GABA Cancer Research Results
GABA, γ-aminobutyric acid: Click to Expand ⟱
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– Some studies have reported upregulated expression of certain GABA receptor subunits (e.g., GABA_A receptor subunits) in breast tumors.
– Increased expression has been associated with enhanced cell proliferation and migration, with some reports linking this to a poorer prognosis.
-GABAergic transmission is deficient in anxiety29.
-Neurons expressing GABAA α1 receptors can mediate sedation,
-while those expressing GABAA α2 receptors mediate anxiolytic.
-In addition, extra-synaptic GABAA α5 receptors can also regulate the activity of hippocampal pyramidal cells, thereby affecting associative temporal and spatial memory
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Scientific Papers found: Click to Expand⟱
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*neuroP↑, Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties
*antiOx↑, shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects
*ROS↓, Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons
*Inflam↓, apigenin has been found to possess anti-inflammatory properties.
*TNF-α↓, inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases
*IL1β↓,
*PI3K↑, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis.
*Akt↑,
*BBB↑, Apigenin has additional neuroprotective properties due to its ability to cross the BBB and enter the brain
*NRF2↑, figure 1
*SOD↑, pigenin has also been shown to activate various antioxidant enzymes, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)
*GPx↑,
*MAPK↓, Apigenin inhibits the MAPK signalling system, which significantly reduces oxidative stress-induced damage in the brain
*Catalase↑, , including SOD, catalase, GPx and heme oxygenase-1 (HO-1) [37].
*HO-1↑,
*COX2↓, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*PGE2↓,
*PPARγ↑, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*TLR4↓,
*GSK‐3β↓, Apigenin can inhibit the activity of GSK-3β,
*Aβ↓, Inhibiting GSK-3 can reduce Aβ production and prevent neurofibrillary disorders.
*NLRP3↓, Apigenin suppresses nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation by upregulating PPAR-γ
*BDNF↑, Apigenin causes upregulation of BDNF and TrkB expression in several animal models
*TrkB↑,
*GABA↑, Apigenin enhances GABAergic signaling by increasing the frequency of chloride channel opening, leading to increased inhibitory neurotransmission
*AChE↓, It blocks acetylcholinesterase and increases acetylcholine availability.
*Ach↑,
*5HT↑, Apigenin has been shown to increase 5-HT levels, decrease 5-HT turnover, and prevent dopamine changes.
*cognitive↑, Apigenin increases the availability of acetylcholine in the synapse after inhibiting AChE, thereby enhancing cholinergic neurotransmission and improving cognitive function and memory
*MAOA↓, apigenin acts as a monoamine oxidase (MAO) inhibitor and MAO inhibitors increase the levels of monoamines in the brain
*Mood↑, All of these studies demonstrated a significant impact on behavioural problems in patients with dementia, with negligible side-effects.
*GABA↑, GABA augmentation
*Sleep↑, ambient lavender oil was as effective in controlling poor sleep patterns
*Mood↑, therapy massage with lavender oil showed a significant improvement in behaviour in the hour after treatment.
*BBB↑, A growing body of evidence confirms that the ‘orifice-opening’ effect of borneol is principally derived from opening the BBB. Borneol is therefore believed to be an effective adjuvant that can improve drug delivery to the brain
*other↑, Borneol also protects the structural integrity of the BBB against pathological damage.
*P-gp↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*toxicity⇅, Natural borneol has been extensively used in aromatherapy and in natural and cosmetic products because of its low toxicity compared to synthetic borneol, which toxicity is relatively high as it degrades slowly during storage, and noxious camphor
*BioAv⇅, In mice, a single oral dose of borneol accumulates in organs in the order of liver > brain > kidney > heart > spleen > muscle > lung, which confirms its considerably higher bioavailability in the brain than in most other organs
*Dose↑, Intranasal drug delivery can avoid gastrointestinal destruction and hepatic first-pass metabolism, resulting in rapid onset of effect and high brain bioavailability.
*ABC↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*MRP1↓, including multidrug resistance protein 1 (Mrp1), 1a (Mdr1a) and 1 b (Mdr1b),
*5HT↑, systemic borneol was found to increase the levels of histamine and serotonin in the hypothalamus
*GABA↑, and levels of l-aspartic acid, glutamate, glycine and γ-aminobutyric acid (GABA) in the corpus striatum of rats (Zhang et al., 2012).
