5HT Cancer Research Results

5HT, Serotonin: Click to Expand ⟱
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Serotonin (5-hydroxytryptamine or 5-HT) is best known as a neurotransmitter; however, it also plays diverse roles in peripheral tissues, including modulation of cell proliferation, angiogenesis, and immune responses.

Several studies have identified the expression of multiple 5-HT receptors (e.g., 5-HT1A, 5-HT2A, and 5-HT7) in breast cancer cells.
Serotonin may promote tumor cell proliferation and can influence breast cancer progression through receptor-mediated signaling pathways.

Expression of 5-HT and its receptors is documented in various cancers including breast, colorectal, pancreatic, prostate, and hepatocellular carcinoma.
Overexpression of particular 5-HT receptors often correlates with increased cell proliferation, angiogenesis, and metastatic potential.
High levels of 5-HT receptor expression generally serve as a marker for poor prognosis, although the exact prognostic implications vary depending on the specific receptor subtype and tumor type.

-Vomiting caused by chemotherapy was thought to result from the fact that the chemotherapeutics stimulated the secretion of 5-HT in intestinal chromaffin cells, and then 5-HT acted on 5-HT receptor which caused excitation of nerves and vomiting reflex.
Scientific Papers found: Click to Expand⟱
3537- 5-HTP,    5-Hydroxytryptophan: a clinically-effective serotonin precursor
- Review, NA, NA
*5HT↑, effective serotonin precursor
*BioAv↑, 5-HTP is well absorbed from an oral dose, with about 70 percent ending up in the bloodstream.
*BBB↑, It easily crosses the blood-brain barrier and effectively increases central nervous system (CNS) synthesis of serotonin

3538- 5-HTP,    Oral Administration of 5-Hydroxytryptophan Restores Gut Microbiota Dysbiosis in a Mouse Model of Depression
- in-vivo, Nor, NA
*GutMicro↑, The diversity and richness of gut microbial communities and relative abundance of specific microbial taxa at both phylum and genus levels were partially recovered.
*BBB↑, 5-HTP, a precursor of 5-HT, can easily cross the blood-brain barrier without requiring a transporter and increase the brain 5-HT levels to yield an antidepressant-like effect
*5HT↑, capacity to increase the brain and gastrointestinal tract 5-HT levels after oral administration
*Weight↓, 5-HTP could reduce the body weights of both healthy mice and mice with depression-like behaviors.

5308- 5-HTP,    The Relationship Between Serotonin and 5-HTP
- Review, Nor, NA
*5HT↑, 5-HTP is the precursor for neurotransmitters, which are chemicals that transmit a nerve impulse across neuronal gaps that are called synapses. These neurotransmitters include serotonin and melatonin.

5303- 5-HTP,    5-HTP shows early promise for cognitive support and in seniors: Singapore study
- Trial, AD, NA
*cognitive↑,
*Dose↝, 100mg nightly
*5HT↑,

5295- 5-HTP,    Safety of 5-hydroxy-L-tryptophan
- in-vivo, Nor, NA
*5HT↑, 5-Hydroxy-L-tryptophan (5-HTP) is the immediate precursor in the biosynthesis of 5-hydroxy-tryptamine (5-HT; serotonin) from the essential amino acid L-tryptophan (L-Trp).
*toxicity↝, The use of L-Trp as a dietary supplement was discontinued in 1989 due to an outbreak of eosinophilia-myalgia syndrome (EMS) that was traced to a contaminated synthetic L-Trp from a single manufacturer.
*toxicity↓, However, no definitive cases of toxicity have emerged despite the worldwide usage of 5-HTP for last 20 years, with the possible exception of one unresolved case of a Canadian woman.

