BloodF Cancer Research Results
BloodF, Blood Flow: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*MMP↓, BC and CBD diminished HG-induced hyperglycemia in Schwann cells, in part by reducing mitochondrial membrane potential, reactive oxygen species, and mitochondrial superoxides.
*ROS↑,
*BloodF↑, while improving blood flow
*Pain↓, CBD and BC treatments also reduced pain hypersensitivity to hyperalgesia and allodynia, with increased antioxidant and anti-inflammatory action in diabetic rats.
*antiOx↑,
*Inflam↓,
*AMPK↑, in vivo effects were attributed to significant upregulation of AMPK, sirT3, Nrf2, PINK1, PARKIN, LC3B, Beclin1, and TFAM functions
*SIRT3↑,
*NRF2↑,
*PINK1↑,
*PARK2↑,
*LC3B↑,
*Beclin-1↑,
*TFAM↑,
*NLRP3↓, while downregulation of NLRP3 inflammasome, NFκB, COX2, and p62 activity was noted
*NF-kB↓,
*COX2↓,
*p62↓,
*NP/CIPN↓, CBD and BC combination ameliorates DN by modulating the mitochondrial quality control system.
*toxicity↓, It has been demonstrated that oral administration of saffron extract at doses from 0.1 to 5 g/kg was non-toxic in mice
*lipid-P↓, crocetin showed significant effects on coronary heart disease by inhibiting lipoprotein oxidation
*neuroP↑, on neurodegenerative diseases [33, 39-44], on retinal function recovery by increasing retinal blood flow [33, 45], on reducing blood pressure and maintaining kidney function
*BloodF↑,
*BP↓,
*RenoP↑,
*ATP↑, enhance oxygen diffusivity during shock and reperfusion that ultimately lead to increased ATP production
AntiCan↑, Saffron and its derivatives particularly crocetin have demonstrated significant anticancer activity in breast, lung, pancreatic and leukemic cells.
TumCP↓, Breast Cancer MCF-7, MDA-MB-231 ↓Proliferation
Apoptosis↑, ↑Apoptosis
lipid-P↓, Liver Cancer Wistar rat (AFB1) C3H1OT1/2 cells ↓Lipid perxidation
ROS↓, Liver Cancer Wistar rat (AFB1)
C3H1OT1/2 cells ↓Reactive oxygen species
GSTs↑, Lung Cancer Swiss albino mice (B[a]P) ↓ Lipid peroxidation, ↑GST, ↑catalases, ↑superoxide dismutase
Catalase↑,
SOD↑,
*BloodF↑, The beneficial effects of dipyridamole on blood flow and vascular density were dependent on NO production as dipyridamole did not augment ischaemic tissue reperfusion, vascular density, or endothelial cell proliferation in endothelial NO synthase (eN
*NO↑, Dipyridamole augments nitrite/NO production, leading to enhanced arteriogenesis activity and blood perfusion in ischaemic limbs.
*AntiAg↑, Dipyridamole, a conventionally used anti-platelet agent for the secondary prevention of cerebrovascular disease, has beneficial effects beyond platelet inhibition, including antithrombotic, anti-inflammatory, anti-proliferative, thrombolytic, and ant
*AntiThr↑,
*antiOx↑,
*angioG↑, rapidly restores ischaemic tissue blood flow and stimulates angiogenesis through a protein kinase A (PKA)-dependent eNOS pathway.
*BloodF↑, Dipyridamole therapy quickly rectified ischemic hind limb blood flow to near pre-ligation levels within three days after starting therapy.
*NO↑, Dipyridamole significantly increased total nitric oxide metabolite levels (NOx) in tissue that were not associated with changes in eNOS expression or phosphorylation.
*AntiAg↑, Dipyridamole anti-platelet therapy has previously been suggested to ameliorate chronic tissue ischemia in healthy animals.
*BloodF↑, Restoration of ischemic tissue blood flow was associated with increased vascular density and endothelial cell proliferation observed only in ischemic limbs.
