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Green Tea Extract (EGCG) How does it work?EGCG and depression -
f,g Western blot of GluN2B levels in brain lysate for total and synaptoneurosomal fraction from hippocampus. i , j Quantitative real-time PCR. Data represent the BDNF and GluN2B gene expressions normalized to GAPDH gene.
To compare the compositions of catechins in HTP-GTE and GTE in detail, we analyzed the constituents of both green tea derivatives by Ultra-performance liquid chromatography photometric diode array UPLC-PDA.
As shown in Table S1 , EGCG and EGC were the major catechins present in both conventional green tea GTE and modified green tea HTP-GTE. However, the levels of GCG and CG i. epimers of EGCG and EGC, respectively were much higher in HTP-GTE than in GTE.
Firstly, each rat was individually fed with GCG, CG, EGCG, or HTP-GTE containing no GCG i. GCG-free HTP-GTE , and exposed to the protocol shown in Fig. S2 , so that we can independently assess the effect of each HTP-GTE catechin component on the LH models of OVX rats. Each animal group was subsequently tested for the escape behaviors to evaluate the induction of LH.
S12 a,b, the administration of GCG and EGCG, and not CG or GCG-free HTP-GTE, significantly increased the rodent resilience against LH in OVX rats. This is an important finding to primarily indicate that HTP-GTE-induced resilience against LH in OVX rats is due to either GCG or EGCG.
Therefore, in the current study, we designed our experimental protocols to use the resilient rats only in the GCG- or EGCG-fed groups.
Meanwhile, the helpless OVX rats were enrolled into two groups to study the CG-only HTP-GTE or GCG-free HTP-GTE-fed effects.
To identify the major active components of the HTP-GTE effect, we investigated the effects of equivalent doses of GCG 5.
Consistent with the results shown in Figs. Notably, only GCG-fed OVX rats exhibited a significant recovery of the suppressed hippocampal BDNF expressions while neither CG-fed nor EGCG-fed OVX rats showed any changes in BDNF expressions. In addition, GCG-free HTP-GTE-fed OVX rats showed no statistically significant alteration in the hippocampal BDNF expressions when compared with the helpless OVX rats Fig.
Administration of GCG nearly completely rescued impairment of LTP induction at SC-CA1 synapses in OVX rats, but CG, EGCG, and GCG-free HTP-GTE treatment showed little effect Fig.
Similarly, the exogenous administration of GCG restored LTP induction to sham-OVX resilient control levels, as observed in the acute hippocampal slices from the helpless OVX rats.
These results suggested that both GCG and EGCG are effective in promoting and maintaining resilience against the induction of depression by LH protocol, but GCG on its own was by far more potent in recovering the depression-related synaptic impairments than EGCG.
In an attempt to further evaluate the effects of HTP-GTE and its major active component, GCG, on memory and learning which are usually malfunctioning during depression , all animal groups were trained to find the hidden platform in a water pool for 4 days, and the Morris water maze test was performed on the 5th day.
On the other hand, the oral administration of HTP-GTE or GCG in the OVX rats significantly restored their ability to perform the tasks to the level of sham-OVX resilient controls. Akin to this finding, GCG-free HTP-GTE had no effect on the improvement of performance, and this further emphasizes the fundamental role of GCG as the major active substance in HTP-GTE underpinning the HTP-GTE-induced rescue of synaptic and cognitive impairments in postmenopausal depression.
GCG, not EGCG, plays a role as a major contributor to HTP-GTE-induced improvement of synaptic and cognitive impairments in helpless OVX rats. c—h Top: representative traces showing EPSPs before average of 20 traces, black line and after average of traces, red line high-frequency stimulus.
Bottom: average time courses for EPSP amplitude during LTP induction on all groups. j Morris water maze learning curves of 4 consecutive days. m—q Representative Morris water maze movement track from all groups. LH is mediated by the failure to learn behavioral responses induced by inescapable aversive events.
Hippocampus, the primary locus for learning and memory, has been known to play a major role in the development of LH where it is associated with its own functional and anatomical changes 38 , 60 , LH can occur with inescapable stress, which disrupts hippocampal LTP induction in vivo.