5293- 5-HTP,    The Role of Tryptophan Metabolism in Alzheimer’s Disease
- in-vivo, AD, NA
*Sleep↑, Finally, trp and various metabolites, including melatonin, are regulators of sleep, with disorders of sleep being an important risk factor for the development of AD.
*5HT↑, Figure 1. Conversion of tryptophan to serotonin.
*memory↑, Sleep has important roles in learning and memory consolidation. Not surprisingly, there are accumulating data suggesting that sleep disorders contribute to cognitive decline and the development of AD [23].
*other↝, People who sleep six hours or less per night are more likely to develop Alzheimer’s dementia later in life, an observation which suggests that inadequate sleep duration increases dementia risk

5290- 5-HTP,    Placebo-controlled comparison of three dose-regimens of 5-hydroxytryptophan challenge test in healthy volunteers
- in-vivo, Nor, NA
*5HT↑, Single-dose administration of 5-hydroxytryptophan (5-HTP) is regularly used as a challenge test of the serotonergic system.

5289- 5-HTP,    5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology
- Review, AD, NA - Review, Arthritis, NA
*5HT↑, 5-HTP plays a major role both in neurologic and metabolic diseases and its synthesis from tryptophan represents the limiting step in serotonin and melatonin biosynthesis.
*Inflam↓, 5-HTP also suppresses inflammation and arthritis through decreasing the production of pro-inflammatory mediators
*memory↑, figure 10
*Sleep↑, In a group of children with sleep terrors, treatment with 5-HTP was able to modulate the arousal level and to induce a long-term improvement of sleep terrors [1
*Weight↓, The effect of 5-HTP on feeding behavior, mood state, and weight loss was studied. 5-HTP promoted decreased food intake and weight loss as well as typical anorexia-related symptoms without changes in mood state during the period of observation
*DNAdam↓, 5-HTP significantly reduced tert-butylhydroperoxide-induced oxidative damage in human fibroblast cells and protected these cells against oxidative DNA damage
*ROS↓, By acting as a reactive oxygen species (ROS) scavenger, 5-HTP has the potential for use in the treatment of inflammatory diseases and as an analgesic
*toxicity↝, An excess of 5-HTP may be responsible for serotonin syndrome (see Section 8.2.1) and an excessive treatment was found to be associated with severe side effects, including behavioral disturbances, abnormal mental functions, and intolerance.

5288- 5-HTP,    The Impact of 5-Hydroxytryptophan Supplementation on Cognitive Function and Mood in Singapore Older Adults: A Randomized Controlled Trial
- Trial, AD, NA
*5HT↑, Moreover, the 5-HTP group showed a significant increase in serum serotonin levels.
*cognitive↑, 5-HTP supplementation can enhance cognitive performance and reduce symptoms of depression in Singaporean older adults, potentially through serotonergic modulation.
*BBB↑, 5-HTP could cross the blood-brain barrier and synthesize serotonin, thereby effectively elevating serotonin levels
*Mood↑, Prior studies have also observed the effect of 5-HTP on mood regulation, especially improvements in patients with depression

5307- 5-HTP,    5-Hydroxytryptophan toxicosis in dogs: 1989-1999
- Case Report, Nor, NA
*toxicity↝, Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care
*5HT↑, The reported mechanism of action of 5-HTP is through an increase of serotonin concentrations within the CNS,1
*Dose↝, The lowest dose at which signs developed was 23.6 mg/kg (10.7 mg/lb); death was reported for 3 dogs at 128, 131.9, and 287 mg/kg (58.2, 60, and 157.7 mg/lb), respectively

4596- AgNPs,    Oral administration of silver nanomaterials affects the gut microbiota and metabolic profile altering the secretion of 5-HT in mice
- in-vivo, NA, NA
*GutMicro↝, decreased the diversity of gut microbiota in mice after short-term (14 days) exposure, while the microbial community tended to recover after long-term exposure (28 days),
*5HT↑, the gut metabolites significantly changed, showing increased 1H-indole-3-carboxylic acid and elevated levels of 5-HT in the gut and blood

3547- ALA,    Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration
- Review, AD, NA - Review, Park, NA
*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,

3545- ALA,    Potential therapeutic effects of alpha lipoic acid in memory disorders
- Review, AD, NA
*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron, zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils

