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⟱
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*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein
*neuroP↑, improved neurological scores when carvacrol was given before or shortly after injury.
*ROS↓, studies showed reduced oxidative damage (MDA, 4-HNE), increased antioxidant enzymes (SOD, CAT, GPx), lower apoptosis (cleaved caspase-3), and variable changes in TRPM7 expression.
*MDA↓,
*4-HNE↓,
*SOD↑,
*Catalase↑,
*GPx↑,
*Apoptosis↓,
*cl‑Casp3↓,
*TRPM7⇅, variable changes in TRPM7 expression
*BBB↓, Natural products such as carvacrol can cross the blood-brain barrier and have been reported to inhibit TRPM7 in vitro
*TRPM7↓,
ChemoSen↑, Combination of HNK with many traditional chemotherapeutic drugs as well as radiation sensitizes cancer cells to apoptotic death
BBB↓, HNK is also capable of crossing the BBB
Ca+2↑, HNK promotes human glioblastoma cancer cell apoptosis via regulation of Ca(2+) channels
Cyt‑c↑, release of mitochondrial cytochrome c and activation of caspase-3
Casp3↑,
chemoPv↑, potent chemopreventive agent against lung SCC development in a carcinogen-induced lung SCC murine model
OCR↓, HNK treatment results in a decreased oxygen consumption rate (OCR) in whole intact cells, rapidly, and persistently inhibiting mitochondrial respiration, which leads to the induction of apoptosis
mitResp↓,
Apoptosis↑,
RadioS↑, Honokiol as a chemo- and radiosensitizer
NF-kB↓, HNK as an anticancer drug is its potential to inhibit multiple important survival pathways, such
as NF-B and Akt
Akt↓,
TNF-α↓, by inhibiting TNF-induced nerve growth factor IB expression in breast cancer cells
PGE2↓, reduced prostaglandin E2 (PGE2) and vascular endothelial growth factor (VEGF) secretion levels
VEGF↓,
NO↝, HNK inhibits cancer cell migration by targeting nitric oxide and cyclooxygenase-2 or Ras GTPase-activating-like protein (IQGAP1) [
COX2↓,
RAS↓,
EMT↓, HNK can reverse the epithelial-mesenchymal-transition (EMT) process, which is a key step during embryogenesis, cancer invasion, and metastasis,
Snail↓, HNK reduced the expression levels of Snail, N-cadherin and -catenin, which are mesenchymal markers, but increased E-cadherin,
N-cadherin↓,
β-catenin/ZEB1↓,
E-cadherin↑,
ER Stress↑, induction of ER stress
p‑STAT3↓, HNK inhibited STAT3 phosphorylation
EGFR↓, inhibiting EGFR phosphorylation and its downstream signaling pathways such as the mTOR signaling pathway
mTOR↓,
mt-ROS↑, We demonstrated that HNK treatment suppresses mitochondrial respiration and increases generation of ROS in the mitochondria, leading to the induction of apoptosis in lung cancer cells
PI3K↓, inhibition of PI3K/Akt/ mTOR, EMT, and Wnt signaling pathways.
Wnt↓,
*neuroP↑, comprehensive overview of resveratrol's neuroprotective role in IS
*NRF2↑, Findings from previous studies suggest that Nrf2 activation can significantly reduce brain injury following IS and lead to better outcomes
*SIRT1↑, neuroprotective effects by activating nuclear factor erythroid 2-related factor 2 (NRF2) and sirtuin 1 (SIRT1) pathways.
*PGC-1α↑, IRT1 activation by resveratrol triggers the deacetylation and activation of downstream targets like peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) and forkhead box protein O (FOXO)
*FOXO↑,
*HO-1↑, ctivation of NRF2 through resveratrol enhances the expression of antioxidant enzymes, like heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which neutralize reactive oxygen species and mitigate oxidative stress in the ischemic bra
*NQO1↑,
*ROS↓,
*BP↓, Multiple studies have demonstrated that resveratrol presented protective effects in IS, it can mediate blood pressure and lipid profiles which are the main key factors in managing and preventing stroke
*BioAv↓, The residual quantity of resveratrol undergoes metabolism, with the maximum reported concentration of free resveratrol being 1.7–1.9 %
*Half-Life↝, The levels of resveratrol peak 60 min following ingestion. Another study found that within 6 h, there was a further rise in resveratrol levels. This increase can be attributed to intestinal recirculation of metabolites
*AMPK↑, Resveratrol also increases AMPK and inhibits GSK-3β (glycogen synthase kinase 3 beta) activity in astrocytes, which release energy, makes ATP available to neurons and reduces ROS
*GSK‐3β↓,
*eff↑, Furthermore, oligodendrocyte survival is boosted by resveratrol, which may help to preserve brain homeostasis following a stroke
*AntiAg↑, resveratrol may suppress platelet activation and aggregation caused by collagen, adenosine diphosphate, and thrombin
*BBB↓, Although resveratrol is a highly hydrophobic molecule, it is exceedingly difficult to penetrate a membrane like the BBB. However, an alternate administration is through the nasal cavity in the olfactory area, which results in a more pleasant route
*Inflam↓, Resveratrol's anti-inflammatory effects have been demonstrated in many studies
*MPO↓, Resveratrol dramatically lowered the amounts of cerebral infarcts, neuronal damage, MPO activity, and evans blue (EB) content in addition to neurological impairment scores.
