BBB Cancer Research Results
BBB, Blood-Brain Barrier Permeability: Click to Expand ⟱
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Blood-Brain Barrier(BBB) is a term often used regarding if a product has the ability to cross the BBB.
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Scientific Papers found: Click to Expand⟱
RadioS↑, enhancing radiation-based anticancer therapy
*ROS↑, Silver nanoparticles (AgNPs) produce a pro-oxidant environment, though it is still unclear exactly how they increase reactive oxygen species (ROS).
*BBB↝, research contends that these particles mainly spare the blood–brain barrier (BBB) from toxicity, other reports found that administering AgNP altered the BBB’s permeability, providing a fascinating potential avenue for future applications
*BBB↝, These results indicated that OCTN2 is functionally involved in ALCAR transfer across the BBB. T
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in-vivo, |
AD, |
NA |
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in-vivo, |
Park, |
NA |
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*neuroP↑, results in reducing symptoms and protecting against neurodegeneration.
*toxicity∅, Bacopa monnieri has been found to be generally non-toxic, with no serious side effects reported.
*AChE↓, The neuroprotective effect of Bacopa monnieri was likely due to its ability to inhibit acetylcholinesterase activity rather than mitigating glutamate-induced toxicity.
*ROS↓, neurons treated with the extract exhibited lower levels of reactive oxygen species, suggesting a reduction in intracellular oxidative stress and an extension of neuronal lifespan.
*antiOx↑, The extract also demonstrated antioxidant properties and inhibited lipid peroxidation
*lipid-P↓,
*cognitive↑, on 72 mice, it was shown that supplementation with Bacopa monnieri (100 mg/kg for 180 days) significantly improved cognitive function.
*memory↑, 60 healthy, elderly volunteers taking 300 mg and 600 mg of Brahmi showed reduced acetylcholinesterase activity, which resulted in improved attention and memory.
*Dose↝, Ethanol extract was most commonly used in the studies. Doses are usually in the range of 300 to 600 mg daily.
*BioAv↓, Bacoside A is one of the main active compounds found in Bacopa monnieri. However, its water insolubility results in low bioavailability when administered orally.
*TumCCA↑, It has been shown to induce cell cycle arrest and apoptosis in colorectal cancer cell lines
*BBB↝, Studies were also conducted in which, similarly to the aforementioned approach, formulated solid lipid nanoparticles (SLNs) were used to facilitate the transport of the bacoside-rich extract across the blood–brain barrier.
*TMAO↑, (HFD) promotes cardiovascular disease, in part because it is rich in quaternary amines such as choline, carnitine, and lecithin, which are converted to trimethylamine (TMA) by the gut microbes and increase levels of circulating TMAO
*cognitive↓, TMAO induces cognitive impairment via disrupting the BBB. TMAO treatment induced cognitive impairment and disrupted the BBB integrity in mice
*BBB↝, TMAO has been reported to regulate blood-brain barrier (BBB) integrity and suppress the expression of tight junction proteins (TJs) in the microvasculature.
*TJ↝,
*BBB↝, It has long been thought that GABA is unable to cross the blood–brain barrier (BBB), but the studies that have assessed this issue are often contradictory and range widely in their employed methods.
*BBB↓, suggestion that the BBB permeability to GABA decreases with age
*fatigue↓, participants who received 50 mg of GABA dissolved in a beverage reported less psychological fatigue after completion of the task
*other↝, To summarize, bacteria from the Lactobacillus spp. strain contribute to the formation of GABA in the ENS. The oral administration of bacteria from this strain can influence GABAergic firing in the mice brain through the vagus nerve.
*BBB↝, While traditional beliefs questioned GABA’s ability to cross the BBB, recent research challenges this notion, proposing specific transporter systems facilitating GABA passage.
*cognitive↑, literature suggests that oral intake of GABA affects the brain illustrated by changes in EEG scans and cognitive performance, with evidence showing that GABA can have beneficial effects for multiple age groups and conditions.
*Dose↝, The gut microbiota is a source of GABA present in the gut, but oral GABA intake needs to be considered as well.
