BDNF Cancer Research Results
BDNF, brain-derived neurotrophic factor: Click to Expand ⟱
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Brain-Derived Neurotrophic Factor (BDNF) is a key neurotrophin (a type of growth factor) involved in brain health, and its role in Alzheimer’s Disease (AD) has been extensively studied.
-AD patients often have lower BDNF levels in key brain regions, such as the hippocampus and cortex.
-This reduction correlates with cognitive decline and brain atrophy.
-BDNF normally protects neurons from Aβ toxicity
-Exercise and cognitive training have been shown to boost BDNF levels and may slow cognitive decline.
- natural compounds (like curcumin or flavonoids) may also upregulate BDNF.
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Scientific Papers found: Click to Expand⟱
*neuroP↑, BCP significantly protected human microglial HMC3 cells from Aβ25-35-induced cytotoxicity, reducing the release of pro-inflammatory cytokines (TNF-α, IL-6) while enhancing IL-10 secretion.
*NF-kB↓, reduced activation of the NF-κB pathway, which emerged as a central mediator of BCP action
*SIRT1↑, BCP restored the expression of SIRT1, PGC-1α, and BDNF, indicating the involvement of neurotrophic pathways.
*PGC-1α↓, BCP effectively counteracted this downregulation and markedly increased the expression of all three genes
*BDNF↓,
*TNF-α↓, BCP was able to suppress Aβ-induced release of TNFα and IL-6, while increasing the secretion of anti-inflammatory IL-10, indicating an anti-inflammatory response.
*IL6↓,
*IL10↑,
*Inflam↓,
*memory↑, Feeding hyperinsulinemic rats with caffeic acid (30 mg/kg b.w./day) for 30 weeks significantly improved their memory and learning impairments caused by a high-fat diet
*cognitive↑, caffeic acid (100 mg/kg for two weeks) significantly improved learning deficits and increased cognitive function
*p‑tau↓, pretreatment with caffeic acid (10 μg/mL) decreased the level of phosphorylated tau protein
*ROS↓, Caffeic acid (100 mg/kg for two weeks) also suppressed oxidative stress, inflammation, NF-κB-p65 protein expression, and caspase-3 activity
*Inflam↓,
*NF-kB↓,
*Casp3↓,
*lipid-P↓, caffeic acid (50 mg/kg/day) improved cognitive functions and inhibited lipid peroxidation and nitric oxide formation in the brain
*AChE↓, Caffeic acid (12 μg/mL) inhibited acetylcholinesterase and butyrylcholinesterase activity in the brain of untreated rats in vitro
*BChE↓,
*GSK‐3β↓, improves cognitive functions, probably by inhibiting NF-κB and GSK3β signaling and acetylcholinesterase and butyrylcholinesterase activity (
*5LO↓, we consider the inhibitory effect of caffeic acid on 5-lipoxygenase as another factor in protecting the brain against damage
*BDNF↓, Caffeic acid also increased the expression of brain-derived neurotrophic factor (BDNF) in stressed mice; the effect was mediated by 5-lipoxygenase inhibition
VEGF↓, the primary way how caffeic acid affects hepatocellular carcinoma in vitro is inhibiting VEGF expression
HSP70/HSPA5↓, affeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve
Showing Research Papers: 1 to 3 of 3
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
ROS↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSP70/HSPA5↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
PCNA↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, EMT↓, 1, miR-34a↓, 1, NOTCH1↓, 1, STAT3↓, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
Ki-67↓, 1, Slug↓, 1, TRIB3↑, 1, TumCI↓, 1, TumMeta↓, 1, TumMeta↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
NF-kB↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
Ki-67↓, 1, TG/TAG↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1,
Total Targets: 28
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, GPx↑, 1, GSH↑, 1, lipid-P↓, 2, NRF2↑, 1, ROS↓, 2, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, PGC-1α↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, AMPK↓, 1, NAD↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 1, BAX↓, 1, Bcl-2↓, 1, Casp3↓, 2, Casp9↓, 1, Cyt‑c↓, 1, GADD34↓, 1, iNOS↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1, LC3II↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1, NO↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IFN-γ↓, 1, IL10↓, 1, IL10↑, 1, IL17↓, 1, IL6↓, 2, Imm↓, 1, Inflam↓, 3, NF-kB↓, 3, PGE2↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1, BChE↓, 1, BDNF↓, 3, p‑tau↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, IL6↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 3, toxicity↝, 1,
Total Targets: 56
Scientific Paper Hit Count for: BDNF, brain-derived neurotrophic factor
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#:1356 State#:% Dir#:1
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