Learn Cancer Research Results

Learn, Learning: Click to Expand ⟱
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Scientific Papers found: Click to Expand⟱
7516- CA,    Caffeic Acid, a Polyphenolic Micronutrient Rescues Mice Brains against Aβ-Induced Neurodegeneration and Memory Impairment
- in-vivo, AD, NA
*neuroP↑, It has been reported that the polyphenolic compound caffeic acid possesses strong neuroprotective and antioxidant effects.
*antiOx↑,
*memory↑, The behavioral results indicated that caffeic acid administration improved spatial learning, memory, and cognitive abilities in AD mice.
*Learn↑,
*cognitive↑,
*ROS↓, ROS and LPO were markedly reduced in the caffeic acid-treated mice
*lipid-P↓,
*NRF2↑, expression of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were regulated with the administration of caffeic acid
*HO-1↑,
*Aβ↓, caffeic acid treatment also decreased Aβ and BACE-1 expression in the Aβ-induced AD mice model.
*BACE/β-secretase↓,

7520- CAPE,    Neuroprotective Effect of Caffeic Acid Phenethyl Ester in A Mouse Model of Alzheimer's Disease Involves Nrf2/HO-1 Pathway
- in-vivo, AD, NA
*ROS↓, intraperitoneal administration of CAPE (10 mg/kg) after i.c.v. AβO-injection counteracted oxidative stress accompanied by an induction of Nrf2 and heme oxygenase-1 via the modulation of glycogen synthase kinase 3β in the hippocampus of mice.
*NRF2↑,
*HO-1↑,
*Apoptosis↓, CAPE treatment decreased AβO-induced neuronal apoptosis and neuroinflammation, and improved learning and memory, protecting mice against the decline in spatial cognition.
*Inflam↓,
*Learn↑,
*memory↑,
*cognitive↑,
*neuroP↑, CAPE could potentially be considered as a promising neuroprotective agent against progressive neurodegenerative diseases such as AD.
*p‑GSK‐3β↓, CAPE treatment reversed the effects of Aβ1-42O and significantly decreased (p<0.05 and p<0.001, 10 and 20 days post-injection) GSK3β inhibitory phosphorylation.
GFAP↓, CAPE treatment significantly decreased the number of reactive Iba-1 (p<0.001) and GFAP (p<0.001) cells in the hippocampus of Aβ1-42O treated mice

7522- DFE,    Diet rich in date palm fruits improves memory, learning and reduces beta amyloid in transgenic mouse model of Alzheimer's disease
- in-vivo, AD, NA
*Aβ↓, The levels of both Aβ proteins were significantly lowered in date fruits supplemented groups than the Tg mice without the diet supplement.
*neuroP↑, The neuroprotective effect offered by 4% date fruits diet to AD mice is higher than 2% date fruits diet.
*motorD↑, Supplementation with 2% and 4% dates to APPsw/Tg2576 mice restored their locomotors activity in both the open-field and rota-rod test after 14 months of supplementation
*memory↑, 2% and 4% date rich diet improved spatial memory in aged amyloid precursor protein sw/Tg2576 mice
*Learn↑, Position discrimination learning ability was improved following date supplementation in amyloid precursor proteinsw/Tg2576

7530- HT,    The Impact of Hydroxytyrosol on the Metallomic-Profile in an Animal Model of Alzheimer's Disease
- in-vivo, AD, NA
*Learn↑, The results also indicated that the control group and the STZ + HT group exhibited enhanced learning curves during the Barnes maze training as compared to the STZ group.
*Copper↓, The most important finding was that copper levels in the frontal cortex from STZ-treated animals were higher than in the control group, and that the STZ + HT group returned to equivalent levels to the control group.

7566- HYP,    Hyperoside improves learning and memory deficits by amyloid β1-42 in mice through regulating synaptic calcium-permeable AMPA receptors
- in-vivo, AD, NA
*Learn↑, Hyperoside enhanced learning and memory in passive avoidance and object recognition tasks.
*memory↑,
*Aβ↓, Finally, hyperoside ameliorated Aβ-induced memory impairments in an AD mouse model.

7544- HYP,    Long-term oral administration of hyperoside ameliorates AD-related neuropathology and improves cognitive impairment in APP/PS1 transgenic mice
- in-vivo, AD, NA
*Learn↑, After 9 months of treatment, we found that hyperoside can improve spatial learning and memory in APP/PS1 transgenic mice, reduce amyloid plaque deposition and tau phosphorylation
*memory↑,
*Aβ↓,
*p‑tau↓,
*Inflam↓, attenuate neuroinflammation and oxidative stress in the brain of APP/PS1 mice.
*ROS↓,
*BACE/β-secretase↓, These beneficial effects may be mediated in part by influencing reduction of BACE1 and GSK3β levels.
*GSK‐3β↓,