*toxicity↓, A study found that consistent administration of GABA to rats and dogs, even at doses up to 1 g/kg/day, did not exhibit any indications of toxicity
*Stress↓, Another study looked at GABA’s ability to affect brain wave patterns and reported increasing alpha and decreasing beta waves suggesting relaxation
*Inflam↓, The anti-inflammatory activity of GABA-enriched products derived from Lactobacillus fermented rice bran solution exhibited inhibitory effects on the expression of inflammatory enzymes, including inducible nitric oxide synthase and cyclooxygenase-2, a
*iNOS↓,
*COX2/PTGS2↓,
*IL6↓, and reduced the generation of pro-inflammatory cytokines like interleukin (IL)-6, IL-1β, tumor necrosis factor α, and monocyte chemoattractant protein-1
*IL1β↓,
*TNF-α↓,
*Sleep↑, GABA rice containing 26.4 mg of GABA three times daily resulted in the improvement of insomnia scores as assessed by the Kupperman Menopause Index.
*Pain↓, oral GABA supplementation or microbial-derived GABA, as a promising avenue for pain management.
*neuroP↑, potential neuroprotective properties of GABA have garnered significant interest
*eff↑, Specifically, glutamate supplementation was found to enhance memory performance by increasing acetylcholine (ACh) levels, distinguishing its effects from those of GABA
*Ach↑,
*AST↓, In support of the impact of dietary GABA on the CNS, FL50 significantly reduced AST and ALT levels induced by EtOH
*ALAT↓,
*BP↓, revealed a significant reduction in blood pressure within 2 to 4 weeks of FMG intake, and this reduction was sustained throughout the 12-week intervention period.
*other↝, Quantitative analysis of the gut microbiota composition revealed a positive correlation between the abundance of Bacteroides and GABA levels. Individuals with higher concentrations of Bacteroides exhibited elevated GABA levels in the fecal samples,
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Review, |
Nor, |
NA |
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Review, |
AD, |
NA |
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*RenoP↓, Thirdly, long-term use of hyperoside is toxic to the kidneys, but the damage is reversible
Casp3↑, Up-regulates caspase-3, caspase-8, Bax, p53 and MDA contents; decreases GSH, SOD and CAT activities; decreases VEGF and Bcl-2 levels; and inhibits cell growth. HeLa 100 μmol/L
Casp8↑,
MDA↑,
GSH↓,
SOD↓,
Catalase↓,
VEGF↓,
Bcl-2↓,
TumCG↓,
p‑Akt↓, Down-regulates BMP-7 expression, AKT phosphorylation and PI3K expression; induces cell cycle arrest; and inhibits cell proliferation. Human HepG2 5, 10, 20, 40 and 80 μM
PI3K↓,
TumCCA↑,
TumCP↓,
BMP7/OP1↓,
*ZO-1↑, up-regulates ZO-1 and claudin5 protein expression; maintains the integrity of the blood–brain barrier; and may protect neural function in CIR-injured mice. CIR injury induced by MCAO in mice 50 mg/kg
*BBB↝,
*p‑Akt↑, increases the phosphorylation of AKT and GSK-3β; alleviates early brain injury after subarachnoid haemorrhage; and promotes nerve function recovery in rats.
*GSK‐3β↑,
*SOD↑, increases SOD and CAT activities and GSH content; increases SIRT1 gene expression; down-regulates NF-κB mRNA
*Catalase↑,
*GSH↑,
*SIRT1↑,
*NF-kB↓,
*IL1β↓, Down-regulates IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax and caspase-3 levels; increases CAT, SOD and GSH activities; up-regulates Bcl-2, BDNF, TrkB, SIRT1 and NGF expression; reduces LPS-induced inflammation, oxidative stress and apoptosis; and protec
*IL6↓,
*IL8↓,
*TNF-α↓,
*ROS↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*Apoptosis↓,
*cardioP↑, Cardioprotective Activity of Hyperoside.
*AST↓, Decreases the levels of AST, CK, CK-MB and c-TnT in rats; the rate of cardiomyocyte apoptosis;
*hepatoP↑, Hepatoprotective Activity of Hyperoside.
*AST↓, Decreases liver index, AST, ALT, MDA and Bach1 complex levels and alleviates the pathological damage of acute liver injury mice.
*ALAT↓,
*MDA↓,
*BACH1↓,
*neuroP↑, Brain-Protective Activity of Hyperoside.
*Stroke↓, Down-regulates TNF-α, IL-1β, IL-6, ICAM-1, VCAM-1, TLR4, COX-2, NF-κB, caspase-3, caspase-9, Bax and Bcl-2 expression and prevents CIR injury. Middle cerebral artery occlusion/reperfusion rat model
*ICAM-1↓,
*VCAM-1↓,
*TLR4↓,
*COX2/PTGS2↓,
*RenoP↑, Renal-Protective Activity of Hyperoside.