*eff↑, Co-incubation with borneol increased the uptake of Huperzine A loaded aprotinin-modified nanoparticles by capillary endothelial cells
*BBB↑, 17 components had a good absorption due to the blood–brain barrier (BBB) limitation;
*GABA↑, further clustering analysis of active ingredient targets by network pharmacology showed that the GABA pathway with GABRG2 as the core target was significantly enriched;
*eff↑, we screened five components, methyl cinnamate, propyl cinnamate, ( +)-procyanidin B2, procyanidin B1, and myristicin as the brain synapse-targeting active substances of cinnamon
*antiOx↑, Cinnamon is multi-targeted and multi-effective and is widely used in treating AD because of its antioxidant, anti-inflammatory, antibacterial, anti-anxiety and antidepressant properties
*Inflam↑,
*Mood↑,
*BDNF↑, recent studies are analyzed that indicate an increase in BDNF levels following physical activity, particularly in young adults.
*eff↑, with the most significant effects seen in aerobic and high-intensity exercises.
*eff↑, Both acute and prolonged exercise increase BDNF, but the effect is more sustained with regular, long-term regimens.
*cognitive↑, Prolonged aerobic exercise increases BDNF and improves vascular and cognitive functions, with positive effects observed in older adults.
*memory↑, In animal models, forced and voluntary exercise increased hippocampal BDNF, improving spatial memory and synaptic function.
*BrainVol↑,
*TrkB↑, The interaction of BDNF with its receptor TrkB is involved in the processes that lead to enhancements in learning and memory associated with exercise
*GABA↑, BDNF increases the expression of markers associated with GABAergic neurotransmission, such as GABA, GAD65, and GAD67
MGO↑, MG levels rise under high-glucose conditions, such as diabetes
ROS↑, MG induces protein and nucleotide modification (advanced glycation end-products, AGEs), reactive oxygen species (ROS), and apoptosis
other↝, To combat MG's cytotoxic effects, GLO1 enzymatically converts MG into the less reactive substance, d-lactate
GABA↑, MG's mechanism of action in behavior: GABAA receptor activation
other∅, GLO1 inhibition was shown to increase MG concentration and reduce anxiety-like behavior in vivo
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*BioAv↑, It has increased bioavailability in comparison to other stilbene compounds. pterostilbene was shown to have 80% bioavailability compared to 20% for resveratrol making it potentially advantageous as a therapeutic agent
*antiOx↑, Multiple studies have demonstrated the antioxidant activity of pterostilbene in both in vitro and in vivo models illustrating both preventative and therapeutic benefits.
*neuroP↑, anticarcinogenesis, modulation of neurological disease, anti-inflammation, attenuation of vascular disease, and amelioration of diabetes.
*Inflam↓,
*ROS↓, pterostilbene reduces oxidative stress (OS) and production of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and superoxide anion (O2 −), which are implicated in the initiation and pathogenesis of several disease processes
*H2O2↓,
*GSH↑, pterostilbene have shown increased expression of the antioxidants catalase, total glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD).
*GPx↑,
*GSR↑,
*SOD↑,
TumCG↓, pterostilbene inhibit breast cancer in vitro and in vivo
PTEN↑, rats fed the blueberry diet exhibited higher mammary branching, increased nuclear immunoreactivity of tumor suppressor phosphatase and tensin homolog deleted in chromosome 10 (PTEN)
HGF/c-Met↓, blueberry extract significantly decreased human-growth-factor (HGF-) induced activation of the PI3 K/AkT/NK-κB pathway, which is implicated in breast carcinogenesis
PI3K↓,
Akt↓,
NF-kB↓,
TumMeta↓, inhibited the metastatic potential of breast cancer cells in vitro by inhibiting HGF-induced cell migration and matrix metalloproteinase-(MMP-) 2 and MMP-9 activity.
MMP2↓,
MMP9↓,
Ki-67↓, blueberry extract produced smaller tumors with decreased expression of Ki-67, a marker of cell proliferation, and increased expression of caspase-3, an apoptosis marker
Casp3↑,
MMP↓, increased mitochondrial depolarization,
H2O2↑, pterostilbene treatment increased GPx antioxidant activity and the production of H2O2 and singlet oxygen indicating a mechanism of ROS-induced apoptosis
ROS↑,
ChemoSen↑, pterostilbene treatment produced a synergistic inhibitory effect when combined with the chemotherapy drug Tamoxifen, demonstrating clinical potential in the treatment of breast cancer
*cardioP↑, blueberries, and pterostilbene alike, exhibit protective effects against cardiovascular disease possibly due to induction of antioxidant enzymes.