7759- ISL,  Rad,    Isoliquiritigenin, a Bioactive Blood Component Derived from Licorice, Activates Nrf2 Enzymes to Confer Protection Against Radiation-Induced Nerve Injury
- vitro+vivo, Nor, PC12
*radioP↑, In vitro, ISL restored the viability of X-ray-irradiated PC12 cells; reduced LDH release and intracellular ROS accumulation; and enhanced SOD1 activity, GSH content, and T-AOC levels.
*LDH↓,
*ROS↓,
*SOD1↑,
*GSH↑,
*TAC↑,
*NRF2↓, Moreover, ISL upregulated the expression of antioxidant-related genes and induced Nrf2 nuclear translocation.
*cognitive↑, In vivo, oral ISL administration ameliorated radiation-induced cognitive impairment, improved spatial learning and memory, alleviated hippocampal neuronal loss, and increased cerebral cortical Nrf2 expression in C57BL/6J mice
*Learn↑,
*memory↑,

7784- ISL,    Isoliquiritigenin attenuates lipopolysaccharide-induced cognitive impairment through antioxidant and anti-inflammatory activity
- in-vivo, AD, NA
*Learn↑, ISL pretreatment reversed these deficits as well as LPS-induced decreases in the hippocampal expression levels of synaptophysin, postsynaptic density-95, brain-derived neurotrophic factor, superoxide dismutase, glutathione peroxidase, and BCL-2.
*PSD95↑,
*BDNF↑,
*SOD↑,
*GPx↑,
*Bcl-2↑,
*SYP↑,
*Bax:Bcl2↓, ISL pretreatment also reversed LPS-induced increases in TUNEL-positive (apoptotic) cells, BAX/BCL-2 ratio, and expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and C-C motif chemokine ligand 3.
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MIP‑1α/CCL3↓,
*p‑GSK‐3β↑, Pretreatment with ISL increased the expression levels of phosphorylated (p)-GSK-3β, nuclear NRF2, HO-1 mRNA, and NQO1 mRNA, and reversed LPS-induced nuclear translocation of nuclear factor (NF)-κB
*NRF2↑,
*HO-1↑,
*NQO1↑,
*cognitive↑, ISL protects against LPS-induced cognitive impairment and neuronal injury by promoting or maintaining antioxidant capacity and suppressing neuroinflammation, likely through phosphorylation-dependent inactivation of GSK-3β, enhanced expression of NRF
*Inflam↓,

7821- ISQ,    Quercitrin improved cognitive impairment through inhibiting inflammation induced by microglia in Alzheimer's disease mice
- in-vivo, AD, NA
*cognitive↑, Quercitrin improved mice cognitive impairment through alleviating the intensity of inflammatory response and is a promising medicinal plant extract in the treatment of AD
*Inflam↓, inhibited the secretion of inflammatory cytokines and chemokines and reduced the accumulation of amyloid-β plaques in AD model mice.
*Aβ↓,
*neuroP↑, Multiple pharmaceutical effects of quercitrin, including antioxidant, anti-inflammatory and neuroprotection, have made it a promising food additive for the prevention of age-related disorders
*memory↑, Quercitrin improved memory impairment in 5XFAD mice
*Learn↑, Quercitrin improved spatial learning and memory impairment in 5XFAD mice

7799- ISQ,    Acer okamotoanum and isoquercitrin improve cognitive function via attenuation of oxidative stress in high fat diet- and amyloid beta-induced mice
- in-vivo, AD, NA
*cognitive↑, administration of A. okamotoanum and IQ improved spatial cognitive ability and object recognition ability in T-maze and novel object recognition tests.
*Learn↑, showed enhanced learning and memory function
*memory↓,
*ROS↓, administration of A. okamotoanum and IQ attenuated oxidative stress in the brain via inhibition of reactive oxygen species production, lipid peroxidation, and nitric oxide formation.
*lipid-P↓,
*NO↓,

7827- KaempF,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, Kaempferol (3,4′,5,7-tetrahydroxyflavone) showed neuroprotective activity in various AD models.
*Learn↑, improved the spatial learning and memory impairment in SZT-injected (i.c.v.) rats
*memory↑,
*antiOx↑, by the mechanisms of antioxidation and antineuroinflammation
*Inflam↓,
*Aβ↓, Aβ-induced damages was also ameliorated by kaempferol as evidenced by the improved cognitive and memory function in Aβ1−40 -injected (i.c.v.) mice
*cognitive↑,
*BDNF↑, Mechanisms for those effects involved the activation of the cytoprotective BDNF/TrkB/ CREB pathway, enhancement of the antiapoptotic Erβ/ERK1/ 2 pathway, and inhibition of oxidative stress.
*TrkB↑,
*CREB↑,
*ERβ/ESR2↑,
*ERK↑,
*ROS↓,
*AChE↓, inhibited AChE activity
*Dose↑, kaempferol-3-Orutinoside, isoquercitrin, isorhamnetin, and rutin increased to 24.25, 18.67, 26.06, and 11.67 mg/100 g dry weight in mung bean sprouts (at the fifth day of sprouting),

