(−)-Epigallocatechin gallate attenuates acute stress responses through GABAergic system in the brain

Adachi, Nami; Tomonaga, Shozo; Tachibana, Tetsuya; Denbow, D. Michael; Furuse, Mitsuhiro

doi:10.1016/j.ejphar.2005.12.024

Cited by 90 publications

(73 citation statements)

References 18 publications

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“…43 It is also consistent with the report that EGCG attenuates acute stress responses through GABAergic system in the brain. 44 In support for this evidence, the plasma Figure 6. Hierarchical clustering heatmap of phenotypes/immunoreactivity measurements and mice.…”

Section: Discussionsupporting

confidence: 48%

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

et al. 2014

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We have previously reported that induction of adenomyosis in mice results in progressive hyperalgesia, uterine hyperactivity, and elevated plasma corticosterone levels and that epigallocatechin-3-gallate (EGCG) treatment dose dependently suppressed myometrial infiltration and improved generalized hyperalgesia. In this study, we examined whether adenomyosis induced in mice results in the loss of GABAergic inhibition as manifested by the diminished glutamate decarboxylase (GAD) 65-expressing neurons in the brainstem nucleus raphe magnus (NRM) that could correlate with heightened hyperalgesia. We also evaluated whether EGCG treatment would reverse these changes and also improve the expression of some proteins known to be involved in adenomyosis. Adenomyosis was induced in 28 female ICR mice and additional 12 were used as blank controls, as reported previously. At the 16th week, all mice with induced adenomyosis received low-or high-dose EGCG treatment or untreated. Mice without adenomyosis received no treatment. After 3 weeks of treatment, their uterine horns and brains were harvested. The right uterine horn was used for immunohistochemistry analysis and for counting the number of macrophages infiltrating into the ectopic endometrium. The brainstem NRM sections were subjected to immunofluorescence staining for GAD65. We found that mice with induced adenomyosis had significantly diminished GAD65-expressing neurons, concomitant with heightened hyperalgesia. Treatment with EGCG increased these neurons in conjunction with improved hyperalgesia, reduced the expression of pp65, cycloxygenase 2, oxytocin receptor, collagen I and IV, and transient receptor potential vanilloid type 1 in ectopic endometrium or myometrium, reduced the number of macrophages infiltrating into the ectopic endometrium while elevated the expression of progesterone receptor isoform B. Thus, adenomyosis-induced pain resembles neuropathic pain in that there is a remarkable central plasticity.

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Section: Discussionsupporting

confidence: 48%

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

et al. 2014

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“…Meanwhile, it was also demonstrated that GABA is a dominant neurotransmitter within the hypothalamus (23). Consistant with the anatomical data mentioned above, there have also been a great number of reports about inhibited corticosterone response to stress induced by the administration of some GABA receptor agonists (13,19,24) and the enhanced CRH release induced by GABA A receptor antagonists (25).…”

Section: Discussionmentioning

confidence: 99%

Sub-Chronic Effects of s-Limonene on Brain Neurotransmitter Levels and Behavior of Rats

