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↓,
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*AntiCan↑, gained increasing interest due to its proposed anti-cancer, anti-obesity, anti-inflammatory, antioxidant, and lipid-lowering effects, in addition to its thermogenic capacity.
*Obesity↓,
*Inflam↓,
*lipid-P↓,
*BioAv↓, intact curcumin in the body may be too low (<1 microM) and not sufficient to affect signaling and gene expression, as observed in vitro with cultured cells (10–20 microM).
*BioAv↑, a myriad of nanoformulations have been developed that either lead to a systemic increase in curcumin or are targeted to specific cells, tissues, or organelles
*BioAv↑, latest generation of curcumin nanoformulations can increase the bioavailability of free curcumin in plasma greater than 100-fold and have superior absorption, cellular uptake, BBB permeability, and tissue distribution
*BioAv↑, In a clinical study, the authors found that 2 g of curcumin administered concomitantly with 20 mg of piperine, an inhibitor of hepatic and intestinal glucuronidation, appeared to promote a significant 2000% increase in the oral bioavailability of cur
*BioAv↑, rats in which piperine pre-administration was performed before receiving curcumin, there was a significant increase in the oral bioavailability of curcumin, especially at 6 h after piperine administration
*BioAv↑, Nanotechnology-based delivery systems such as micelles, liposomes, and polymeric, metal, and solid lipid nanoparticles have also been applied to enhance curcumin bioavailability
*ROS↓, Curcumin was effective against ischemia/reperfusion (I/R) lesions, as well in various experimental models, primarily through antioxidant actions such as scavenging ROSs [153], increasing mitochondrial superoxide dismutase (SOD) activity and decreasin
*mt-SOD↑,
*MDA↓,
*BBB↓, Curcumin has poor bioavailability, especially in the brain, where the BBB further limits its absorption
*Aβ↓, curcumin appears to reduce the production of Aβ also by affecting a second enzyme required for the cleavage of APP
*GSK‐3β↓, the inhibition of GSK3β by curcumin would hinder both Aβ production and tau aggregation
*tau↓,
*neuroG↑, prolonged treatment of aged rats with curcumin stimulates neurogenesis in the hippocampus
*memory↑, chronic curcumin administration improved memory acquisition and consolidation in both adult and aged rats
cardioP↑, curcumin has been investigated to promote cardioprotective effects against chemotherapy-induced cardiotoxicity
*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.
*toxicity↓, Data showed no serious adverse events associated with GABA at intakes up to 18 g/d for 4 days and in longer studies at intakes of 120 mg/d for 12 weeks.
*BP↓, GABA was associated with a transient and moderate drop in blood pressure (<10% change). intake of 80 mg/day of GABA was associated with a significant reduction of the BP in adults with mild hypertension, and no adverse effects were reported.
*AntiDiabetic↑, other biological activities, which include anti-hypertension, anti-diabetes, anti-cancer, antioxidant, anti-inflammation, anti-microbial, and anti-allergy effects
*AntiCan↑,
*antiOx↑,
*Inflam↓,
*AntiBio↑,
*other↝, GABA is a popular ingredient in sports dietary supplements and other wellness dietary supplements.
*cognitive↑, The NNHPD monograph for Cognitive Function Products recommends a daily intake of 50–3000 mg GABA that does not exceed 750 mg per single dose; it also says to consult a healthcare practitioner for use of products providing 300 mg/day or more when GABA
*GH↑, GABA has been reported to increase serum GH levels and has been considered an ergogenic aid. Many sports supplements include GABA as an ingredient.
*Sleep↑, insomnia improved more with 300 mg of GABA compared to 150 mg
*BioAv↑, GABA was rapidly absorbed (Tmax: 0.5~1 h)
*Half-Life↝, with a half-life of 5 h.
*BBB↓, very low amounts of GABA cross from the plasma into the brain through the BBB even when GABA is exogenously administered orally or intravenously
*eff↑, GABA and L-theanine had a synergistic effect on the sleep behavior of mice
*neuroP↑, Hydroxycinnamic acids, including ferulic acid, caffeic acid, chlorogenic acid, rosmarinic acid, and salvianolic acids, exhibit pleiotropic neuroprotective effects involving antioxidant, neuroinflammation, amyloid and tau modulation, and mitochondrial
*antiOx↓,
*Inflam↓,
*tau↓,
*BioAv↓, Translation is limited by poor oral bioavailability, rapid metabolism, and restricted blood–brain barrier penetration.
*BBB↓,
*BioAv↑, Nanoformulation and prodrug approaches show promise in improving CNS exposure in preclinical models.