However, cumulative evidences have raised questions regarding the role of the hippocampus in the development of depression.
Passive response to inescapable shock is mediated by the serotonergic activity of the dorsal raphe nucleus DRN , which results in escape failure. This passivity is overcome by learning control via the ventromedial prefrontal cortex vmPFC , which inhibits DRN activity, making the rats possible to learn the fact that an escape from aversive stress is possible.
Thus, the alterations in the vmPFC-DRN pathway serve as the main influence on the development of LH Consistent with these findings, we showed that both EGCG and GCG can effectively increase the resilience to escape the stress against foot shock-induced LH; however, only GCG can ameliorate hippocampal synaptic dysfunction and cognitive deficits induced by LH, and this difference between EGCG and GCG was clearly observed in Morris water maze tests in our results Figs.
These results demonstrated that the failure of escaping behavior due to LH is mediated by a neural circuit, which is different from the hippocampal circuit responsible for the cognitive impairments by LH. Likewise, the administration of GCG is more effective in ameliorating depression-induced behavior than EGCG.
Although many studies have stressed the role of hippocampal synaptic plasticity as a possible mechanism underlying the cognitive impairment commonly accompanying depression 14 , 15 , 16 , 17 , a detailed synaptic and molecular mechanism remains to be elucidated.
In the present study, we provided a possible mechanism to account for depression-induced cognitive deficits in terms of synaptic plasticity for the first time. The proportion of silent synapses containing NMDA receptor, but not AMPA receptor, in the hippocampus is significantly reduced in a PMD rodent model Fig.
In addition, the reemergence of silent synapses serves as the fundamentally mandatory mechanism for HTP-GTE-induced restoration of LTP in the hippocampus of a depressive animal model Figs. BDNF plays a pivotal role in regulating a long-term synaptic plasticity in the hippocampus 48 , 49 , 50 , and the down-regulation of BDNF levels contributes to the depression-related cognitive impairments 5 , 51 , 52 , Concurrently, GluN2B-containing NMDA receptor plays a critical role in the formation and maintenance of silent synapses 58 , However, GluN2B deletion increases the number of functional synapses, which in turn prevents premature synapse maturation until correlated activity allows the induction of functional synapses Despite this circumstantial evidence indicating the involvement of BDNF in GluN2B-mediated regulation of silent synapses, the evidences to elucidate the relationship between BDNF and silent synapse formation has not yet been provided.
In this study, we demonstrated that hippocampal BDNF expression is notably reduced in the helpless OVX rats, and that the suppressed BDNF-TrkB signaling pathway interferes with the hippocampal GluN2B expression, resulting in the reduced formation of silent synapses in the helpless OVX rats.
Taken together, HTP-GTE rescues the dysfunctional long-term plasticity by reversing this process by increasing the hippocampal GluN2B expressions through the activation of BDNF-TrkB signaling pathway in the helpless OVX rats.
In conclusion, we developed a modified green tea extract, HTP-GTE, which is safer and more bioactive than conventional green tea extract. We demonstrated its therapeutic efficacy in overcoming postmenopausal depression as well as improving the cognitive dysfunctions associated with it. We also elucidated the potential mechanism underlying the effect of HTP-GTE by identifying GCG as a major bioactive component responsible for the effect.
Our findings suggest that GCG-based green tea derivatives may serve as a potential therapeutic agent to prevent or ameliorate the cognitive deficits induced by postmenopausal depression.
Female Sprague—Dawley rats 6-week-old, — g were randomized by weight and housed in cages. and lights off at 7 p. The animals were initially distributed into two groups: placebo surgery Sham and ovariectomized OVX groups.
On post-operative day 3, the OVX group was subdivided into three more groups which received vehicle 0. Animal care was performed in accordance with the Yonsei University College of Medicine Animal Care Project license number: 00,; — and all experimental protocols were approved by Yonsei University College of Medicine and use Committee or the NIH Guide for the Care and Use of Laboratory Animals.
Fresh green tea Camellia sinensis, CS leaves were collected in spring from Osulloc Tea Garden in Jeju, Korea and were dried at °C for 10 min. Bioactive components in HTP-GTE were determined by UPLC with a PDA detector using a Zorbax Eclipse XDB C18 column 2. The mobile phases were 0.
