EGCG and memory -
Green tea extract enhances parieto-frontal connectivity during working memory processing. Psychopharmacology , ; DOI: Cite This Page : MLA APA Chicago University of Basel. ScienceDaily, 7 April University of Basel. Green tea extract boosts your brain power, especially the working memory, new research shows.
Retrieved February 14, from www. htm accessed February 14, Explore More. Ceramic Tea Set Glazing Affects Health Benefits of Tea, Finds New Study. Now, researchers reveal that the glazing on ceramic tea sets plays a crucial role in retaining the beneficial Put the Kettle On!
How Black Tea and Other Favorites May Help Your Health Later in Life. The key is flavonoids, which are Are There DBPs in That Cup of Tea? When boiled tap water is used to brew tea, residual chlorine in the water can react with tea compounds to form Drinking Matcha Tea Can Reduce Anxiety.
July 9, Using the 'elevated plus maze' test with mice, researchers have shown that Matcha green tea can reduce anxiety.
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From inflammaging to healthy aging by dietary lifestyle choices: is epigenetics the key to personalized nutrition? Clin Epigenetics. Kuriyama S, Hozawa A, Ohmori K, Shimazu T, Matsui T, Ebihara S, et al. Citation: Gu H-F, Nie Y-X, Tong Q-Z, Tang Y-L, Zeng Y, Jing K-Q, et al. PLoS ONE 9 11 : e Editor: Jianhua Zhang, university of alabama at birmingham, United States of America.
Received: July 14, ; Accepted: October 10, ; Published: November 13, Copyright: © Gu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information files.
Funding: This work was supported by grants from the National Natural Science Foundation of China grant no. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist, and all the authors listed have approved the manuscript that is enclosed.
Accumulating evidence suggests that chronic unpredictable mild stress CUMS is a significant etiological factor for neurodegenerative disorders characterized by amyloid-β Aβ deposition [1] , neuron loss [2] , learning and memory deficits [3] , [4].
CUMS increases corticosterone secretion, which causes dysregulation of hypothalamic—pituitary—adrenocortical HPA axis and impairment of hippocampus-dependent learning and memory processes. Moreover, in humans and animals, the offspring of mothers that experience stress during pregnancy have been reported to display cognitive dysfunctions [6].
These findings suggest that chronic stress plays a critical role in the development of learning and memory impairment. The etiological role of dysregulated autophagy in cognitive dysfunctions has been a subject of intense investigation. However, the majority of present studies examining stress contributions to learning and memory deficits have focused on HPA dysfunction, tau phosphorylation and Aβ aggregation in AD transgenic mice [1] , [2] , [4] , and only few studies have focused on the role of autophagy in stress-induced memory impairment.
The macroautophagy pathway hereafter referred to as autophagy is the main degradation route for damaged organelles [7] and protein aggregates [8] , [9].
Autophagy is a highly regulated process characterized by the formation of double or multimembrane vesicles autophagosomes that sequester portions of cytosol. Autophagosome then fuses with a lysosome to form an autolysosome where the captured material is degraded together with the inner membrane.
Above dynamic process of autophagy is termed autophagic flux [10] , [11]. When autophagic flux is impaired, the subsequent accumulation of damaged organelles and protein aggregates may impair cellular functions and lead to neuronal cells death [12] , [13].
These data suggest that autophagy may be intimately associated with stress-induced cognitive dysfunctions. Thus, we investigated whether autophagy mechanism was involved in learning and memory impairment in experimental model of CUMS rats. In neurons, autophagy acts predominantly as a pro-survival pathway to protect the cells from stress [12] , [14] , [15].
Autophagic flux impairment is often associated with a number of diseases [8] , [16] , such as some forms of cancers and neurodegenerative disorders. Several studies have identified specific defects in the autophagy process in AD mouse model [7] , [17] , [18]. In fact, the strategies to restore autophagic flux were reported to prevent neuropathological and cognitive deficits in the AD mouse model [19] — [21].
These data indicate that activation of autophagy may be a therapeutic strategy in learning and memory deficits. Epigallocatechin gallate EGCG , a natural anti-oxidant flavonoid, has a variety of beneficial therapeutic roles, such as anti-inflammatory and neuroprotective effects [22] , [23].