4279- Api,    The Beneficial Role of Apigenin against Cognitive and Neurobehavioural Dysfunction: A Systematic Review of Preclinical Investigations
- Review, NA, NA
*antiOx↑, potent antioxidant and has been shown to exhibit anti-inflammatory, antitumorigenic and antimicrobial activities
*Inflam↓,
*BBB↑, Its ability to cross the blood–brain barrier is important as it contributes to its pharmacological activity against neurological disorders
*5HT↑, Apigenin improved serotonin, dopamine and epinephrine levels, which were altered in depressive animals
*CREB↑, Apigenin further regulates the cAMP-CREB-BDNF signalling pathway and N-methyl-D-aspartate (NMDA) receptors, which play important roles in neuronal survival, synaptic plasticity, cognitive function and mood behaviour
*BDNF↑, Apigenin improved BDNF levels and enhanced ERK1/2 and CREB expression
*memory↑, All the studies showed that apigenin improved learning and memory, except for two studies.
*motorD↑, In the open field test, apigenin improved locomotor activity
*Mood↑, The splash test revealed that apigenin improved grooming activity and locomotion in streptozotocin-induced depressive-like behaviour in a mouse model via an improvement in grooming activity.
*cognitive↑, The studies included in this systematic review showed that apigenin improved cognitive function and neurobehaviour in impaired or stressed animals.
*ROS↓, inhibition of ROS production

4280- Api,    Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms
- Review, AD, NA - Review, Park, NA
*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/PTGS2↓, 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

4275- BBR,    Pharmacological effects of berberine on mood disorders
- Review, NA, NA
*antiOx↑, Berberine has multiple therapeutic actions, including antioxidant, anti‐inflammatory, antitumour, antimicrobial, hepatoprotective, hypolipidemic, and hypoglycemic actions.
*Inflam↓,
*hepatoP↑,
*eff↑, recent studies show that berberine has a protective effect on central nervous system disorders, such as Alzheimer's, cerebral ischaemia, mental depression, schizophrenia, and anxiety
*5HT↑, Chronic administration of berberine (5 mg/kg, ip) for 15 days significantly increased the levels of norepinephrine (29%), serotonin (19%) as well as dopamine (52%)
*Mood↑, An antidepressant effect of berberine results from elevation of brain‐derived neurotrophic factor (BDNF) levels.
*BDNF↑,

5649- BNL,    Borneol, a novel agent that improves central nervous system drug delivery by enhancing blood–brain barrier permeability
- Review, Nor, NA
*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/ABCB1↓, 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/ABCC1↓, 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

4263- CA,    Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action
- Review, AD, NA
*neuroP↑, neuroprotective effect of CA on neuronal cells subjected to ischemia/hypoxia injury via the scavenging or reduction of ROS (reactive oxygen species) and NO (nitric oxide) and inhibition of COX-2 and MAPK pathways
*ROS↓,
*NO↓,
*COX2/PTGS2↓,
*MAPK↓,
*NRF2↑, CA is known to activate the Keap1/Nrf2 pathway, thereby resulting in the production of cytoprotective proteins.
*GSH↑, activation of GSH metabolism
*HO-1↑, activation of Nrf2 target genes, including heme oxygenase 1 (HO-1) and thioredoxin reductase 1 (TXNRD1)
*5HT↑, Observations of increased serotonin and BDNF suggest that CA may represent a novel therapeutic avenue for depressive behaviors that should be further explored.
*BDNF↑, 10 μM CA results in a 1.5-fold increase in levels of BDNF
*PI3K↑, CA has been shown to mediate the activation of the PI3K/Akt/NF-κB pathway
*Akt↑,
*NF-kB↑,
*BBB↑, CA was shown to ameliorate brain edema and blood-brain barrier (BBB) disruption
*SIRT1↑, CA was also shown to increase SIRT1
*memory↑, CA was shown to significantly improve short-term and spatial memory attributes in rat models of AD
*Aβ↓, CA also delayed the deposition of Aβ and protected cells against Aβ-induced cholinergic and mitochondrial dysfunction in a Caenorhabditis elegans model of AD
*NLRP3↓, CA also inhibits the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome, which plays a critical role in the pathogenesis of neurodegenerative disorders, including AD and PD and COVID-19

