BloodF Cancer Research Results
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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/PTGS2↓,
*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↑,
*hepatoP↑, Artichoke leaf extract (ALE) has shown potential as a hepatoprotective agent.
*Dose↝, 100 subjects with ultrasound-diagnosed NAFLD were randomized to either ALE 600 mg daily or placebo for a 2-month period.
*toxicity↓, with no side effects reported.
*BloodF↑, Doppler sonography showed increased hepatic vein flow (p < .001), reduced portal vein diameter (p < .001) and liver size (p < .001), reduction in serum ALT (p < .001) and AST (p < .001) levels, improvement in AST/ALT ratio
*ALAT↓,
*AST↓,
*Bil↓, and reduction in total bilirubin
*LDL↓, ALE supplementation reduced total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and triglyceride concentrations
*HDL↓,
*TG/TAG↓,
*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↑,
*toxicity↓, Taking a 240-mg daily dose of Ginkgo biloba extract (EGb761) is effective and safe in the treatment of dementia.
*Dose↝, The standard composition of EGb761 preparations is 22.0% to 27.0% flavonoids and 5.0% to 7.0% terpenoids (ginkolides A, B, C; bilobalide; etc.) as active ingredients, and less than 5 ppm of ginkgolic acid,
*ROS↓, Flavonoids inactivate deleterious toxic active oxygen, and terpenoids act as antagonists of platelet activating factor and exert neuroprotection in the brain
*PAF↓,
*memory↑, Ginkgo biloba is thought to improve memory and learning ability, blood flow in the microcirculation, hypoxia tolerance in brain cells, and blood viscosity due to its antioxidant, antiinflammatory, and other activities.
*BloodF↑,
*antiOx↑,
*Inflam↓,
*Tinn↓, Although Ginkgo biloba extract has been reported to be effective in the treatment of vertigo [3], tinnitus [4], headache [5], and anxiety disorders [6] in clinical trials, consistent, conclusive results were not reported because of small sample sizes
*Dose↝, A standardized formulation, EGb 761®, also sold as Tanakan® or Tebonin®, was created to normalize the constituents to assure reliable and consistent drug performance and the absence of ginkgolic acid, a known allergen naturally found in Ginkgo
*PAF↑, Ginkgolides have been clinically shown to act as platelet-activating factor (PAF) antagonists, inhibiting platelet aggregation and promoting increased blood flow.
*AntiAg↑,
*BloodF↑,
*Inflam↓, Additionally, BB(bilobalide) has shown anti-inflammatory properties and neuroprotection in preclinical models of stroke16 and AD
*neuroP↑,
*Stroke↓, Alternatively, promising results have been observed that support administration of EGb 761 soon after the onset of ischemia and during the recovery period.
*Dose↝, The standard clinical dose of EGb 761 is 120 mg (~1.7 mg/kg) once or twice daily; thus, a standard dose will contain ~3–4 mg ginkgolides A, B, and C, 3–4 mg BB, and 29 mg flavonoids.
*Sepsis↓, Patients treated with antimicrobials plus GB showed a significant drop in mortality as compared to patients treated with antimicrobials and placebo; this finding led to the development of other PAF antagonists for the treatment of sepsis
*memory↑, when administered daily, EGb 761 (240 mg daily) may improve some aspects of memory better than others
*BioAv↑, Ferulic acid (4-hydroxy-3-methoxycinnamic acid) is abundant in some cereal grains and shows relatively higher absorption in the gastrointestinal mucosa compared to other phenolic acids
*cognitive↓, oral administration of ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks improved the mild cognitive impairment in populations aged 65−85 years old.
*Dose↝, ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks
*neuroP↑, ferulic acid might possess great neuroprotective potential in the neurodegenerative diseases.
*Aβ↓, ferulic acid reduced Aβ plaque deposits via inhibiting β-secretase (BACE1) activity and cleavage, as well as enhancing α-secretase (ADAM10) activity and cleavage in APP/PS1 mice
*BACE/β-secretase↓,
*ADAM10↑,
*Ac-histone H3↑, ferulic acid improved the cholinergic deficits as indicated by the increased ACh level in the cortex of Aβ1−42 -injected (i.c.v.) mice after ferulic acid treatmen
*BloodF↑, rerulic acid improved the cerebral blood flow (CBF) and insulin resistance, which helped to reduce the progression of AD pathology
*IRes↑,
*memory↑, while ferulic acid treatment (20 mg/kg, p.o.) improved the capillary hypofunction and reduced the memory deficits of APP/PS1 mice.