*TLR4↓, TLR4, NF-κB p65, COX-2, MMP-9, TNF-α, and IL-1β all had greater levels of expression after cerebral ischemia, whereas resveratrol decreased these amounts
*NF-kB↓,
*p65↓,
*MMP9↓,
*TNF-α↓,
*IL1β↓,
*PPARγ↑, Previous studies have shown that resveratrol activates the PPAR -γ coactivator 1α (PGC-1 α), which has free radical scavenging properties
*MMP↑, Resveratrol can prevent mitochondrial membrane depolarization, preserve adenosine triphosphate (ATP) production, and inhibit the release of cytochrome c
*ATP↑,
*Cyt‑c∅,
*mt-lipid-P↓, mitochondrial lipid peroxidation (LPO), protein carbonyl, and intracellular hydrogen peroxide (H2O2) content were significantly reduced in the resveratrol treatment group, while the expression of HSP70 and metallothionein were restored
*H2O2↓,
*HSP70/HSPA5↝,
*Mets↝,
*eff↑, Shin et al. showed that 5 mg/kg intravenous (IV) resveratrol reduced infarction volume by 36 % in an MCAO mouse model.
*eff↑, This study indicates that resveratrol holds the potential to improve stroke outcomes before ischemia as a pre-treatment strategy
*motorD↑, resveratrol treatment significantly reduced infarct volume and prevented motor impairment, increased glutathione, and decreased MDA levels compared to the control group,
*MDA↓,
*NADH:NAD↑, Resveratrol treatment significantly enhanced the intracellular NAD+/NADH ratio
eff↑, Pretreatment with resveratrol (20 or 40 mg/kg) significantly lowered the cerebral edema, infarct volume, lipid peroxidation products, and inflammatory markers
eff↑, Intraperitoneal administration of resveratrol at a dose of 50 mg/kg reduced cerebral ischemia reperfusion damage, brain edema, and BBB malfunction
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*Inflam↓, its anti-inflammatory, anti-oxidant, and anti-apoptotic properties.
*antiOx↓,
*neuroP↑, potential applications of UA in neuroprotective strategies
*p‑tau↓, mainly in AD and ischemic neuronal injury resulting in improved cognition, reduced neuroinflammation, neuronal loss, tau phosphorylation, and amyloid plaques
*Aβ↓,
*eff↑, The bioavailability of ellagitannin is very low; however, their absorption may be increased by the co-intake of dietary fructooligosaccharides.
*BioAv↓, only 40% of individuals could naturally convert the polyphenolic precursors to UA
*BioAv↑, administration of UA is proposed to be an answer for urolithin non-producers, which could allow for the exploration of its health benefits
*GSH↑, UA administration protected against the cisplatin-induced depletion of the renal GSH pool, the inhibition of GPx and superoxide dismutase (SOD) activity
*SOD↑,
*lipid-P↓, declined lipid peroxidation and protein nitration were observed
*Catalase↑, UA not only enhanced the cellular antioxidant mechanism attributed to increased CAT, SOD, glutathione reductase (GR), and GPx activity, but also inhibited oxidizing enzymes contributing to reactive oxygen species (ROS)
*GSR↑,
*GPx↑,
*ROS↓,
*NRF2↑, Beneficial effects of UA, including antioxidant activity, are believed to be mediated through the activation of the Nrf2/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway
*GutMicro↑, enhancing the gut barrier integrity caused by the UA administration
*Risk↓, Urine UA elevation was reported to also be associated with decreased age-related hippocamp atrophy—a biomarker of neurodegeneration and cognitive decline
*BBB↓, free form of UA crossing the blood–brain barrier (BBB) in animal model studies
*NLRP3↓, UA downregulated NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome-mediated inflammation,
*MAOA↓, Another aspect of the role of UA in PD management is its inhibitory effects on monoamine oxidase (MAO).
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
NADH↓, 1, ROS↑, 1, mt-ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
mitResp↓, 1, MMP↓, 1, MPT↑, 1, OCR↓, 1,
Core Metabolism/Glycolysis ⓘ
SIRT1↓, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 2, Casp↑, 1, Casp3↑, 1, Cyt‑c↑, 2, p38↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, mTOR↓, 1, PI3K↓, 1, RAS↓, 1, p‑STAT3↓, 1, TOP1↓, 1, TOP2↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
Ca+2↑, 1, E-cadherin↑, 1, N-cadherin↓, 1, Snail↓, 1, TRIB3↑, 1, TumCMig↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
EGFR↓, 1, NO↝, 1, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, eff↑, 2, RadioS↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, TRIB3↑, 1,
Functional Outcomes ⓘ
chemoPv↑, 1, Obesity↓, 1,
Total Targets: 46
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
4-HNE↓, 1, antiOx↓, 1, antiOx↑, 1, Catalase↑, 2, GPx↑, 2, GSH↑, 1, GSR↑, 1, H2O2↓, 1, HO-1↑, 1, lipid-P↓, 1, mt-lipid-P↓, 1, MDA↓, 2, Mets↝, 1, MPO↓, 1, NQO1↑, 1, NRF2↑, 2, ROS↓, 4, SOD↑, 2,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, MMP↑, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, NADH:NAD↑, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 1, cl‑Casp3↓, 1, Cyt‑c∅, 1, TRPV1↑, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↝, 1,
Proliferation, Differentiation & Cell State ⓘ
FOXO↑, 1, GSK‐3β↓, 1, TRPM7↓, 1, TRPM7⇅, 1,
Migration ⓘ
AntiAg↑, 1, Ca+2↑, 1, MMP9↓, 1,
Barriers & Transport ⓘ
BBB↓, 4,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 1, Inflam↓, 3, NF-kB↓, 1, p65↓, 1, TLR4↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
MAOA↓, 1, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 2, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 2, BioAv↝, 1, eff↑, 4, Half-Life↓, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, GutMicro↑, 2,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 1, motorD↑, 1, neuroP↑, 4, Risk↓, 1,
Total Targets: 61
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
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