7834- VA,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, Vanillic acid (4-hydroxy-3-methoxybenzoic acid) showed neuroprotective activities in various CNS disorders, such as AD, Parkinson’ disease, cerebral ischemia, and excessive iron-induced damage
*memory↑, vanillic acid improved the memory and learning deficits via multiple mechanisms
*Learn↑,
*Aβ↓, First, vanillic acid inhibited Aβ production, β-secretase (BACE-1) activity, and Aβ plaque deposits in Aβ or lipopolysaccharide (LPS)-induced AD models,
*BACE/β-secretase↓,
*NeuroI↓, vanillic acid exerted antineuroinflammatory effects by inhibition of the receptor for advanced glycation end products (RAGE)-mediated c-Jun n-terminal kinase (JNK) activation
*RAGE↓,
*antiOx↑, vanillic acid enhanced the antioxidant Nrf2/HO-1 pathway by inhibiting GSK-3β, thus reducing the oxidative stress of Aβ1−42 -injected (i.c.v.) mice.
*NRF2↑,
*HO-1↑,
*GSK‐3β↓,
*ROS↓,
*AChE↓, vanillic acid also ameliorated the cholinergic deficits as evidenced by the inhibited AChE activity in STZ-induced AD mice
*Dose↝, effective dose of vanillic acid in rodents was 30−100 mg/kg, while its content of vanillic acid in mung bean (0.97 mg/100 g) was quite low, which implied its limited contribution to the neuroprotective activity of mung bean

7902- VT,    Vitexin Protects Against Scopolamine-Induced Cognitive Impairment by Preserving Synaptic Integrity and Modulating Nrf2/HO-1 and NF-κB Signaling Pathways
- in-vivo, AD, NA
*Dose↝, Sco (2 mg/kg/day, i.p.), Sco + vitexin (30 mg/kg/day, oral), Sco + donepezil (1.5 mg/kg/day, i.p.), vitexin alone, and donepezil alone
*Learn↑, co significantly impaired spatial learning and memory while increasing anxiety-like behaviors. Vitexin treatment markedly improved these deficits, with efficacy comparable to donepezil
*memory↑,
*AChE↓, Sco elevated acetylcholinesterase activity, lipid peroxidation, and oxidative/nitrosative stress markers (TOS, OSI, MDA, Peroxynitrite, NO, and NOS) while decreasing total antioxidant status (TAS). Vitexin reversed these changes.
*lipid-P↓,
*TOS↓,
*MDA↓,
*ONOO↓,
*NO↓,
*NOS2↓,
*TAC↑,
*BDNF↑, Sco reduced hippocampal BDNF, GDNF, PSD95, and synaptophysin levels and increased GFAP, IL-6, TNF-α, NF-κB p65, and COX-2 expression. Vitexin restored neurotrophic and synaptic proteins, suppressed astrocyte activation and inflammatory signaling, a
*GDNF↑,
*PSD95↑,
*GFAP↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, and activated the Nrf2/HO-1 pathway.
*HO-1↑,
*neuroP↑, vitexin exerts significant neuroprotective and synaptoprotective effects against Sco-induced cognitive impairment by simultaneously restoring redox balance
*NeuroI↓, suppressing neuroinflammation, and preserving synaptic integrity.


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

GFAP↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

GDNF↑, 1,   GFAP↓, 1,   Learn↑, 13,   NeuroI↓, 2,   ONOO↓, 1,   SYP↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Copper↓, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 5,   lipid-P↓, 3,   MDA↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 5,   ROS↓, 7,   SOD↑, 1,   SOD1↑, 1,   TAC↑, 2,   TOS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CREB↑, 1,   LDH↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Bax:Bcl2↓, 1,   Bcl-2↑, 1,  

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

ERK↑, 1,   GSK‐3β↓, 2,   p‑GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,  

Migration(tgid=13) ⓘ

RAGE↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 5,   MIP‑1α/CCL3↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3,   BDNF↑, 3,   PSD95↑, 2,   p‑tau↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 7,   BACE/β-secretase↓, 3,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ERβ/ESR2↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↑, 1,   Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   LDH↓, 1,   NOS2↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 7,   memory↓, 1,   memory↑, 10,   motorD↑, 1,   neuroP↑, 7,   radioP↑, 1,  
Total Targets: 59

Scientific Paper Hit Count for: Learn, Learning
2 Hyperoside
2 Isoliquiritigenin
2 isoquercitrin
2 Mung Bean Sprouts
1 Caffeic acid
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Date Fruit Extract
1 HydroxyTyrosol
1 Radiotherapy/Radiation
1 Kaempferol
1 Vanillic Acid
1 Vitexin
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#:1656  State#:%  Dir#:2
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