The mobile phase flow-rate was 1. Primary hippocampal neuronal cell culture was produced and maintained using a method described previously 3 , with some modifications.
All experiments were performed in accordance with the Yonsei University College of Medicine Animal Care and Use Committee or NIH Guide for the Care and Use of Laboratory Animals.
Briefly, primary hippocampal neuron cultures were prepared from Sprague—Dawley rat embryos embryonic day 18 of either sex. The hippocampi were dissected and the cells were dissociated by trituration using a fire-polished Pasteur pipette. The cells were then plated onto cover glasses coated with poly-L-lysine.
The test group of female rats underwent ovariectomy ovaries removed by surgical method and the other group underwent sham surgery the skin was cut and sewed back in place. The surgery consisted of a dorsolateral incision of the skin between the last rib and pelvis and muscle dissection to expose periovarian fat.
Forceps were used to find the ovaries surrounded by variable amount of fat. The ovary was pulled out and the junction between the fallopian tube and uterine horn was cut. Bleeding was usually light and stopped soon. The horn and periovarian fat were returned into the abdominal cavity.
The muscle wound was first sutured shut and the skin incision was closed. In sham surgery, the rats underwent the same incision but no ovaries were removed. To reduce pain, ketoprofen 2. The rats in the shock-exposed group received inescapable and unpredictable foot shock in an electric foot shock chamber The shock chamber was equipped with metal rod stainless steel flooring connected to a shock generator and a shock control box LE, LE; Panlab, Barcelona, Spain.
Inescapable foot shocks were delivered to rats repeatedly 50 times at an amplitude of 0. Learned helplessness LH was assessed 24 h after the third shock procedure by testing escape performance, which comprised 30 escape trials. Each trial adopted a single 0.
Each trial was terminated when the rat escaped to the non-shock side of the shuttle box or the maximum duration 15 s was reached. Thirty shocks lasting for 15 s each were applied with an inter-trial time of 20 s.
The rats with more than 20 escape failures in the 30 trials were regarded as being "helpless" and as having attained a state of learned helplessness 36 , In vivo Toxicity test was carried out in compliance with the OECD Guidelines for the testing of chemicals, Acute Oral Toxicity — Fixed Dose Procedure No.
All rats were given a single oral dose of test articles after a h fasting period. All visible signs of reaction to treatment and mortality were recorded daily.
On the first day of treatment for each dose level, the animals were observed at the following approximate time points: at the end of dosing and 0. Then, body weights were recorded on the day of dosing, Day 1,4, 7, 10, 13, 16, 19, 22, 25 and At the end of the observation period all animals were euthanized by a CO 2 gas overdose.
In terms of necropsy and gross pathology, any abnormalities were recorded, including details of location, color, shape, and size, and then appropriately sampled and identified.
In vitro toxicity test was done as follows. Cell viability was measured by the CCK-8 assay Dojindo laboratories, Shanghai, China.
At h post-treatment with vehicle [dimethyl sulfoxide DMSO ], conventional green tea extract GTE , or modified GCG-enriched green tea extract HTP-GTE , the cells were incubated with 10 μL CCK-8 reagent for 2 h at 37 °C.
The optical density was measured at a wavelength of nm using a microplate reader Molecular devices, San Jose, CA, USA. Cell viability was calculated by dividing the optical density of the treated group by that of the control group. At 2-h post-treatment with GTE or HTP-GTE, the medium was carefully replaced with fresh neurobasal medium containing dilute MTT Sigma Aldrich, St.
After removing the incubation medium, the formazan crystals were dissolved in μL DMSO. MTT reduction was quantified by measuring the light absorbance at nm using the microplate reader The cell viability was calculated by dividing the optical density of the treated group by that of the control group.
Hippocampal slices μm thick were prepared from learned helplessness LH -tested week-old female Sprague Dawley rats. After perfusion, the brains were quickly removed from the skull and slices were cut on a vibratome Leica biosystems, Wetzlar, Germany. The slices were transferred to an incubation chamber containing incubation solution with the following concentrations in mM: NaCl, 2.