We and others have shown that EGCG has beneficial health effects in various pathophysiological conditions including neuronal cells injury [24] and AD-related cognitive deficits [25]. Furthermore, recent research has uncovered an important role for EGCG regulation of autophagic flux in reducing intracellular lipid accumulation in hepatic [26] and vascular endothelial cells [27].
However, it remains largely unknown whether EGCG protects against CUMS-induced memory impairment in rats through its regulation of autophagic flux. In this study, we investigated the effects of EGCG treatment on the spatial learning and memory functions, pathological changes, and hippocampal autophagic flux in CUMS rats.
Here, we found that EGCG treatment could significantly alleviate CUMS-induced memory impairment in rats likely through restoring autophagic flux. Hence, pharmacological manipulation of autophagic flux by EGCG treatment may offer an alternative therapeutic approach in cognitive dysfunctions.
Antibodies against GAPDH, LC3, p62, p-mTOR Ser and p-p70S6K Thr were purchased from Abcam Cambridge, UK. Chloroquine CQ was purchased from Sigma Sigma, USA. They were allowed to acclimatize for a week before the onset of the experiment.
EGCG was dissolved in sterile saline. Rats received 28 injections of EGCG by intraperitoneally i. CQ was injected into the right lateral ventricle of the rat with a constant infusion technique. Briefly, the rats were stereotaxically implanted with the cannulas leading into the right lateral ventricle at coordinates of 0.
The rats received daily intraventricular injections of 5 µl chloroquine diphosphate salt 20 µM for 28 days. The doses of EGCG and CQ were selected based on previous studies [23] , [28]. The drugs EGCG and CQ were given 30 min before the stress exposure.
The stress scheme was slightly modified from previous study [29]. Briefly, rats in CUMS groups were exposed to different stressors, namely, h food deprivation, h water deprivation, 5-min cold swimming at 6°C , 1-min tail pinch 1 cm from the end of the tail , physically restraint for 2 h, exposure to rat odor removal of the cage containing the experimental rats from the procedure room and placing the experimental rats into cages in which cats had been held for 1 h and overnight illumination.
One of these stressors in random order was given every day for 4 weeks. The control rats were housed under identical conditions in a separate room and had no contact with the stressed animals.
After behavioral tests, rats were sacrificed and blood samples were obtained by heart puncture. Samples were centrifuged at 4°C for 30 min at rpm. The plasma corticosterone concentration was determined by solid-phase I radioimmunoassay using a commercially available reagent kit Diagnostic Products, Los Angeles, CA.
In the last week of treatment, spatial memory was assessed by the Morris water maze MWM test. The task was conducted in a circular tank 1. An 8-cm-diameter platform was placed at the center of northwest quadrant of the tank.
On the first day, all rats were trained to remember the visible platform. During the following 5 d, the hidden platform trials were used to evaluate spatial learning ability.
On each day, the rats were subjected to three trials with 10 min interval between trials. Each trial lasted for 90 s unless the rats reached the platform first. If the rats failed to escape within 90 s, they were gently conducted to the platform and allowed to stay there for 20 s. Escape latency s was recorded by video-tracking system.
On the 6th day, the platform was removed from the tank and each rat was allowed one 90 s swim probe trial. Finally, the data for the escape latency, the number of platform location crosses and percentage of time spent in the target quadrant between groups were analyzed.
After being dehydrated, the brain was embedded in paraffins. Consecutive coronal paraffin sections 4 µm were collected throughout the hippocampus according to the rat stereotaxic atlas and stained with HE. Cells that underwent morphological changes, such as pyknosis or nuclear fragmentation were excluded.
Dewaxed sections of rats of each group were washed three times 5 min each in 0. Endogenous peroxidase was deactivated by 0. These sections were washed 3 times again.
Then they were incubated with TdT at 37°C for 1 h, and incubated with antibody at 37°C for 1 h. These sections were stained by 3, diaminobenzidine DAB. After hematoxylin post-staining, they were mounted and observed under light microscope. The number of TUNEL-positive cells was counted with about cells counted per slide.
The brains were removed and immediately immersed in 2. After hippocampal CA1 region dissection, fixation was continued for 1 h at 4°C. Ultrathin sections were cut on a Reichert 2 microtome and a minimum of 10 sections from each hippocampus were observed under a transmission electron microscope JEMEX; JEOL, Tokyo, Japan.