4264- CA,    Carnosic Acid Mitigates Depression-Like Behavior in Ovariectomized Mice via Activation of Nrf2HO-1 Pathway
- in-vivo, NA, NA
*NRF2↑, CA treatment alleviated depressive behavior, induced the expression of Nrf2, HO-1, thioredoxin-1, and brain-derived neurotrophic factor, and enhanced serotonin levels.
*HO-1↑,
*Trx1↑,
*BDNF↑,
*5HT↑,
*ROS↓, CA also suppressed oxidative stress, reduced TNF-α, IL-1β, and iNOS mRNA expression, and ameliorated OVX-induced histopathological changes.
*TNF-α↓,
*IL1β↓,
*iNOS↓,

6128- CHr,    Chrysin: A Comprehensive Review of Its Pharmacological Properties and Therapeutic Potential
- Review, Nor, NA - Review, Var, NA - Review, AD, NA
*antiOx↑, Chrysin exhibits a range of biological activities, including antioxidant, anti-inflammatory, anticancer, neuroprotective, and anxiolytic effects.
*Inflam↓,
AntiCan↑,
*neuroP↑, exhibits neuroprotective effects in neurological disorders such as epilepsy, neuronal apoptosis, neuroinflammation [80], anxiety [81], depression [82], multiple sclerosis [83], Parkinson’s disease, Alzheimer’s disease, cognitive deficits,
*ROS↓, facilitate the neutralization of free radicals
*BioAv↓, Despite its therapeutic potential, chrysin’s bioavailability is significantly limited due to poor aqueous solubility and rapid metabolism in the gastrointestinal tract and liver, which reduces its systemic efficacy.
*BioAv↑, Ongoing research aims to enhance chrysin’s bioavailability through the development of delivery systems such as lipid-based carriers and nanoparticles.
*cardioP↑, Chrysin exerts cardioprotective effects by modulating certain cellular signaling pathways involved in inflammation, oxidative stress [66]
*COX2/PTGS2↓, it suppresses cyclooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis that promotes inflammation
*TNF-α↓, inhibits phosphorylation and degradation of IκB-α, as well as the translocation of NF-κB, and reduces levels of TNF-α and IL-1β by inhibiting NF-κB expression
*IL1β↓,
*NF-kB↓,
*lipid-P↓, Chrysin protects against ROS by reducing lipid peroxidation levels in the liver and increasing both enzymatic and non-enzymatic antioxidant levels
*Apoptosis↓, chrysin counteracted oxidative stress, reduced neuronal apoptosis, and increased expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) [80].
*NRF2↑,
*HO-1↑,
*MDA↓, In rat models, chrysin was shown to lower serum corticosterone and malondialdehyde (MDA) levels while increasing glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (Gpx), glutathione reductase (GR), and catalase (CAT).
*GSH↑,
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*5HT↑, Moreover, chrysin increased serotonin (5-HT) levels and reduced the activity of indoleamine 2,3-dioxygenase.
*Casp3↓, It also decreased the expression of caspases-3 and -9 [97,98].
*Casp9↓,
TumCCA↑, it causes cell cycle arrest in cancer cells, reduces expression of MAPK and PI3K/Akt signaling pathways, and disrupts overall cell proliferation
MAPK↓,
PI3K↓,
Akt↓,
TumCP↓,
TET1↑, chrysin promoted TET1 and 5-hydroxymethylcytosine expression, which stimulated apoptosis and disrupted the migration of gastric cancer cells
TLR4↓, Chrysin’s effects in lung cancer include decreasing the expression of TLR4 and Myd88 in the signaling cascade from activated receptor to the cell interior.
HER2/EBBR2↓, pyrotinib combined with chrysin, it was confirmed that adding chrysin positively enhanced the inhibition of HER2-positive breast cancer growth both in vitro and in vivo,
HK2↓, As HK-2 levels decreased, chrysin inhibited glycolysis (which impairs glucose uptake and lactate production) in the tumor and activated mitochondria-related apoptosis
Glycolysis↓,
glucose↓,
lactateProd↓,
ROS↑, chrysin was shown to promote the generation of reactive oxygen species (ROS) and reduce mTOR expression, thereby stimulating autophagy [127]
mTOR↓,
TumAuto↑,
tumCV↓, chrysin significantly reduces cell viability by inducing ER stress through stimulation of UPR, PERK, ATF4, and eIF2α
ER Stress↑,
UPR↑,
PERK↑,
ATF4↑,
eIF2α↑,
BioAv↑, Solid Lipid Nanoparticles (SLNs) High biocompatibility and low toxicity due to the use of physiological lipids.