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/PTGS2↓,
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↓,
*BioAv↝, through different routes of administrations, including intravenously (IV), via hypodermic (IH) or intraperitoneal (IP) injection, and orally, have indicated that ISL exhibits a robust absorption capacity (absorption rate: ~60–90 min; oral absorptio
*BBB↓, ISL distribution mainly relies on the blood circulation, with the brain showing the lowest level of ISL due to the blood–brain barrier (BBB)
*BioAv↑, To improve solubility, enhancing its bioavailability and distribution, encapsulated ISL nanoparticles or nano-ISL have been developed.
selectivity↑, A selective cytotoxicity effect of ISL has been reported (Table 2 and Table 3), and the effective dose in tumor cell lines shows very little cytotoxic effect on normal cells.
*neuroP↑, Figure 4
*Inflam↓,
NF-kB↓,
TNF-α↓,
IL6↓,
IL1β↓,
IL10↓,
ICAM-1↓,
COX2/PTGS2↓,
PPARγ↑,
MMP2↓,
cFos↓,
VEGF↓,
CHOP/DDIT3↓,
CTSK↓,
CycB/CCNB1↑,
cycD1/CCND1↑,
TOP2↑,
PI3K↓, ISL also can inhibit the PI3K/AKT pathway and thus suppresses EMT and increases the antiproliferative effect
Akt↓,
mTOR↓,
MMP9↓,
TIMP1↓,
ChemoSen↑, ISL not only inhibits cancer cell growth by inducing apoptosis and autophagy, but can also enhance chemosensitivity
CSCs↓, ISL can interact synergistically with these first-line chemotherapy drugs through mediating cell death (apoptosis) and autophagy and suppressing breast CSCs
*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 10 of 10
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CTSK↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
NADH↓, 1, ROS↑, 1, mt-ROS↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
mitResp↓, 1, MMP↓, 1, MPT↑, 1, OCR↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
PPARγ↑, 1, SIRT1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Apoptosis↑, 2, Casp↑, 1, Casp3↑, 1, Cyt‑c↑, 2, p38↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, ER Stress↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CycB/CCNB1↑, 1, cycD1/CCND1↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
cFos↓, 1, CSCs↓, 1, EMT↓, 1, mTOR↓, 2, PI3K↓, 2, RAS↓, 1, p‑STAT3↓, 1, TOP1↓, 1, TOP2↓, 1, TOP2↑, 1, TumCG↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 1, E-cadherin↑, 1, MMP2↓, 1, MMP9↓, 1, N-cadherin↓, 1, Snail↓, 1, TIMP1↓, 1, TRIB3↑, 1, TumCMig↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
EGFR↓, 1, NO↝, 1, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, ICAM-1↓, 1, IL10↓, 1, IL1β↓, 1, IL6↓, 1, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 2, eff↑, 2, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, IL6↓, 1, TRIB3↑, 1,
Functional Outcomes(tgid=23) ⓘ
cardioP↑, 1, chemoPv↑, 1, Obesity↓, 1,
Total Targets: 64
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
4-HNE↓, 1, antiOx↓, 2, antiOx↑, 2, Catalase↑, 2, GPx↑, 2, GSH↑, 1, GSR↑, 1, H2O2↓, 1, HO-1↑, 1, lipid-P↓, 2, mt-lipid-P↓, 1, MDA↓, 3, Mets↝, 1, MPO↓, 1, NQO1↑, 1, NRF2↑, 2, ROS↓, 5, SOD↑, 2, mt-SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, NADH:NAD↑, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 1, cl‑Casp3↓, 1, Cyt‑c∅, 1, TRPV1↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 2,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP70/HSPA5↝, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
FOXO↑, 1, GH↑, 1, GSK‐3β↓, 2, neuroG↑, 1, TRPM7↓, 1, TRPM7⇅, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 1, Ca+2↑, 1, MMP9↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 9, BBB↝, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 1, Inflam↓, 7, NF-kB↓, 1, p65↓, 1, TLR4↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
MAOA↓, 1, tau↓, 2, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 3, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 5, BioAv↑, 10, BioAv↝, 2, eff↑, 5, Half-Life↓, 1, Half-Life↝, 2,
Clinical Biomarkers(tgid=22) ⓘ
BP↓, 2, GutMicro↑, 2,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, AntiDiabetic↑, 1, cardioP↑, 1, cognitive↑, 1, fatigue↓, 1, memory↑, 1, motorD↑, 1, neuroP↑, 6, Obesity↓, 1, Risk↓, 1, Sleep↑, 1, toxicity↓, 1,
Total Targets: 75
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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