*NLRP3↓, Suppresses NLRP3, caspase-1 and ASC expression and prevents acute kidney injury induced by lipopolysaccharide. Mouse acute kidney injury model
*Casp1↓,
*ASC↓,
*BioAv↓, low oral bioavailability
*BioAv↑, hyperoside is compatible with other traditional Chinese medicines and they can improve its bioavailability and oral absorption.
*toxicity↓, Firstly, an acute toxicity test of hyperoside showed that its LD50 > 5000 mg/kg
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vitro+vivo, |
Nor, |
RAW264.7 |
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*Inflam↓, Isoorientin has anti-inflammatory effects; however, the mechanism remains unclear.
*GSK‐3β↓, isoorientin is an inhibitor of glycogen synthase kinase 3β (GSK3β) in vitro
*TNF-α↓, isoorientin decreased the production of TNF-α, IL-6, and IL-1β and increased the expression of p-GSK3β in vitro and in vivo, similar to LiCl.
*IL6↓,
*IL1β↓,
*p‑GSK‐3β↑,
*eff↑, Coadministration of isoorientin and LiCl showed antagonistic effects
*COX2/PTGS2↓, Isoorientin decreased the expression of COX-2, inhibited the activation of ERK and NF-κB, and increased the activation of Nrf2/HO-1 in LPS-induced RAW264.7 cells
*ERK↓,
*NF-kB↓,
*NRF2↑,
*HO-1↑,
*OCLN↑, Isoorientin increased the expressions of occludin and ZO-1 in the brain of endotoxemia mice.
*ZO-1↑,
*BBB↝, protect the integrity of the blood-brain barrier and the homeostasis in the brain.
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in-vitro, |
AML, |
HL-60 |
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in-vitro, |
AML, |
K562 |
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in-vitro, |
BC, |
KAIMRC1 |
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ROS↑, Myrrh caused a dose-dependent effect on macrophages to increase the reactive oxygen species (ROS) level
M1↑, promote their polarization to classically activated macrophages (M1) and alternatively activated macrophages (M2) phenotypes, and consequently induce apoptosis
M2 MC↑,
Apoptosis?,
BBB↝, myrrh resin extract, only compounds 3, 4, 5, and 8 are potentially not permeable to the blood-brain barrier (BBB)
*cognitive↑, extra virgin olive oil (EVOO), particularly high-phenolic varieties, may be associated with improvements in cognitive domains such as memory, attention, executive function, and global cognition.
*memory↑,
*BBB↝, Proposed mechanisms include reduced blood–brain barrier permeability, enhanced brain functional connectivity, and the neuroprotective effects of compounds such as hydroxytyrosol and oleuropein.
*neuroP↑,
*neuroP↑, Neuroprotection by quercetin has been reported in several in vitro studies
*lipid-P↓, It has been shown to protect neurons from oxidative damage while reducing lipid peroxidation.
*antiOx↑, In addition to its antioxidant properties, it inhibits the fibril formation of amyloid-β proteins, counteracting cell lyses and inflammatory cascade pathways.
*Aβ↓,
*Inflam↓,
*BBB↝, It also has low BBB penetrability, thus limiting its efficacy in combating neurodegenerative disorders.
*NF-kB↓, downregulating pro-inflammatory cytokines, such as NF-kB and iNOS, while stimulating neuronal regeneration
*iNOS↓,
*memory↑, Quercetin has shown therapeutic efficacy, improving learning, memory, and cognitive functions in AD
*cognitive↑,
*AChE↓, Quercetin administration resulted in the inhibition of AChE
*MMP↑, quercetin ameliorates mitochondrial dysfunction by restoring mitochondrial membrane potential, decreases ROS production, and restores ATP synthesis
*ROS↓,
*ATP↑,
*AMPK↑, It also increased the expression of AMP-activated protein kinase (AMPK), which is a key cell regulator of energy metabolism.
*NADPH↓, Activated AMPK can decrease ROS generation by inhibiting NADPH oxidase activity
*p‑tau↓, Inhibition of AβAggregation and Tau Phosphorylation
*BioAv↓, confirmed that the intestinal permeability of RA is <1% of its intake volume
*BBB↝, migrates to the brain with difficulty due to the presence of the BBB
*monoA↑, RA administration increases monoamines in the brain
*TGF-β↓, Several studies have reported that RA suppresses the expression of Tgf-β1 in vivo and in vitro2
*Aβ↓, Suppression of Aβ aggregation by DA and other monoamines
*Aβ↓, We have previously shown that pantethine treatment reduces amyloid-β (Aβ)-induced IL-1β release and alleviates pathological metabolic changes in primary astrocyte cultures
*Mood↑, We observed that long-term pantethine treatment significantly reduced glial reactivity and Αβ deposition, and abrogated behavioral alteration in Tg mice.