7429- CS,    Functional and Therapeutic Potential of Cynara scolymus in Health Benefits
- Review, Nor, NA - Review, IBD, NA - Review, AD, NA
*Inflam↓, C. scolymus exhibits anti-inflammatory, antioxidant, liver-protective, bile-expelling, antimicrobial, and lipid-lowering neuroprotective properties.
*antiOx↑, Of particular interest is the abundance of chlorogenic acid, a type of caffeoylquinic acid known also by its antioxidant activity.
*hepatoP↑,
*lipid-P↓,
*TNF-α↓, Pectins from artichoke reduced the expression of inflammatory markers such as TNF-α, ICAM-I, IL-1β, and IL-6 in mice. This has resulted in a decrease in iNOS and TLR4 expression in favor of reducing inflammation.
*ICAM-1↓,
*IL1β↓,
*IL6↓,
*MUC1↑, artichoke pectin increased the intestinal barrier genes expression, MUC-1 and Occludin.
*OCLN↑,
*IBI↑, artichoke pectin has the potential to improve IBD by inhibiting inflammation and promoting the expression of genes involved in intestinal barrier function
*ROS↓, The beneficial components derived from artichoke have shown important scavenging activity against reactive oxygen species (ROS) and free radicals.
*cardioP↑, Moreover, artichoke leaf extracts supplementation has also decreased the cardiac markers and increased the antioxidant enzyme SOD, GPx, and GSH activities [80].
*SOD↑,
*GPx↑,
*GSH↑,
*TG/TAG↓, resulting in lower triglyceride (TG) levels
*LDL↓, 8 weeks with artichoke leaf extracts (administered as two daily doses of 250 mg). This treatment significantly reduced total cholesterol (TC), LDL cholesterol (LDL-c),
*neuroP↑, Growing evidence highlights the neuroprotective role of polyphenols
*5HT↑, Polyphenols have been shown to improve mood by increasing serotonin levels in the brain, stimulating the production of brain-derived neurotrophic factor (BDNF), and reducing inflammation
*BDNF↑,

4253- EA,    The effects of Ellagic acid supplementation on neurotrophic, inflammation, and oxidative stress factors, and indoleamine 2, 3-dioxygenase gene expression in multiple sclerosis patients with mild to moderate depressive symptoms: A randomized, triple-blind, placebo-controlled trial
- Human, MS, NA - NA, IBD, NA
*Mood↑, The current study indicates that Ellagic acid intervention has a favorable effect on depression in MS patients.
*BDNF↑, we found a significant elevation in circulating levels of BDNF and serotonin.
*5HT↑,
*antiOx↑, associated to its antioxidative, anti-inflammatory, immunomodulatory, antidiabetic, and anticancer properties (Gupta et al., 2021)
*Inflam↓,
*AntiCan↑,
*QoL↑, Ellagic acid improves bowel function and enhances the quality of life for individuals suffering from irritable bowel syndrome (IBS)
*neuroP↑, Ellagic acid may have neuroprotective effect by regulating the hypothalamic–pituitary–adrenal (HPA) axis and neurotransmitters in animal's brain
*cognitive↑, Ellagic acid supplementation may also improve mood and cognitive function like memory and learning in rats (Gupta et al., 2021).
*memory↑,
*Dose↝, 180 mg Ellagic acid

6954- FA,    Folic acid as a potential therapeutic agent for Alzheimer's disease: Effects on inflammatory cytokines, amyloid deposition, and neurotransmitter metabolism
- Trial, AD, NA
*Inflam↓, FA supplementation can effectively delay AD progression by inhibiting neuroinflammation, reducing amyloid deposition, regulating neurotransmitter metabolism and improving nutritional status.
*Aβ↓,
*IL1β↓, levels of inflammatory factors (IL-1b, IL-6, and TNF-a), Ab1-42, and Tau were significantly lower (P<0.05), and neurotransmitters (GABA, 5-HT, and Ach) and nutritional indexes (albumin and hemoglobin) were substantially higher.
*IL6↓,
*TNF-α↓,
*tau↓,
*GABA↑,
*5HT↑,
*Ach↑,
*Albumin↑,
*HemoG↑,
*neuroP↑, GABA, 5-HT, and Ach in both groups increased after treatment, with more significant increases in the experimental group (P<0.001), indicating better neurological function
*Hcy/homoC↓, FA supplementation has been shown to effectively promote plasma conversion of Hcy to reduce plasma Hcy concentrations in patients with metabolic syndrome