*Dose↝, Notably, the effective doses of ferulic acid in rodents were 5.3−30 mg/kg when administered for more than 4 weeks, which could be achieved through daily intake of appropriate amount of mung bean
*GlyFlow↑, 40 Hz light flickering enhanced glymphatic influx and efflux independently of anesthesia and sleep,
*e-ADO↑, First, brief 40 Hz light flickering produces a robust and sustained increase in the extracellular adenosine levels in the primary visual cortex and other brain regions
*Sleep↑, Second, 40 Hz light flickering promotes sleep18, when the glymphatic system is mostly active
*Dose↝, 30-min exposure to light flickering (white light, illuminance of 3000 lux, irradiance of 1.10 mW/cm2 at 20 cm distance, 50% duty cycle) at 40 Hz
*AQPs↑, Accordingly, we found that 40 Hz light flickering increased the gene expression of AQP4-M23
BloodF↑, 40 Hz light flickering increases vasomotion and cerebral blood flow (CBF)
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vitro+vivo, |
Nor, |
HUVECs |
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vitro+vivo, |
Diabetic, |
NA |
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*BloodF↑, Formononetin (FMN), a phytoestrogen from Astragalus roots, is traditionally used to enhance blood function and microcirculation; however, its mechanism remains unclear.
*Ferroptosis↓, FMN effectively reduced ferroptosis markers in HG-treated HUVECs,
*eff↓, and Erastin treatment abolished this protective effect.
*mtDam↓, block ferroptosis through two mechanisms: restoration of mitochondrial integrity and reactivation of the xCT/GPX4 antioxidant system
*xCT/SLC7A11↑,
*GPx4↑,
*Wound Healing↑, When we tested FMN in diabetic mice, wound closure rates improved substantially, the expression of xCT and GPX4 was increased, and CD31 expression in wound vessels increased, which matched what we observed in vitro.
*CD31/PECAM-1↑,
*mt-ROS↓, mitigation of mitochondrial reactive oxygen species (mtROS) accumulation through xCT/GPX4 activation.
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.
*antiOx↑, The antioxidant effects of EGb 761 are mainly related to its influence on cerebral blood flow, the neurotransmitter system, cellular redox state and the level of nitric oxide
*ROS↓, EGb 761 works directly by scavenging ROS or increasing the expression of genes encoding antioxidant enzymes
*mitResp↑, When used, it reduces oxidative stress, improving mitochondrial respiration (Müller et al., 2019) and protects cells from NO-induced neurotoxicity by reducing the increase in caspase-9 activity that activates caspase-3, leading to cell apoptosis
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*ATP↑, EGb 761 reduces the production of ROS in the mitochondria and protects the mitochondrial complexes of the respiratory chain and increases the availability of ATP
*neuroP↑, Neuroprotective Effect of G. biloba
*IL1β↓, IL-1β, IL-6 and TNFα, causing pro-inflammatory reactions, however, anti-inflammatory cytokines such as IL-4, IL-13 and Arg-1 are also secreted in microglia activation. The use of EGb 761 significantly reduces the above-mentioned cytotoxic mediators,
*IL6↓,
*TNF-α↓,
*PGE2↓, EGb 761 extract strongly inhibits LPS-induced prostaglandin E2 (PGE 2) production mediated by cyclooxygenase 2 (COX-2)
*memory↑, The main reasons for the improvement in memory and cognitive functions after the use of G. biloba include: increased blood flow in the brain, protective effect against peroxidation of brain lipids, easier utilization of oxygen and glucose by brain ce
*cognitive↑,
*BloodF↑,
*lipid-P↓,
*Aβ↓, reduction of amyloid plaque deposition
*MAOA↓, EGb 761 can effectively reduce the activity of MAO, as well as increasing the level of dopamine, especially in the prefrontal cortex
*DA↑,
*Dose↝, In general, the EGb 761 extract is well tolerated and safe up to a dose of 240 mg/day
*toxicity↓, The oral LD50 in mice is 2,100 times the recommended daily dose
Dose↝, Body temperature during heating was maintained at 39.5 ± 0.5 °C for 4 h
BloodF↑, Heating tumour-bearing mice resulted in significant decrease in intratumoural IFP, increased the number of perfused tumour blood vessels as well as relative tumour perfusion in both tumour models
Hypoxia↓, Intratumoural hypoxia was also reduced in tumours of mice that received heat treatment.