*neuroP↑, Pantethine elicits broad physiological activities involving multiple cellular pathways. It has been shown to exert neuroprotective effects
*Inflam↓, but also to decrease inflammation and mediate immune responses
*TNF-α↓, We have previously shown that pantethine is able to protect mice against cerebral malaria by preserving blood–brain barrier integrity and by lowering TNF-α levels
*BBB↝, Cysteamine can cross the blood–brain barrier [110] and was shown to induce the release of BDNF (brain-derived neurotrophic factor)
*other↝, The present study demonstrated the efficiency of pantethine to reverse AD features such as astrogliosis, microgliosis, Aβ deposition, and to AD-associated aggressive behavior.
*Dose↝, Based on our results, pantethine, provided routinely as a dietary supplement, could be considered as a serious therapeutic option for preventing, slowing, or halting AD progression.
*BBB↝, BBB: not penetrant, but cysteamine (metabolite) is penetrant
*LDL↓, Pantethine has reduced total and LDL cholesterol though effects have been modest.
*lipid-P↓, Therapeutic Lifestyle Change (TLC) diet alone did
not significantly affect lipid profiles but when combined with pantethine supplementation, significantly
decreased lipid levels.
*AST↓, significantly reduced levels of liver enzymes (AST reduced from 66 to 33 IU/L, and ALT
reduced from 113 to 51 IU/L, or by 58%)
*ALAT↓,
*TGF-β↓, mean serum TGF-β level was significantly decreased
*adiP↑, while the mean serum level of high molecular adiponectin was increased.
*Inflam↓, inflammation was improved,
TumCG↓, mouse model of ovarian tumor, pantethine treatment (750 mg/kg/day, i.p.) for 4 weeks resulted in slower tumor progression,
FASN↓, Pantethine inhibits fatty acid synthase (FAS). Inhibition of FAS activity has been shown to be cytotoxic to human cancer cells in vitro and in
vivo [17].
Showing Research Papers: 1 to 14 of 14
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
BMP7/OP1↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↓, 1, GSH↓, 1, MDA↑, 1, ROS↑, 1, SOD↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
FASN↓, 1,
Cell Death(tgid=5) ⓘ
p‑Akt↓, 1, Apoptosis?, 1, Bcl-2↓, 1, Casp3↑, 1, Casp8↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
PI3K↓, 1, TumCG↓, 2,
Migration(tgid=13) ⓘ
TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↝, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
M1↑, 1, M2 MC↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
RadioS↑, 1,
Total Targets: 21
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
Stress↓, 1, Stroke↓, 1, TMAO↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, Catalase↑, 1, GSH↑, 1, HO-1↑, 1, lipid-P↓, 3, MDA↓, 2, NRF2↑, 1, ROS↓, 3, ROS↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
adiP↑, 1, ALAT↓, 3, AMPK↑, 1, LDL↓, 1, NADPH↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
p‑Akt↑, 1, Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, Casp1↓, 1, Casp3↓, 1, iNOS↓, 2,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, other↝, 3,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↓, 1, GSK‐3β↑, 1, p‑GSK‐3β↑, 1,
Migration(tgid=13) ⓘ
BACH1↓, 1, TGF-β↓, 2, TJ↝, 1, VCAM-1↓, 1, ZO-1↑, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 1, BBB↝, 13, OCLN↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
ASC↓, 1, COX2/PTGS2↓, 3, ICAM-1↓, 1, IL1β↓, 3, IL6↓, 3, IL8↓, 1, Inflam↓, 5, NF-kB↓, 3, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 2, BDNF↑, 1, monoA↑, 1, NGF↑, 1, p‑tau↓, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 3, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 1, Dose↝, 3, eff↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 3, AST↓, 4, BP↓, 1, IL6↓, 3,
Functional Outcomes(tgid=23) ⓘ
cardioP↑, 1, cognitive↓, 1, cognitive↑, 4, fatigue↓, 1, hepatoP↑, 1, memory↑, 3, Mood↑, 1, neuroP↑, 6, Pain↓, 1, RenoP↓, 1, RenoP↑, 1, Sleep↑, 1, toxicity↓, 2, toxicity∅, 1,
Total Targets: 83
Scientific Paper Hit Count for: BBB, Blood-Brain Barrier Permeability
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#:1123 State#:% Dir#:4
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