*NOX↑, Dipyridamole significantly increased total nitric oxide metabolite levels (NOx) in tissue that were not associated with changes in eNOS expression or phosphorylation.
*antiOx↑, importance of dipyridamole antioxidant activity in restoring tissue NO bioavailability during diabetes.
*NO↑,
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AD, |
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Park, |
NA |
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MS, |
NA |
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Stroke, |
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*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*eff↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats
*Inflam↓, Commercially, and in the modern apothecary, it is used for its anti-inflammatory, antiseptic, and scent properties to treat joint, ligament, and soft tissue pain.
*Pain↓,
*BioAv↝, Ten to 20 percent of MS is absorbed through the skin after application.
*BloodF↑, produces a local vasodilatory action which increases dermal blood flow, a local rise in temperature, and a sense of warmth;
*toxicity↑, Ingestion of pure oil of Wintergreen, such as in aromatherapy products, has caused poisoning and death in children due to its high concentration of MS — up to 98 percent in some products
other↑, Magnetic fields have been found to stimulate collagen density in and around the joints, and help to trigger Ca2+ flow to the defect site resulting in faster bone healing
BloodF↑, blood microcirculation revealed that magnetic fields have strong influence on relaxation and constriction of capillary blood vessels which alters the blood flow.
Glycolysis↓, In general, the glycolysis and glucose oxidations are decreased in diabetic patients leading to lower ATP production.
ATP↓,
VEGF↓, Application of magnetic fields can significantly decrease VEGF level and therefore reduces the growth and distribution of cancer to other parts of the body
ROS↑, SMF interacts with the charged molecules (ions, proteins etc.) of biological system through several physical mechanisms and alters the activity, concentration, and life time of paramagnetic free radicals i.e. ROS (reactive oxygen species),
P-gp↓, study demonstrated that 8.8 mT SMF enhances cytotoxic potency of Adriamycin on K562 cells due to decrease in the P-gp expression
Apoptosis↑, n vitro analysis in terms of apoptosis and cell electrical properties showed that MCF7 cells are highly reactive to 3 mT flux density and normal cells (MCF10) are unaffected.
selectivity↑,
Ca+2↑, Long PMF (50 Hz, 0.1–1 mT) for 7 days Undifferentiated PC12, increased intracellular Ca+ concentration and Catalase activity.
Catalase↑,
*BioAv↝, although intra-nasal use of tea tree oil may cause irritation to mucous membranes.
*toxicity↝, Side effects were reported in 60% of included studies and were minor, except where tea tree oil was applied topically in concentrations ≥ 25%.
*BloodF↑, Blood flow was significantly higher in fingers immersed in the saline with tea tree oil solution, compared with saline alone.
*Sleep↑, Tea tree oil was found to be as effective as lavender essential oil in improving sleep quality, although baseline scores for sleep quality were higher in the tea tree oil grou
Showing Research Papers: 1 to 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 2, GSTs↑, 1, lipid-P↓, 1, ROS↓, 1, ROS↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 2,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1,
Total Targets: 17
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 4, HO-1↑, 1, lipid-P↓, 1, NRF2↑, 2, PARK2↑, 1, ROS↓, 1, ROS↑, 1, SIRT3↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 2, MMP↓, 1, PINK1↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, CREB↑, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Bax:Bcl2↓, 1, Casp3↓, 1, Casp9↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, TFAM↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
GRP78/BiP↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↑, 1, NO↑, 3,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, IL1β↓, 1, IL33↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 3, NF-kB↓, 2, TNF-α↓, 1,
Cellular Microenvironment(tgid=17) ⓘ
NOX↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 1, tau↓, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 3, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↑, 8, BP↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
cognitive↑, 1, memory↑, 1, neuroP↑, 2, NP/CIPN↓, 1, Pain↓, 2, RenoP↑, 1, Sleep↑, 1, toxicity↓, 1, toxicity↑, 1, toxicity↝, 1,
Total Targets: 60
Scientific Paper Hit Count for: BloodF, Blood Flow
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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