ABSTRACT
After an ischemic stroke, various harmful mechanisms contribute to tissue damage, including the inflammatory response. The increase in pro-inflammatory cytokines has been related to greater damage to the neural tissue and the promotion of neurological alterations, including cognitive impairment. Recent research has shown that the use of prebiotics and/or probiotics counteracts inflammation and improves cognitive function through the production of growth factors, such as brain-derived neurotrophic factor (BDNF), by reducing inflammatory molecules. Therefore, in this study, the effect of the symbiotic inulin and Enterococcus faecium on neuroprotection and memory improvement was evaluated in a rat model of transient middle cerebral artery occlusion (tMCAO). In order to accomplish this, the animals were subjected to ischemia; the experimental group was supplemented with the symbiotic and the control group with the vehicle. The neurological deficit as well as spatial and working memory were evaluated using the Zea Longa scale, Morris water maze, and the eight-arm maze tests, respectively. Infarct size, the levels of BDNF, and tumor necrosis factor-alpha (TNF-α) were also assessed. The results show that supplementation with the symbiotic significantly diminished the neurological deficit and infarct size, improved memory and learning, increased BDNF expression, and reduced TNF-α production. These findings provide new evidence about the therapeutic use of symbiotics for ischemic stroke and open up the possibilities for the design of further studies.
ABSTRACT
Obesity has been linked to cognitive impairment through systemic low-grade inflammation. High fat and sugar diets (HFSDs) also induce systemic inflammation, either by induced Toll-like receptor 4 response, or by causing dysbiosis. This study aimed to evaluate the effect of symbiotics supplementation on spatial and working memory, butyrate concentration, neurogenesis, and electrophysiological recovery of HFSD-fed rats. In a first experiment, Sprague-Dawley male rats were given HFSD for 10 weeks, after which they were randomized into 2 groups (n = 10 per group): water (control), or Enterococcus faecium + inulin (symbiotic) administration, for 5 weeks. In the fifth week, spatial and working memory was analyzed through the Morris Water Maze (MWM) and Eight-Arm Radial Maze (RAM) tests, respectively, with 1 week apart between tests. At the end of the study, butyrate levels from feces and neurogenesis at hippocampus were determined. In a second experiment with similar characteristics, the hippocampus was extracted to perform electrophysiological studies. Symbiotic-supplemented rats showed a significantly better memory, butyrate concentrations, and neurogenesis. This group also presented an increased firing frequency in hippocampal neurons [and a larger N-methyl-d-aspartate (NMDA)/α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) current ratio] suggesting an increase in NMDA receptors, which in turn is associated with an enhancement in long-term potentiation and synaptic plasticity. Therefore, our results suggest that symbiotics could restore obesity-related memory impairment and promote synaptic plasticity.
Subject(s)
Agave , Spatial Memory , Rats , Animals , Male , Agave/metabolism , Inulin/pharmacology , Inulin/therapeutic use , Rats, Sprague-Dawley , Hippocampus/metabolism , Neuronal Plasticity/physiology , Receptors, N-Methyl-D-Aspartate/metabolism , Maze Learning/physiology , Obesity/therapy , Dietary Supplements , InflammationABSTRACT
INTRODUCTION: The mechanism underlying the memory improvement induced by prebiotic and probiotic supplementation remains unclear. Glucagon-like peptide type 1 (GLP-1) could play an important role since it is induced by prebiotics and enhances memory and learning. AIMS: We correlated the levels of GLP-1 with spatial memory in senile animals to determine its role in memory improvement after prebiotic and probiotic supplementation. METHODS: Senile rats were randomly assigned to four groups: (1) water (control); (2) Enterococcus faecium (probiotic); (3) agave inulin (prebiotic); and (4) E. faecium + agave inulin (symbiotic). Each supplement was administered by an orogastric cannula for 5 weeks. In the fifth week, spatial memory was assessed using the Morris Water Maze test (MWM). We extracted the hippocampus, intestine, and serum. GLP-1 levels were quantified by enzyme-linked immunosorbent assay. RESULTS: A significant decrease in escape latency time in the MWM was observed in all groups treated with supplements. The symbiotic group achieved the highest reduction (15.13 s ± 6.40) (p < 0.01). We did not find a significant increase in GLP-1 levels nor a direct correlation of its levels with spatial memory improvement (p > 0.05). CONCLUSION: Prebiotic and probiotic supplementation improved spatial memory in senile animals. However, this beneficial effect did not correlate with GLP-1 levels.
Subject(s)
Prebiotics , Probiotics , Rats , Animals , Glucagon-Like Peptide 1 , Inulin , Dietary SupplementsABSTRACT
INTRODUCTION: Sarcopenia refers to a progressive and generalized muscle mass and strength loss. In liver diseases, it has been related to worse outcomes and high risk of decompensations. AREAS COVERED: Sarcopenia is caused by a set of cellular processes in the muscle such as denervation, mitochondrial dysfunction, endotoxemia and inflammation; which are manifested through the alteration of several proteolytic pathways such as lysosomal, proteasomal and caspase systems. In autophagy, myostatin and oxidative stress; such as hyperammonemia, contributes importantly to liver sarcopenia through loss of muscle mass already demonstrated in in vitro and in vivo models. In addition, hormones and the regulation of the intestinal microbiota, influence in a not less important magnitude. In the clinical setting, early identification of sarcopenia has been established as a mandatory item to prevent progression of muscle mass loss; however, diagnostic methods have extreme variation according to methodology, population, etiology and severity of liver disease. Reversing sarcopenia should be an integral therapeutic strategy. EXPERT OPINION: Clinical and nutritional interventions should be adapted to liver injury etiology and stage of disease, each of them shares a similar sarcopenia development pathway. There are specific biomarkers that condition or exacerbate loss of skeletal muscle.