6981- Form,    Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;

3723- GBE,    Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies
- Review, AD, NA
*memory↑, GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration.
*antiOx↑, Antioxidant properties
*Casp3↓, ↓caspase-3
*APP↓, ↓APP
*AChE↓, ↓AChE activity
*Aβ↓, ↓Aβ oligomers
*5HT↑, ↑5-HT in the striatum
*SOD↓, ↓SOD ↓MDA ↓NO
*MDA↓,
*NO↓,
*GSH↑, ↓SOD ↑GSH ↓MDA
*Bcl-2↑, ↑Bcl-2 ↓Bax
*BAX↑,
*TNF-α↓, ↓TNF-α, IL-1β, ccl-2, iNOS, and IL-10
*IL1β↑,
*iNOS↓,
*IL10↓,
*p‑tau↓, ↓tau phosphorylation
*ROS↓, ↓ROS
*MAOB↓, ↓MAO-B enzyme activity
*cognitive↑, A total of 819 patients who had been diagnosed with AD, or that had AD-like symptoms, received lower SKT scores after GBE treatment for 12 to 24 weeks
*neuroP↑, Neuroprotective Mechanism Analysis
*Apoptosis↓, GBE Inhibits Cell Apoptosis

3942- MF,    Chronic-Exposure Low-Frequency Magnetic Fields (Magnetotherapy and Magnetic Stimulation) Influence Serum Serotonin Concentrations in Patients with Low Back Pain-Clinical Observation Study
- Human, AD, NA
*5HT↑, Magnetotherapy and magnetic stimulation, acting in a similar way, increase the concentration of serotonin.

3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

3587- PI,    Piperine: A review of its biological effects
- Review, Park, NA - Review, AD, NA
*hepatoP↑, piperine has also been documented for its hepatoprotective, anti-allergic, anti-inflammatory, and neuroprotective properties
*Inflam↓,
*neuroP↑,
*antiOx↑, antiangiogenesis, antioxidant, antidiabetic, antiobesity, cardioprotective,
*angioG↑,
*cardioP↑,
*BioAv↑, nano-encapsulation and resulting piperine-loaded nanoparticles enhance the bioavailability of piperine via oral administration
*P450↓, piperine inactivates cytochrome P450 (CYP) 3A (CYP3A), which plays a critical role in drug metabolism
*eff↑, enhances the anti-inflammatory effects when combined with resvera- trol
*BioAv↑, piperine increases the bioavailability of various compounds such as ciprofloxacin, norfloxacin, metronidazole, oxytetracycline, nimesulide, pentobarbitone, phenytoin, resveratrol, beta-carotene, curcumin, gallic acid, tiferron, nevirapine, and sparte
E-cadherin↓, Downregulates the E-cadherin (E-cad), estrogen receptor (ER), matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP- 9), vascular endothelial growth factor (VEGF) levels, and c-Myc.
ER(estro)↓,
MMP2↓,
MMP9↓,
VEGF↓,
cMyc↓,
BAX↑, Increases the expressions of Bax and p53.
P53↑,
TumCG↓, Lowers the tumor growth and elevates survival time
OS↑,
*cognitive↑, piperine ameliorated the neuro-chemical, neuroinflammatory, and cognitive alterations caused by chronic exposure to galactose
*GSK‐3β↓, piperine reversed D-Gal-induced GSK-3β activation through modulating PKC and PI3K/AKT pathways, s
*GSH↑, Piperine stimulates glutathione levels in rats' striatum, reduced caspase-3 and 9 activation, and diminished release of cytochrome-c from mitochondria along with a reduction in lipid peroxidation
*Casp3↓,
*Casp9↓,
*Cyt‑c↓,
*lipid-P↓,
*motorD↑, piperine also caused improvement in motor coordination and balance behavior along with reduction in contralateral rotations.
*AChE↓, significantly amended impaired memory and hippo-campus neurodegeneration and lowered lipid peroxidation and acetylcholinesterase enzyme
*memory↑,
*cardioP↑,
*ROS↓, fig 6
*PPARγ↑,
*ALAT↓, piperine lowers alanine aminotransferase (ALT), AST, and ALP levels in sera of cholesterol-fed albino mice
*AST↓,
*ALP↓,
*AMPK↑, reversed the downregulation of AMPK signaling molecules, which are responsible for fatty acid oxidation, insulin signaling, and lipogenesis in mouse liver.
*5HT↑, t causes a significant decrease in serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) contents in the hippocampus and frontal cortex.
*SIRT1↑, , it may enhance the SIRT1 expression in cells and SIRT1 activity enhancing its potential to prevent SIRT1-mediated disease
*eff↑, combination ther- apy of resveratrol and piperine as an approach to enhance the biologi- cal effects with respect to cerebral blood flow and improved cognitive functions