*CDK2↓, Pterostilbene also produced downregulation of the cell-cycle mediators, cyclin-dependent kinase (CDK)-2, CDK-4, cyclin E, cyclin D1, retinoblastoma (Rb), and proliferative cell nuclear antigen (PCNA), all of which promote unchecked VSMC proliferation
*CDK4↓,
*cycE/CCNE↓,
*cycD1/CCND1↓,
*RB1↓,
*PCNA↓,
*CREB↑, The authors found that treatment with blueberry extract decreased dopamine- (DA-) induced upregulation of the oxidative mediators, CREB and pPKCγ, indicating a significant antioxidant effect
*GABA↑, blueberry-fed aged rats had significant improvements in GABA potentiation and increased GSH compared to aged controls
*memory↑, 1- or 2-month blueberry diet showed significantly higher object memory recognition compared to control rats
*IGF-1↑, supplementation with blueberry extract was shown to enhance hippocampal plasticity and increase levels of insulin-like growth factor (IGF-) 1, IGF-2, and ERK resulting in improved spatial memory
*ERK↑,
TIMP1↑, increased endogenous tissue inhibitors of metalloproteinases (TIMPs)
BAX↑, ↑Bax, ↑cytochrome C, ↑Smac/Diablo, ↑MnSOD
Cyt‑c↑,
Diablo↑,
SOD2↑,
*BDNF↑, PCR (qPCR) showed that diabetic rats presented lower α2 GABAA subunit and BDNF mRNA expression than non-diabetic rats and taurine increased both parameters in these sick rats.
*GABA↑,
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*ROS↓, prevention of oxidative stress, and inflammation.
*Inflam↓,
*GABA↑, It serves as an agonist of GABAA receptors and, through them, exerts its neuronal inhibitory, anxiolytic, and calming effect
*memory↑, Consequently, taurine promotes emotional learning ability, memory, and cognitive performance
*cognitive↑,
*iNOS↓, It reduces inducible nitric oxide synthase (iNOS), C-reactive protein (CRP),
*CRP↓,
*HO-1↑, In parallel, it increases the expressions of cytoprotective antioxidant proteins, such as heme oxygenase 1 (HO-1), peroxiredoxin (PRX), and thioredoxin (TRX), in macrophages [74].
*Prx↑,
*Trx↑,
*NRF2↑, inhibits reactive oxygen species by Kelch-like ECH-associated protein 1 (Keap-1)/nuclear factor erythroid-2-related factor (Nrf2)/heme oxygenase-1 (HO-1) pathway
*GSH↑, enhanced liver antioxidant capacities via glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), and catalase (CAT), decreased lipid peroxidation and malondialdehyde (MDA) levels [
*SOD↑,
*Catalase↑,
*lipid-P↓,
*MDA↓,
*eff↝, Similar to free taurine [62,63,64], TUDCA has proven neuroprotective properties which were researched in the models of Alzheimer’s disease (AD)
*GutMicro↑, taurine has been associated with inhibited growth of harmful bacteria, including Proteobacteria and especially Helicobacter, and also increasing the production of SCFA in mouse feces [351] as well as the metabolism of taurine by microbiota
other↑, Similarly, taurine plays a protective role in acute ischemic stroke
*neuroP↑, neuroprotective action of taurine is blocked by picrotoxin, an antagonist of GABA(A) receptors
*GABA↑, activation of GABA receptors decreases neuronal vulnerability to excitotoxic damage and that pharmacological manipulation of the excitatory and inhibitory neurotransmitter tonus may protect neurons against a variety of insults.
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*antiOx↑, Taurine has antioxidative, osmoregulatory, and anti-inflammatory functions, among other cytoprotective properties.
*Inflam↓,
*Ca+2↓, Taurine intracellular effects are directed toward calcium homeostatic pathway, reducing calcium overload and thus preventing excitotoxicity, mitochondrial stress, and apoptosis.
*neuroP↑, significant relationship between taurine and astrocytes, as well as its homeostatic and neuroprotective role in the nervous system.