Quantification of autophagosomes was performed as previously described [17]. Pictures were taken from randomly selected cells from each sample. For each picture, the number of autophagosomes and the total cellular area were determined and the number of autophagic structures per cell cytoplasmic area was calculated.
The immunoreaction was visualized using Amersham Enhanced Chemiluminescence Amersham Pharmacia Bio-tech, Piscataway, NJ, USA.
The densities of blots were analyzed using a scanning densitometer that was operated by Scanner Control software Molecular Dynamics, Sunnyvale, CA, USA.
Results were obtained by calculating the density using Imagequant software American Biosciences, Pittsburg, PA, USA and reported as relative optical density of the specific proteins.
After the behavioral test, rats were sacrificed, and the brains were removed. The homogenates were mixed for 3 h in room temperature and centrifuged with 15, rpm for 20 min at 4°C.
A spectrophotometer was used to read the absorbance of the plates at nm. All data were presented as mean ± SEM. Student's t-test or one-way ANOVA followed by Newman—Keuls post-hoc test PRISM software was used.
To ensure that CUMS paradigms induced sufficient stress, plasma corticosterone concentrations were determined as a means of quantifying stress. As shown in Fig. The plasma corticosterone concentrations were assayed using a radioimmunoassay as described in Methods.
The drugs EGCG and CQ were given to rats 30 min before the stress exposure. First, we performed the MWM assay to examine the effect of EGCG on CUMS-induced memory impairment.
The change in the escape latency time to reach the hidden platform was observed in this trial. MWM test was performed to evaluate spatial memory in rats. A In 5 d training trials, the escape latencies were measured to assess the rat memory ability.
B, C In the probe trial, the time spent in target quadrant and the time for rats to cross the area where the submerged platform was placed in training trails were analyzed. Next, platform was removed on day 28 to evaluate the retention of memory.
Considering the principal role of hippocampal CA1 region in the learning and memory, we examined the number and arrangement of the CA1 cells by HE staining. In the CUMS group, however, the CA1 cells were irregularly arranged.
In many of these cells, the edge, nucleus and nucleolus became ambiguous. For the number of cells in the CA1 area Fig. Conversely, these CUMS-induced abnormalities were significantly improved by EGCG treatment.
These results suggested that EGCG decreased CUMS-induced neuron loss in CA1 areas of hippocampus via restoring autophagic flux. A Representative light micrographs of HE-stained CA1 hippocampal cells.
B Statistical analyses for the number of cells in the CA1 region. Scale bar, µm. After characterization of cell number, apoptotic cells in the hippocampal CA1 region of rat were detected by TUNEL method Fig.
The TUNEL-positive cells were rarely detected in the CA1 region of the control group. In contrast, the total number of TUNEL-positive cells was obviously increased in the CUMS rats Fig. These results further indicated that EGCG decreased CUMS-induced apoptosis in CA1 regions of rats.
A The TUNEL assay was used to detect apoptotic cells in the CA1 region of rats as described in Methods.
EGCG and memory tea, qnd tea, EGCG and memory black menory EGCG and memory Shellfish-free performance foods from dried leaves of Camellia sinensisa perennial evergreen shrub. EGCG could theoretically promote brain health, but no studies have evaluated whether it can protect from cognitive decline or dementia. EGCG supplements are considered safe for most people but high doses may affect liver function. Long-term studies are lacking and no studies have evaluated whether EGCG may slow cognitive decline or prevent dementia. Our search identified:.Video
EGCG In Green Tea Linked To Better Memory EGCG and memory memorg Ding et al. This andd an open access article distributed under the terms of Annd Commons Attribution Diuretic effect on pregnancy. Postoperative cognitive mmory POCD mekory to alterations in cognitive abilities experienced by mmemory following anesthesia, affecting functions such EGCG and memory orientation, memory, attention and insight 1. Furthermore, changes in personality, social skills and other cognitive functions may have a negative impact upon patient recovery, such as extension of hospital stays and regression of quality of life 2. POCD is a common central nervous system complication affecting elderly people following surgery and presents as a mild cognitive dysfunction 2. Learning and memory are closely associated with the central nervous system, particularly with the function of the hippocampus.
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