4114- SAMe,    S-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders: A Clinician-Oriented Review of Research
- Review, AD, NA
*Mood↑, review of SAMe in the treatment of major depressive disorder found promising but limited evidence of efficacy and safety to support the use of SAMe as a monotherapy and as an augmentation for other antidepressants.
*BBB↑, SAMe crosses the blood-brain barrier and increases CSF levels
*5HT↑, increases concentrations of CNS monoamine neurotransmitters, serotonin and norepinephrine
*p‑tau↓, SAMe affects site-specific methylation of DNA-promoter regions that regulate gene function, and carboxymethylation of proteins that can regulate b-amyloid and Tau proteins, neuropathological hallmarks of Alzheimer's disease
*Aβ↓,
*other↑, twelve of the nineteen RPCTs showed the antidepressant effect of SAMe to be significantly greater than placebo for depressive syndromes

3944- Shank,    Role of Shankhpushpi (Convolvulus pluricaulis) in neurological disorders: An umbrella review covering evidence from ethnopharmacology to clinical studies
- Review, AD, NA
*memory↑, exhibited a wide range of in vitro and in vivo neuropharmacological effects, including memory enhancement, anxiolytic, tranquilizing, anti-depressant, anti-stress
*neuroP↑, neurodegenerative, anti-inflammatory, anti-oxidant, analgesic, sedative, anti-convulsant, and Alzheimer's disease-reversing effects.
*Inflam↓,
*5HT↑, and increasing serotonin concentration in synapses.

4206- SIL,    Silymarin ameliorates experimentally induced depressive like behavior in rats: Involvement of hippocampal BDNF signaling, inflammatory cytokines and oxidative stress response
- in-vivo, NA, NA
*BDNF↑, improved BDNF expression, 5-HT, DA, NE and antioxidant paradigms in cerebral cortex as well as hippocampus.
*5HT↑,
*antiOx↑,
*IL6↓, silymarin attenuated IL-6, and TNF-α significantly in hippocampus and cerebral cortex in OBX rats.
*TNF-α↓,
*Mood↑, silymarin exhibits anti-depressant-like activity in OBX rats due to alterations in several neurotransmitters, endocrine and immunologic systems, including BDNF, 5-HT, DA, NE, MDA formation, IL-6, and TNF-α in hippocampus

4205- SIL,    The Therapeutic Effect of Silymarin and Silibinin on Depression and Anxiety Disorders and Possible Mechanism in the Brain: A Systematic Review
- Review, AD, NA
*BDNF↑, Silymarin and silibinin upregulated brain-derived neurotrophic factor (BDNF) and improved neural stem cells (NSCs) proliferation in the cortex and hippocampus.
*5HT↑, They also increased neurochemical serotonin (5-HT), dopamine (DA), and norepinephrine (NE) levels.
*MDA↓, Silymarin and silibinin reduced malondialdehyde (MDA) formation and increased glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities.
*GSH↑,
*SOD↑,
*Catalase↑,
*IL6↓, silymarin and silibinin reduced interleukin (IL)-6, IL-1β, and IL-12β, reducing tumor necrosis factor α (TNF-α) induced neuroinflammation.
*IL1β↓,