After incubation, the slices were transferred to a container filled with aCSF solution at 23—24 °C for 1 h. Field recordings were made with a concentric bipolar electrode positioned in the stratum radiatum of the CA1 region using an extracellular glass pipette 3—5 MΩ filled with aCSF.
Stimulation was delivered through a bipolar electrode FHC, Bowdoin, ME, USA placed in the Schaffer collateral-CA1 SC. Baseline synaptic responses were recorded for 30 min, and then long-term potentiation LTP was induced by high-frequency stimulation HFS; Hz, 4 trains, 1 s duration, 20 s inter-train interval.
Recordings were made every 10 s for 1 h using Axopatch 1D amplifier Molecular Devices, San Jose, CA, USA digitized at 10 kHz, and filtered at 2 kHz with Digidata A and pClamp For the minimal stimulation experiment, the lowest intensity was found to induce a combination of synaptic responses and failures by adjusting the SC stimulation intensity.
The criterion of single axon stimulation was co-initiation or no response, and the average EPSC amplitude remained unchanged because of the small increase in stimulus intensity 4 , 5.
To measure miniature EPSCs, the electrode was filled with internal solution concentration in mM: Cs methanesulfonate, 8 NaCl, 10 HEPES, 0. Miniature currents were recorded in the presence of tetrodotoxin 1 μM TTX, Tocris, Bristol, England to block sodium currents and propagate action potentials.
Spontaneous firing was recorded in the cell attached mode from CA3 principal cells and stratum radiatum interneurons. Total lysate and synaptoneurosome SN were prepared from the hippocampus.
The isolated hippocampus was homogenized with 0. The resulting supernatant total lysate was stored, and the remaining pellets were re-suspended with 0. To lyse the sample, the pellets were re-suspended in dd H 2 O in order to provide a hypo-osmotic shock, transferred to a glass—Teflon tissue homogenizer, and homogenized rapidly by hand 3 strokes.
The sample was transferred to a new collection tube, suspended in 4 mM HEPES solution prepared by the addition of 1 M HEPES, and rotated for 30 min at 4 °C to ensure complete lysis. Pellets were re-suspended in 0. Protein concentration was determined using a BCA Protein Assay Kit Thermo Fisher Scientific, Waltham, CA, USA.
Louis, MO, USA , BDNF Alomone, Jerusalem, Israel , and β-actin for normalization SCBT, Dallas, TX, USA. All full blots are represented in Figs. S13 , S The Superscript III First-strand synthesis system for RT-PCR kit Invitrogen, Carlsbad, CA, USA was used for the Real-Time PCR analysis to see the expression levels of BDNF and GluN2B.
The reaction carried out in a system of 10 μl, containing 50 ng cDNA templates, specific primers 2. The amplification procedures were performed in Applied Biosystems real-time PCR system Applied Biosystems, Foster City, CA, USA. The expression levels of the target genes were calculated using 2 -ΔΔCt method.
The rats were trained in the water maze to find a hidden platform for 6 consecutive days. On the first day, the trial began by placing the rats into the tank facing the mark on the wall at one of the four quadrants and ended when the rats climbed on the platform. If the rats were not able to find the platform within 1 min, they were guided to the platform and allowed to stay on the platform for 10 s only once.
From the second day to the fifth day, the trial began by placing the rats into the tank facing the same mark as in the first day trial and were evaluated for their ability to find the platform in 2 min. Four trials were conducted per day with a min interval.
On the sixth day of the test, the hidden platform was removed. The percentage of time spent in the target quadrant and the platform crossing number were recorded using a video camera and tracking data were visualized by EthoVision XT software Noldus, Wageningen, Netherlands.
In brief, the brain was immersed in 10 mL of a mixture containing equal amounts of solution A and B and stored at 23—24 °C for 2 weeks with gentle agitation. The brain was then transferred to solution C, stored at 4 °C for 48 h, and then frozen in optimal cutting temperature OCT compound at °C for 12 h.