Zhou

Yoshioka

Yokogoshi

2009

J Nutr Sci Vitaminol

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SummaryThe present study was designed to gain insight into the effects of s -limonene on the brain after 1-wk administration. For this purpose, neurotransmitters such as dopamine (DA), serotonin (5-HT), ␥ -aminobutyric acid (GABA), glutamic acid (Glu) and some of their metabolites (DOPAC and 5-HIAA) were determined by HPLC-ECD and amino acid analyzer after 1-wk administration of s -limonene of different concentrations (0, 5, 25, 50 mg/ kg). Significant changes, such as GABA, 5-hydroxyindoleacetic acid (5-HIAA) and 5-HT, were confirmed. At the same time, basal hypothalamic-pituitary-adrenal (HPA) activity after 1-wk administration of s -limonene was evaluated by corticosterone. Considering the increment of GABA and the changes of other neurotransmitters, anti-stress effects after 1-wk administration were observed. The experimental results showed that s -limonene could inhibit HPA activity under physical stress and this anti-stress effect of s -limonene may act through the GABA A receptor. Key Words s -limonene, anti-stress effects, GABA, 5-HT, foot shock s -Limonene is a component of lemon essential oil. It has been reported that acute administration of slimonene at high concentration can relieve physical and psychological stress ( 1 ). There are other reports about its acute functions in modifying monoamine levels in rat brains and brain waves from human tests ( 2 ). In addition, some researchers have also demonstrated by the microdialysis method that lemon essential oil components could stimulate the release of acetylcholine when rats were facing persistent painful stimulation ( 3 ). From these reports, we thought that s -limonene showed potential to be used as a medical additive or substitute therapy in the pharmaceutical field for helping people troubled by stress. However, it is unknown what happens in the brain after chronic or sub-chronic administration of s -limonene.In this study, the effects of 1-wk administration of slimonene on neurotransmitters were determined, and the possible anti-stress effects were evaluated. The possible relationship between neurotransmitter changes and anti-stress effects was also explored. MATERIALS AND METHODS Animals.Wistar male rats (200-250 g) (Japan SLC, Inc., Shizuoka, Japan) were individually housed at 23 Ϯ 1˚C in a room with a 12-h light-dark cycle. Rats were given a commercial diet (stock diet: CE-2, CLEA Japan, Inc., Tokyo, Japan). Foodstuff and water were freely available. Rats in each group were only used once with one purpose. The experimental procedures were in accordance with the guidelines of the University of Shizuoka for the Care and Use of Laboratory Animals, based on those of the American Association for Laboratory Animal Science.Dose-dependent changes of neurotransmitters induced by 1-wk administration of s-limonene. Seventy-two rats were split randomly into 4 groups (18 rats per group) , with similar body weights among the groups. The rats were orally administered corn oil (1 mL/kg, vehicle) or s -limonene dissolved in corn oil (5, 25, or 50 mg/kg) accord...

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“…The identity of the primary flavonoid interacting sites in neurons is unknown and could be either at the cell surface or intracellular, although the ERK and PI3K dependence to CREB phosphorylation is very similar to ionotropic receptor signalling [133]. Receptors reported to act as flavonoid-binding sites, that are present in cortical neurons, are adenosine [79] and GABA A receptors [4,80]. However, a specific plasma membrane binding site for polyphenols has recently been described in rat brain [69].…”

Section: Extracellular Signal-regulated Protein Kinase Pathwaymentioning

confidence: 99%

The interactions of flavonoids within neuronal signalling pathways

2007

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Emerging evidence suggests that dietary phytochemicals, in particular flavonoids, may exert beneficial effects in the central nervous system by protecting neurons against stress-induced injury, by suppressing neuroinflammation and by promoting neurocognitive performance, through changes in synaptic plasticity. It is likely that flavonoids exert such effects in neurons, through selective actions on different components within a number of protein kinase and lipid kinase signalling cascades, such as phosphatidylinositol-3 kinase (PI3K)/Akt, protein kinase C and mitogen-activated protein kinase. This review details the potential inhibitory or stimulatory actions of flavonoids within these pathways, and describes how such interactions are likely to affect cellular function through changes in the activation state of target molecules and/or by modulating gene expression. Although, precise sites of action are presently unknown, their abilities to: (1) bind to ATP binding sites on enzymes and receptors; (2) modulate the activity of kinases directly; (3) affect the function of important phosphatases; (4) preserve neuronal Ca 2+ homeostasis; and (5) modulate signalling cascades lying downstream of kinases, are explored. Future research directions are outlined in relation to their precise site(s) of action within the signalling pathways and the sequence of events that allow them to regulate neuronal function in the central nervous system.

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(−)-Epigallocatechin gallate attenuates acute stress responses through GABAergic system in the brain

Cited by 90 publications

References 18 publications

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

Possible Loss of GABAergic Inhibition in Mice With Induced Adenomyosis and Treatment With Epigallocatechin-3-Gallate Attenuates the Loss With Improved Hyperalgesia

Sub-Chronic Effects of s-Limonene on Brain Neurotransmitter Levels and Behavior of Rats

The interactions of flavonoids within neuronal signalling pathways

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