*other↑, taurine has been proposed as a novel therapeutic agent for many human diseases including stroke, epilepsy, neurodegenerative diseases like Alzheimer’s disease (AD)
*Dose↝, concentration declines with age, with decreasing values that range from 4–20 μmol/g during development to 1–9 μmol/g at adulthood
*PKCδ↓, taurine’s inhibitory effect on the protein kinase C (PKC), thereby blocking the phosphorylation and activation of voltage-gated calcium channels (VGCC), and therefore, decreasing calcium influx
*VGCC↓,
*GABA↑, may have a similar effect as GABAB receptors, so that its activation by taurine may lead to the activation of coupled inhibitory G-proteins,
TumCP↓, thymoquinone can inhibit cancer cell proliferation through disruption of the PI3K/AKT pathway by upregulating phosphatase and tensin homolog
*antiOx↑, thymoquinone improve antioxidant enzyme activities, effectively scavenges free radicals, and thus protect cells from oxidative stress.
*ROS↓, modulate reactive oxygen species levels in tumor cells,
NRF2↑, regulate responses to oxidative stress and inflammation via Nrf2 and NF-κB pathways
NF-kB↓, Inhibits inflammatory response
TumCCA↑, arrest the cell cycle in the G2/M phase
*GABA↑, N. sativa and thymoquinone can elevate brain GABA content, and thus it may ameliorate epilepsy
P53↑,
P21↑,
AMPK↑,
neuroP↑, thymoquinone, exhibit various pharmacological activities, including neuroprotective, nephroprotective, cardioprotective, gastroprotective, hepatoprotective, and anti-cancer effects.
cardioP↑,
hepatoP↑,
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
H2O2↑, 1, MGO↑, 1, NRF2↑, 1, ROS↑, 2, SOD2↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1,
Cell Death ⓘ
Akt↓, 1, BAX↑, 1, Casp3↑, 1, Cyt‑c↑, 1, Diablo↑, 1, HGF/c-Met↓, 1,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 1, other∅, 1,
DNA Damage & Repair ⓘ
P53↑, 1,
Cell Cycle & Senescence ⓘ
P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1, PTEN↑, 1, TumCG↓, 1,
Migration ⓘ
Ki-67↓, 1, MMP2↓, 1, MMP9↓, 1, TIMP1↑, 1, TumCP↓, 1, TumMeta↓, 1,
Immune & Inflammatory Signaling ⓘ
NF-kB↓, 2,
Synaptic & Neurotransmission ⓘ
GABA↑, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1,
Clinical Biomarkers ⓘ
Ki-67↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, hepatoP↑, 1, neuroP↑, 1,
Total Targets: 35
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 5, Catalase↑, 2, GPx↑, 2, GSH↑, 2, GSR↑, 1, H2O2↓, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 1, NRF2↑, 2, Prx↑, 1, ROS↓, 4, SOD↑, 3, Trx↑, 1,
Core Metabolism/Glycolysis ⓘ
CREB↑, 1, PPARγ↑, 1,
Cell Death ⓘ
Akt↑, 1, iNOS↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1, other↑, 2,
DNA Damage & Repair ⓘ
PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, RB1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, GSK‐3β↓, 1, IGF-1↑, 1, PI3K↑, 1, VGCC↓, 1,
Migration ⓘ
Ca+2↓, 1, PKCδ↓, 1,
Barriers & Transport ⓘ
BBB↑, 3, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, CRP↓, 1, IL1β↓, 1, Inflam↓, 4, Inflam↑, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↑, 2, AChE↓, 1, BDNF↑, 3, BrainVol↑, 1, GABA↑, 11, MAOA↓, 1, TrkB↑, 2,
Protein Aggregation ⓘ
Aβ↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
ABC↓, 1, BioAv↑, 1, BioAv⇅, 1, Dose↑, 1, Dose↝, 1, eff↑, 4, eff↝, 1, MRP1↓, 1,
Clinical Biomarkers ⓘ
CRP↓, 1, GutMicro↑, 1,
Functional Outcomes ⓘ
cardioP↑, 1, cognitive↑, 3, memory↑, 3, Mood↑, 3, neuroP↑, 4, Sleep↑, 1, toxicity⇅, 1,
Total Targets: 70
Scientific Paper Hit Count for: GABA, γ-aminobutyric acid
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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