RadioS?, Mice bearing FaDu tumours heated 24 h prior to five daily radiation treatments exhibited significantly enhanced tumour response compared to tumours in control mice.
NA↑, As an adjunct to radiotherapy and chemotherapy, hyperthermia enhances the therapeutic efficacy against both primary and recurrent tumors.
RadioS↑, The present review explores the mechanisms underlying the synergy between radiotherapy and hyperthermia, while reviewing the outcomes of relevant clinical trials.
DNArepair↓, Key mechanisms of action include inhibition of DNA repair, reduction of hypoxic tumor cell populations, enhancement of drug uptake and improved perfusion and oxygenation.
Hypoxia↓,
EPR↑,
LC↑, Its application has improved both local control and overall survival (OS),
OS↑,
*toxicity↓, Randomized clinical trials (4–6) have demonstrated that combined therapy effectively prolongs disease-free survival and ensures local tumor control without added toxicity.
Dose↝, fever-range temperatures (39–40°C), moderate heating to induce cellular stress (41–43°C) and high-intensity thermal ablation >43°C for cell destruction.
BloodF↑, Hyperthermia is particularly toxic to cells in acidic environments (29), and increased blood flow helps clear acidic metabolites, restore normal extracellular pH
pH↝,
Imm↑, Under heat stress, tumor cells release heat shock protein 70 (HSP70), triggering antitumor immune responses
HSP70/HSPA5↑,
LC↑, moderate RHT in improving local tumour control, survival outcomes and quality of life scores were observed across the different cancer subsites with minimal increase in toxicities.
OS↑,
QoL↑,
toxicity↓,
Dose↝, Various heating methods include direct (e.g., intracavitary and whole-body waterbed), infrared, perfusional (e.g., isolated limb perfusion, intravesical and intraperitoneal), nanoparticles, ultrasound and regional radiofrequency (RF) radiation
Dose↝, Moderate HT is usually described at a range of 39–44 °C a
ROS↑, Figure 1
DNArepair↓,
EPR↑,
DNAdam↑,
HSP70/HSPA5↑,
BloodF↑,
Hypoxia↓,
RadioS↑, Mild hyperthermia (mHT, 39–42 °C) is a potent modality when combined with existing radio-, chemo-, or immunotherapy, leading to enhanced microcirculatory blood flow and improved tumor oxygenation
ChemoSen↑, Hyperthermia enhances cytotoxicity of anticancer drugs:
Imm↑,
BloodF↑,
Hypoxia↓, HT-induced improvements of tumor oxygenation status (“reversal of tumor hypoxia”) a
Dose↝, Mild hyperthermia (mHT, 39–42 °C) is a potent cancer treatment modality when delivered in conjunction with radiotherapy.
DNArepair↓, Hyperthermia inhibits DNA repair enzymes: In the upper range of mHT (41–43 °C), several DNA damage repair enzymes responsible for the repair
e-pH↓, Tissue exposure to mHT triggers a series of events that aggravate tumor tissue acidosis (pH↓), finally reaching extracellular pH values of ≈ 6.20:
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in-vitro, |
Cerv, |
HeLa |
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in-vitro, |
Laryn, |
FaDu |
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RadioS↑, Hyperthermia has a number of biological effects that sensitize tumors to radiotherapy in the range between 40-44 °C.
TumCD↑, For treatment temperatures above 41 °C, we found a decrease in cell survival, an increase in sensitization towards irradiation, a decrease of BRCA2 protein levels, and altered RAD51 focus formation.
BRCA2↓,
Dose↝, This study demonstrates that optimal inhibition of HR is achieved by subjecting cells to hyperthermia at 41-43 °C for 30 to 60 minutes.
BloodF↑, The second explanation is that hyperthermia has multiple biological effects, including increased blood flow [33], increased oxidation [34], and activation of the immune system
ROS↑,
Imm↑,
*Dose↝, They regularly consumed 500 mL of beverage containing 110 mg of quercetin glycoside as isoquercitrin for 40 weeks.