Brain sections with μm thickness were dissected with dry ice using a cryostat microtome. Each section was mounted onto a slide and allowed to dry naturally at room temperature. In the next step, the slide was stained with a solution a mixture of solution D, E, and distilled water in a ratio for 5—10 min, and washed with distilled water twice for 5 min each.
Finally, the slides were visualized using a Zeiss LSM confocal microscope Carl Zeiss, Jena, Germany. Confocal z-series image stacks encompassing entire dendrite segments were analyzed using MetaMorph software Molecular Devices, San Jose, CA, USA. To measure dendritic spine density, we evaluated the dendritic segments 50 μm from the first branch of main axon from soma of the hippocampus CA1.
Spines 0. Rotarod tests were performed to compare motor dysfunction before and after ovariectomy or electrical shock, animals were tested on the rotarod B. S Technolab, Daejeon, Korea.
Before ovariectomy, they had time for adaptive training sessions first 5 RPM, 5 min and three consecutive sessions under an accelerating speed 5—40 RPM, s. The day after electric shock for learned helpless test, rotarod performance was evaluated with three sessions under accelerated speed as described above.
Each group were exposed to the rod three times for training before taking the test. For each of the test, results are expressed as the mean latency to fall for trials.
The 17β-estradiol levels were detected by chemilluminescence. An estradiol ELISA kit Enzo life sciences, Farmingdale, NY, USA was used to detect the level of corresponding substances.
The results were detected with Multiskan sky microplate spectrophotometer Thermo Fisher Scientific, Waltham, MA, USA. Statistical comparisons were made using the two-tail unpaired t test to compare the two independent group means.
Kolmogorov—Smirnov two-sample test was used to compare the cumulative distributions of two data sets Figs. Data were analyzed using Prism software GraphPad, La Jolla, CA, USA. All data generated or analysed during this study are included in this published article and its Raw data zip file.
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Henn, F. Check out CONTINUE SHOPPING. Blayne Andrews. HOW EGCG MAKES YOU HEALTHIER, AND THE BEST WAYS TO TAKE IT. If you drink tea or have looked into its benefits, you might have stumbled across some of these benefits being attributed to something called EGCG.
EGCG is a plant compound that is generally most concentrated in green tea. It is also found in white, oolong, and black tea, as well as in small amounts in certain foods.
These positive effects of EGCG can be found in simple bags of green tea. What is EGCG? EGCG also known as epigallocatechingallate is the main and most significant green tea polyphenol. The benefits associated with tea consumption are believed to be due to this polyphenolic compound and other related green tea catechins.
EGCG is also a potent antioxidant that helps suppress inflammation by neutralizing free radicals. This is important because an increasing amount of evidence has shown that chronic inflammation causes and advances many common diseases.
EGCG has been shown to have cancer-protective effects. It achieves this through its interaction with a protein called p This protein is a gene that essentially creates blueprints for the creation of proteins involved with the death of cancer cells in healthy individuals.
Cancer itself knows how to turn this gene off so it can continue to grow. This weakens our own innate defense mechanism against cancer cells and gives them a more suitable environment to thrive.
EGCG has also been shown to starve cancer cells by inhibiting a growth factor that promotes the formation of new blood vessels. By inhibiting this, you can take away the fuel that these cells need to survive.
Can EGCG support brain health? Yes, another benefit of EGCG is its ability to help support brain health. Brain health is imperative to overall health. One of these ways is through drinking green tea. When it clumps together and misfolds it can cause amyloid plaques. Getting adequate EGCG may also help support your mental health.
There is a new scientific theory of depression being presented in recent years. But researchers are starting to find that inflammation can play a role in mental health as well.
This theory explains that inflammatory cytokines a type of signaling molecule can pass through the blood-brain barrier and cause symptoms of depression. EGCG has been shown to have an anti-inflammatory effect by decreasing inflammatory cytokine production. These studies are still preliminary, but a start to a larger conversation.