Subject(s)
Gastrointestinal Microbiome/physiology , Liver Diseases/physiopathology , Sarcopenia/physiopathology , Carcinoma, Hepatocellular/physiopathology , Chronic Disease , Humans , Liver Diseases/etiology , Liver Neoplasms/physiopathology , Liver Transplantation , Muscle, Skeletal/physiopathology , Sarcopenia/diagnosis , Sarcopenia/etiology , Sarcopenia/therapyABSTRACT
Cognitive functions, such as learning and memory, may be impaired during aging. Age-related cognitive impairment is associated with selective neuronal loss, oxidative changes that lead to microglia activation and neuroinflammation. In addition, it is associated to alteration reduction in trophic factors affecting neurogenesis and synaptic plasticity. In recent years, attention has been paid to the relationship between gut microbiota and brain. In aging, there is an alteration in microbiota, gut microbiota diversity is perturbed with an increase in pathogenic bacteria at the expense of beneficial ones. Dysbiosis may lead to chronic inflammation, and a decrease in bacteria metabolites such as short-chain fatty acids which have been related to an upregulation of neurotrophic factors. Supplementation with prebiotics and probiotics can modulate gut microbiota, returning it to a more physiological state; thus, they may be considered as a possible treatment for age-related cognitive impairment.
Subject(s)
Cognitive Dysfunction/therapy , Dysbiosis/therapy , Prebiotics , Probiotics/therapeutic use , Aging/psychology , Brain-Derived Neurotrophic Factor/physiology , Cell Death , Cognitive Dysfunction/microbiology , Cognitive Dysfunction/physiopathology , Cognitive Dysfunction/prevention & control , Dysbiosis/psychology , Gastrointestinal Microbiome/physiology , Humans , Inflammation , Microglia/immunology , Mitochondria/physiology , Neurogenesis , Neurons/pathology , Oxidative Stress , Reactive Oxygen Species/metabolismABSTRACT
Aging is associated with morphological, physiological and metabolic changes, leading to multiorgan degenerative pathologies, such as cognitive function decline. It has been suggested that memory loss also involves a decrease in neurotrophic factors, including brain-derived neurotrophic factor (BDNF). In recent years, microbiota has been proposed as an essential player in brain development, as it is believed to activate BDNF secretion through butyrate production. Thus, microbiota modulation by supplementation with probiotics and prebiotics may impact cognitive decline. This study aimed to evaluate the effects of probiotics and prebiotics supplementation on the memory of middle-aged rats. Sprague-Dawley male rats were randomized in four groups (n = 13 per group): control (water), probiotic (E. faecium), prebiotic (agave inulin), symbiotic (E. faecium + inulin), which were administered for 5 weeks by oral gavage. Spatial and associative memory was analyzed using the Morris Water Maze (MWM) and Pavlovian autoshaping tests, respectively. Hippocampus was obtained to analyze cytokines [interleukin (IL-1ß) and tumor necrosis factor (TNF-α)], BDNF and γ-aminobutyric acid (GABA) by enzyme-linked immunosorbent assay (ELISA). Butyrate concentrations were also evaluated in feces. The symbiotic group showed a significantly better performance in MWM (p < 0.01), but not in Pavlovian autoshaping test. It also showed significantly lower concentrations of pro-inflammatory cytokines (p < 0.01) and the reduction in IL-1ß correlated with a better performance of the symbiotic group in MWM (p < 0.05). Symbiotic group also showed the highest BDNF and butyrate levels (p < 0.0001). Finally, we compared the electrophysiological responses of control (n = 8) and symbiotic (n = 8) groups. Passive properties of CA1 pyramidal cells (PCs) exhibited changes in response to the symbiotic treatment. Likewise, this group showed an increase in the N-methyl-D-aspartate receptor (NMDA)/AMPA ratio and exhibited robust long-term potentiation (LTP; p < 0.01). Integrated results suggest that symbiotics could improve age-related impaired memory.
ABSTRACT
Dyslipidemia is an important modifi able risk factor for cardiovascular and metabolic diseases, which are responsible for a large number of mortality and disability cases around the globe. Different strategies have been used within the treatment of dyslipidemia, including lifestyle modifi cations, pharmacologic therapy, as well as functional foods and nutraceuticals. Functional foods have been used worldwide since ancient times, particularly, the prehispanic civilizations utilized several as medicinal foods. In the current pandemic of dyslipidemia as well as the nutritional transition, particularly in Latin America, the use of native functional foods represents an attractive target for the treatment and/ or prevention of these conditions. In this mini-review, evidence regarding different functional foods such as cacao, amaranth, chia, nopal, spirulina, as well as their nutraceutical compounds, including fl avonoids, omega-3 PUFAs, fi ber, prebiotics, lovastatin, c-phycocyanin, among others, and their mechanism of action are presented and discussed. Although such foods certainly are considered as attractive potential agents to target dyslipidemia thus decrease the associated cardiometabolic risk, we conclude that for most of the presented functional foods there is currently not enough evidence to support its recommendation and every-day use.