*RT↓, Cognitrax demonstrated that the reaction time significantly improved in the quercetin glycoside intake group
*BloodF↑, The CBF measurement suggested that quercetin glycoside intake could likely suppress the decrease in cerebral blood volume, CBF
*Aβ↓, inhibit the decrease in CBF and suppress Aβ accumulation.
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Review, |
AD, |
NA |
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Park, |
NA |
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Review, |
MS, |
NA |
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Review, |
Stroke, |
NA |
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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/β-secretase↓, 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
*Dose↝, PEMF (5 min, twice a day for 3 weeks) was performed on 20 dogs affected by BPH. (Magcell® Vetri, Physiomed Elektromedizin AG, Schnaittach, Germany
*toxicity↓, The efficacy of PEMF on BPH in dogs, with no side effects, suggests the suitability of this treatment in humans and supports the hypothesis that impairment of blood supply to the lower urinary tract may be a causative factor in the development of BPH
*BloodF↑,
*Dose↝, A frequency of 4–12 Hz and intensity of 1000 Gauss was used. The magnetic field maximum strength was 200 mT. ( ±105 mT ) pulse rate of 12.5 ms
*PV↓, progressive reduction of prostatic volume was recorded from T0 to T3. Prostate volume decreased an average of 57% over the course of the study,
*Inflam↓, The anti-inflammatory function of electromagnetic-fields [34] should also be considered.
*PV↓, PEMF) to treat men suffering from benign prostatic hyperplasia (BPH). After one month of
treatment, prostate volume and symptoms significantly decreased.
*Inflam↓, The electromagnetic field is produced by a device that reduces inflammation by promoting growth of new blood vessels, dilation of blood vessels, and tissue remodeling.
*BloodF↑, PEMF was able to significantly reduce prostate volume after just 28 days of therapy,
resulting in a median decrease of 5.4%
*Dose↝, handheld PEMF device (Magcell® Microcirc, Physiomed Elektromedizin) for five minutes twice daily for 28 consecutive days.
*eff↑, Among groups, all parameters showed highly significant differences in favor of Group A. (PEMF)
*eff↑, Pelvic floor exercises deliver distinctive unmistakable effects on the prostate, particularly in individuals who present with BPH
*BloodF↑, Exercise can enhance blood circulation to the pelvic region, enabling the body to actively eliminate harmful agents and waste products;
*Diff↝, EMF is thought to have the ability to affect the cells that induce different cellular changes including cell reproduction and differentiation
*Dose↝, EMF device (PMT-120 Desktop, ElectroMeds, USA) was worked with impact to patient with damped trains of magnetic oscillations with a period of 20–1,100 nanoseconds and an intensity of 0.12–18 microtesla
*Dose↝, and a decreased damping of at least 0.05 and a repetition rate between the trains in the range of 25–30 Hz.
*Dose↝, application was directed to the perineum with the patient lying in the lateral recumbent position.
*Dose↝, 30 minutes for each day, five times each week for 4 progressive weeks.
*Dose↝, Aerobic exercises: regular aerobic exercise for 20–60 minutes undertaken five times each week at 55–90% of the maximal heart rate is estimated as 220 −age in years.
*Dose↝, pelvic floor exercises to be performed in daily sessions in lying, sitting, and standing positions consisting of 10 seconds of contractions followed by 10 seconds of relaxation and repeating the exercises 15 times each session.
*Dose↝, While, fast twitch muscle fibers can be trained through asking the patient to contract as if he controls his urine by quick contraction and relaxation of the levator ani muscles 20 times, rest for ten seconds, and then repeat again for a total of 2 t
*UFR↑, RU: post void residual urine volume, FR: urine flow rate, PSA: Intragroup comparisons showed a significant difference (p<0.05) in Groups A and B in all parameters
*UR↓,
*PSA↓,
*other↑, The results of the current study demonstrated that the use of PEMF and exercise therapy is beneficial in the treatment of BPH.
*Inflam↓, The anti-inflammatory capacity of PEMF should additionally be granted16)
*UFR↑, Our meta-analysis revealed that extracorporeal MS significantly reduced NIH-CPSI scores [MD = -6.65; 95% CI (-8.15, -5.15), P < 0.00001] and improved Qmax [MD = 2.98; 95% CI (1.36, 4.59), P = 0.0003] compared to the control group.