The aim of this study is to ahd the antidepressant-like effect ddpression EGCG and get deeper insights into implications of modulating serotonin sepression in the colon and depressikn. Before conducting andd designed set EGCG and depression behavior tests, Autophagy and neurodegeneration rats were EGCG and depression depresdion then forced swimming test FST znd open field test OPT were EGCG and depression in all rats for the measurement and analysis of EGCG and depression depreseion colonic serotonin levels. In order to determine the extent of CUMS-induced injuries and examine neurological deficits, the method of Nissl staining was implemented accordingly. The study found that, due to the involvement of CUMS, the body weight of experimental rats declined, their time of immobility in FST was greater, and the avoidance of central sections in OPT was also greater and more obvious. However, through intervention of the EGCG treatment, either weight loss or depression-related behavior induced by the involvement of CUMS was alleviated in the experimental rats. However, it should be noted that the level of 5-HT in peripheral blood did not show any significant difference between both groups. Furthermore, CUMS caused the morphological changes of the hippocampus and structural changes of the colon were noteworthy.
EGCG and depression -
This article is part of Nature Outlook: Tea , an editorially independent supplement produced with the financial support of third parties. About this content. Kim, J.
Nutrients 10 , Article Google Scholar. Feng, L. Health Aging 14 , — Article PubMed Google Scholar. Steptoe, A. et al.
Psychopharmacology , 81—89 White, D. Nutrients 8 , 53 Haskell, C. Scholey, A. Appetite 58 , — Camfield, D. Download references. The growth of tea.
Culturing better tea research. How climate change might affect tea. Genomic focus brings tea research to the boil. Brewing nanotechnology from tea. Article 14 FEB Career News 06 FEB Comment 06 FEB Summarily, the investigation results of this experimental study indicated that the intervention of EGCG treatment might have considerable implications in several aspects such as anti-depression, regulation of 5-HT concentration, enhancement of intestinal hyper-permeability, and neuroprotection in the hippocampus.
Abstract The aim of this study is to examine the antidepressant-like effect of EGCG and get deeper insights into implications of modulating serotonin 5-HT in the colon and brain.
Substances Antidepressive Agents Serotonin Catechin epigallocatechin gallate. This protein is a gene that essentially creates blueprints for the creation of proteins involved with the death of cancer cells in healthy individuals.
Cancer itself knows how to turn this gene off so it can continue to grow. This weakens our own innate defense mechanism against cancer cells and gives them a more suitable environment to thrive. EGCG has also been shown to starve cancer cells by inhibiting a growth factor that promotes the formation of new blood vessels.
By inhibiting this, you can take away the fuel that these cells need to survive. Can EGCG support brain health? Yes, another benefit of EGCG is its ability to help support brain health. Brain health is imperative to overall health. One of these ways is through drinking green tea.
When it clumps together and misfolds it can cause amyloid plaques. Getting adequate EGCG may also help support your mental health.
There is a new scientific theory of depression being presented in recent years. But researchers are starting to find that inflammation can play a role in mental health as well. This theory explains that inflammatory cytokines a type of signaling molecule can pass through the blood-brain barrier and cause symptoms of depression.
EGCG has been shown to have an anti-inflammatory effect by decreasing inflammatory cytokine production. These studies are still preliminary, but a start to a larger conversation. For more information on tea's mental health benefits, check out Can Drinking Tea Help PTSD Symptoms? Tips for boosting EGCG Green tea is the best natural source of EGCG.
Matcha is a particularly potent variety. Black tea provides less EGCG than other tea varieties but more than most foods.
Thank you for EGCG and depression nature. You deprssion using EGCG and depression browser version with EGCG and depression ddepression for CSS. To obtain the Boost Vitality Levels experience, we EGCG and depression you use a depressioj up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Post-menopausal depression PMD is a common psychological disorder accompanied by a cognitive deficit, which is caused by a series of uncontrolled emotional disruptions by strong environmental stressors during menopause. Epigallocatechin 3-gallate EGCG is a natural polyphenolic antioxidant in green tea depressino with well-known health-promoting EGCG and depression. However, EGCG and depression influence depressino EGCG on a chronic Non-GMO diet pills model of depression remains to be fully investigated, and the details of the molecular and cellular changes are still unclear. Therefore, the present study aimed to investigate the antidepressant effect of EGCG in mice subjected to chronic unpredictable mild stress CUMS. by oral gavage for two weeks. A forced swimming test FST was used to assess depressive symptoms.
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