Showing Research Papers: 1 to 32 of 32

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 32

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   glucose↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   BAX↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,   P53↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   mitA↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1,   GSK‐3β↑, 1,   mTOR↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   E-cadherin↓, 1,   LAMs↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TET1↑, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   NF-kB↓, 2,   PD-1↓, 1,   TLR4↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   NP/CIPN↓, 1,   OS↑, 1,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 10,   Catalase↑, 6,   GPx↑, 6,   GSH↑, 9,   GSR↑, 1,   HO-1↓, 1,   HO-1↑, 5,   Keap1↝, 1,   lipid-P↓, 5,   MDA↓, 4,   NQO1↑, 1,   NRF2↑, 5,   ROS↓, 12,   mt-ROS?, 1,   SOD↓, 1,   SOD↑, 6,   Trx1↑, 1,   VitC↑, 2,   VitE↑, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↑, 2,   Insulin↑, 1,   MMP↑, 1,   PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   AMPK↑, 1,   CREB↑, 1,   glucose↓, 1,   GlucoseCon↑, 1,   LDL↓, 1,   PPARγ↑, 2,   SIRT1↑, 2,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   p‑Akt↓, 1,   Apoptosis↓, 2,   BAX↑, 1,   Bcl-2↑, 1,   Casp3↓, 4,   Casp9↓, 2,   Cyt‑c↓, 1,   iNOS↓, 2,   MAPK↓, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 4,   other↑, 2,   other↝, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   PARP1↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cFos↑, 1,   GSK‐3β↓, 2,   IGF-1↑, 1,   mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 2,  

Migration(tgid=13) ⓘ

APP↓, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP9↓, 1,   MUC1↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   VCAM-1↓, 2,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 8,   GLUT3↑, 1,   GLUT4↑, 1,   IBI↑, 1,   OCLN↑, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 3,   COX2/PTGS2↑, 1,   ICAM-1↓, 1,   IL10↓, 1,   IL18↓, 1,   IL1β↓, 8,   IL1β↑, 1,   IL6↓, 5,   Inflam↓, 14,   pol-M2 MC↑, 1,   NF-kB↓, 3,   NF-kB↑, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 9,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 32,   AChE↓, 6,   BDNF↑, 12,   ChAT↑, 2,   GABA↑, 3,   MAOA↓, 1,   NGF↑, 2,   tau↓, 1,   p‑tau↓, 3,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 7,   MAOB↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABC↓, 1,   BioAv↓, 1,   BioAv↑, 6,   BioAv⇅, 1,   BioAv↝, 1,   Dose↑, 1,   Dose↝, 3,   eff↑, 5,   Half-Life↓, 1,   MRP1/ABCC1↓, 1,   P450↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   Albumin↑, 1,   ALP↓, 1,   AST↓, 2,   GutMicro↑, 2,   GutMicro↝, 1,   Hcy/homoC↓, 1,   HemoG↑, 1,   IL6↓, 5,   TG/TAG↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   antiPs↑, 1,   cardioP↑, 4,   chemoP↑, 1,   cognitive↑, 11,   hepatoP↑, 4,   memory↑, 12,   Mood↑, 6,   motorD↑, 3,   neuroP↑, 13,   Obesity↓, 1,   QoL↑, 1,   Sleep↑, 2,   toxicity↓, 3,   toxicity⇅, 1,   toxicity↝, 3,   Weight↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 144

Scientific Paper Hit Count for: 5HT, Serotonin
10 5-Hydroxytryptophan
2 Alpha-Lipoic-Acid
2 Apigenin (mainly Parsley)
2 Carnosic acid
2 Magnetic Fields
2 Silymarin (Milk Thistle) silibinin
1 Silver-NanoParticles
1 Berberine
1 borneol
1 Chrysin
1 Cynara scolymus/Globe Artichoke/Artichoke Extract
1 Ellagic acid
1 Folic Acid, Vit B9
1 Formononetin
1 Ginkgo biloba
1 Magnetic Field Rotating
1 Piperine
1 S-adenosyl-L-methionine
1 Shankhpushpi
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1119  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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