*other?, MS uses magnetic fields to stimulate the central and peripheral nervous systems non-invasively, thereby enhancing the activity of enzymes that catalyze the hydrolysis of pain-inducing substances
*Pain↓, This action contributes significantly to reducing the presence of these substances, thus mitigating pain and discomfort.
*BloodF↑,
*other↑, Furthermore, positioning magnetic coils at the sacral nerve roots significantly promotes bladder emptying. MS at this location stimulates the sacral nerve, inducing muscle contractions that trigger urination
*Inflam↓, MS modulates macrophage regenerative phenotypes and enhances the synthesis of anti-inflammatory mediators, thereby mitigating inflammatory response.
*QoL↑, Specifically, all three dimensions of the questionnaire - pain symptoms, urination symptoms, and quality of life - showed marked improvement.
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/ABCB1↓, 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 27 of 27
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
LC↑, 2, NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 2, GSTs↑, 1, lipid-P↓, 1, ROS↓, 1, ROS↑, 3, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 2, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP70/HSPA5↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
BRCA2↓, 1, DNAdam↑, 1, DNArepair↓, 3,
Migration(tgid=13) ⓘ
Ca+2↑, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
EPR↑, 2, Hypoxia↓, 4, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Imm↑, 3,
Cellular Microenvironment(tgid=17) ⓘ
pH↝, 1, e-pH↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↝, 6, RadioS?, 1, RadioS↑, 3, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↑, 7,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, OS↑, 2, QoL↑, 1, toxicity↓, 1,
Total Targets: 36
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
e-ADO↑, 1, Buty↑, 1, DA↑, 1, diuretic↑, 1, GLP-1R↑, 1, GlyFlow↑, 1, IRes↑, 1, PAF↓, 1, PAF↑, 1, PV↓, 2, RT↓, 1, SCFAs↑, 1, Stroke↓, 1, Tinn↓, 1, UFR↑, 2, UR↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 7, Bil↓, 1, Catalase↑, 1, Ferroptosis↓, 1, GPx↑, 1, GPx4↑, 1, HDL↓, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 1, NRF2↑, 3, PARK2↑, 1, ROS↓, 4, ROS↑, 1, mt-ROS↓, 1, SIRT3↑, 1, SOD↑, 2, uricA↓, 1, xCT/SLC7A11↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 3, mitResp↑, 1, MMP↓, 1, mtDam↓, 1, PINK1↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Ac-histone H3↑, 1, ALAT↓, 1, AMPK↑, 1, CREB↑, 1, LDL↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 1, Bax:Bcl2↓, 1, Casp3↓, 2, Casp9↓, 1, Casp9↑, 1, Ferroptosis↓, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, other?, 1, other↑, 2, TFAM↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
GRP78/BiP↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
Diff↝, 1, ERK↑, 1, GSK‐3β↓, 1, PI3K↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 3, CD31/PECAM-1↑, 1, COL1↓, 1, Fibrosis↓, 1, RAGE↓, 1, TGF-β1↓, 1, TJ↑, 1, α-SMA↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↑, 1, NO↑, 3,
Barriers & Transport(tgid=15) ⓘ
AQPs↑, 1, BBB↑, 1, IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, HMGB1↓, 1, IL1β↓, 2, IL33↓, 1, IL6↓, 2, IL8↓, 1, Inflam↓, 10, JAK2↓, 1, NF-kB↓, 3, PGE2↓, 1, PSA↓, 1, TNF-α↓, 2,
Cellular Microenvironment(tgid=17) ⓘ
NOX↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
ADAM10↑, 1, BDNF↑, 1, MAOA↓, 1, tau↓, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 4, BACE/β-secretase↓, 2, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 3, Dose↝, 20, eff↓, 1, eff↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, Bil↓, 1, BloodF↑, 20, BP↓, 1, GutMicro↑, 1, IL6↓, 2, PSA↓, 1, RAGE↓, 1, TG/TAG↓, 1,
Functional Outcomes(tgid=23) ⓘ
cognitive↓, 1, cognitive↑, 2, hepatoP↑, 1, memory↑, 5, neuroP↑, 5, NP/CIPN↓, 1, Pain↓, 3, QoL↑, 1, RenoP↑, 2, Sleep↑, 2, toxicity↓, 6, toxicity↑, 1, toxicity↝, 1, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Sepsis↓, 1,
Total Targets: 135
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1374 State#:% Dir#:2
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