with control mice. The 15% okara-fed mice displayed decreased body weight, increased fecal weight, and altered cecal microbiota composition compared with the control group; however, there was no significant difference in the serum lactic acid and butyric acid levels among these mice groups. The 7.5% okara-fed mice had significantly higher NeuN intensity in the hippocampus compared with control mice. Furthermore, a decrease in inflammatory cytokine TNF- and an increase in brain-derived neurotrophic factor (BDNF) was observed in the 7.5% okara-fed group. The expression of synthesizing enzyme of acetylcholine was increased by the okara diets, and the acetylcholine level in the brain was higher in the 7.5% okara-fed group than in the control. These suggest that oral administration of okara could delay cognitive decline without drastically changing gut microbiota.
Assuntos
Envelhecimento , Ração Animal/análise , Disfunção Cognitiva/tratamento farmacológico , Dieta/veterinária , Glycine max/química , Animais , Fator Neurotrófico Derivado do Encéfalo/genética , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Microbioma Gastrointestinal/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Camundongos , Fator de Necrose Tumoral alfa/metabolismoRESUMO
This study investigated the preventive effects of fermented rice peptides (FRPs) against scopolamine-induced memory impairment in mice and their potential mechanisms. Mice were pretreated with FRPs (25 and 100â¯mg/kg body weight) via intraperitoneal injection for 7â¯days, followed by intraperitoneal injection of scopolamine. FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice. Additionally, scopolamine-treated mice showed significantly decreased acetylcholine levels and increased acetylcholine-esterase activity in the hippocampus as compared with controls; however, these changes were suppressed by FRP pretreatment. Among the fractions separated by size-exclusion chromatography, the non-glycosylated peptide fraction of FRP suppressed H2O2-induced neuronal damage in SK-N-SH cells via upregulated BDNF levels. Our findings demonstrated that FRP prevented memory impairment, and that the underlying mechanism might involve regulation of the ERK/CREB/BDNF signaling pathway. These results suggest FRP as a potential agent for the prevention of age-related cognitive decline and dementia.
Assuntos
Transtornos da Memória/tratamento farmacológico , Peptídeos/farmacologia , Acetilcolinesterase/metabolismo , Animais , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Disfunção Cognitiva/metabolismo , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Alimentos Fermentados , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Peróxido de Hidrogênio/metabolismo , Memória/efeitos dos fármacos , Transtornos da Memória/induzido quimicamente , Transtornos da Memória/metabolismo , Camundongos , Fatores de Crescimento Neural , Oryza/metabolismo , Fosforilação , Escopolamina/metabolismo , Transdução de Sinais/efeitos dos fármacos , Lobo Temporal/metabolismoRESUMO
This study aimed to assess the suppressive effect of long-term diet supplementation with Lactobacillus strains on cognitive decline in the senescence-accelerated mouse prone 8 (SAMP8) model. For 43 weeks, fourteen-week-old female SAMP8 mice were fed a standard diet containing 0.05% (w/w) Lactobacillus casei subsp. casei 327 (L. 327) or Lactobacillusparacasei K71 (L. K71) derived from rice grains and sake lees, respectively. SAMP8 mice that were fed a L. K71-supplemented diet had better cognitive performance compared with the control and L. 327 groups in the Barnes maze and passive avoidance tests. An ELISA analysis revealed that the levels of serotonin were elevated in the serum and brain tissue of L. K71-fed mice. The protein expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), and phosphorylated CREB were evaluated using western blot. Long-term administration of L. K71 resulted in increased protein expression of BDNF and CREB phosphorylation in the hippocampus. These results suggest that prolonged intake of a diet supplemented with a Lactobacillus strain derived from sake lees may prevent age-dependent cognitive decline by upregulating BDNF expression in the hippocampus.