AntiThr Cancer Research Results
AntiThr, antithrombotic: Click to Expand ⟱
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An antithrombotic agent is a drug that reduces the formation of blood clots.
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Scientific Papers found: Click to Expand⟱
*Wound Healing↑, Antimicrobial effect of AgNPs allows effective use in wound healing and dentistry
*AntiThr↑, AgNPs possess antithrombotic activity useful to treat cardiovascular diseases.
*AntiAg↑, Their anti-platelet effects can be attributed to their ability to prevent or inhibit platelets from adhering to each other.
eff↑, AgNPs makes them excellent agents for photothermal therapy in the treatment of tumours and cancers.
*AntiAg↑, Potentially, materials exhibiting antiplatelet activity may be applied in devices that prevent arterial thrombotic events like ischemic stroke, coronary heart disease, and ischemic gangrene.
*AntiThr↑,
*Dose↝, All four types of AgNPs were spherical in shape with the primary size close to 10 nm
*AntiThr↑, However, advent of biogenic silver nanoparticles with anticoagulant and thrombolytic potentials has opened up a window of opportunity to address most of the shortcomings of the chemical synthesized anticoagulants.
eff↑, Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin.
AntiThr↑, ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities.
Bacteria↓,
LDH↓,
TumCP↓, Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1
TumCCA↑, Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
Bcl-2↓, The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3.
Cyt‑c↑,
Casp3↑,
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*BioAv↝, Pure anethole is a colorless to faintly yellow liquid at above 23 °C [10]. It is poorly soluble in water, is highly soluble in alcohol, and is miscible with ether and chloroform.
*other↝, Trans-anethole has a sweet herbaceous smooth odor profile [7] and a sweet taste, being more than 10 times sweeter than common sugar
eff↓, Ultraviolet (UV) light and visible (VIS) light, temperature, atmospheric oxygen, the prolonged storage significantly influence the chemical stability of anethole.
TNF-α↓, Figure 3
IL10↑,
CXCR4↓,
MMP2↓,
MMP9↓,
TIMP1↑,
NF-kB↓,
AP-1↓,
STAT↓,
JNK↓,
ERK↓,
MAPK↓,
PI3K↓,
Akt↓,
JAK↓,
*AntiDiabetic↓,
*neuroP↑, Anethole dithiolethione (Fig. 4), a synthetic analogue of anethole, has an attractive potential in the development of neuroprotective agents in Parkinson’s disease due to its multifaceted antioxidant activity coupled with inhibition of monoamine oxid
*Imm↑, immunomodulatory profile of anethole may offer promising alternative therapy to counteract the effects of cytotoxic chemotherapeutic agents
chemoP↑,
*AntiThr↑, Anethole as well as fennel essential oil exhibit antithrombotic properties which are linked to a broad spectrum antiplatelet activity,
*AntiAg↑,
*antiOx↑, anticataract activity through the inhibition of lens aldose reductase (IC 50 = 3.8 lg/mL) and antioxidant activity. It increases SOD and catalase activities and restores GSH levels in the sugar induced lens opacification
*SOD↑,
*GSH↑,
*Wound Healing↑, administration of pharmaceutical formulation with 20 % anethole twice daily for 15 days accelerates wound closure of injured tissue
chemoPv↑, Cancer chemoprevention activity of anethole dithiolethione may be related to the increase of intracellular glutathione, up-regulation of phase II detoxification enzymes such as glutathione-S-transferase, and inhibition of NF-kB signaling activation
*GSTs↑,
*NF-kB↓,
Dose↝, Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications.
TumCP↓, CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis.
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
angioG↓,
*Inflam↓, including anti-inflammatory (3), antioxidant (4), antiviral (5), anti-bacterial (6), antithrombic (7), hypoglycemic (8), hepatoprotective (9), anti-diabetic (10), neuroprotective (11) and anticancer effects
*antiOx↑,
*Bacteria↓,
*AntiThr↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
AntiCan↑,
ChemoSen↑, can enhance the effectiveness of anticancer drugs and ensure patient safety.
*BioAv↝, the bioavailability of intravenous administration of CA was superior to that of oral administration
*BioAv↑, A into CA solid lipid nanoparticles, which increased the oral bioavailability of CA by >1.69 times.
eff↑, Especially when combined with hyperthermia therapy at 42°C and 43°C, CA could inhibit cell proliferation
CDK1↓, CB403 (Fig. 1) is a cinnamaldehyde derivative that inhibits the activity of cyclin-dependent kinases (CDKs), particularly CDK1, CDK2 and CDK4, thereby halting cell cycle progression.
CDK2↓,
CDK4↓,
cJun↓, 2-hydroxycinnamaldehyde (HCA; Fig. 1) inhibits the growth of SW620 colon cancer cells by reducing the expression of c-Jun and c-Fos, inhibiting the DNA binding activity of activator protein 1, and inducing cell apoptosis
cFos↓,
Apoptosis↑,
PI3K↓, CA can induce apoptosis in colon cancer cells by inhibiting the PI3K/Akt signaling pathway
Akt↓,
E-cadherin↑, CA upregulates the expression of E-cadherin while downregulating the expression of matrix metalloproteinase-2 (MMP2) and MMP9
MMP2↓,
MMP9↓,
TOP1↓, increases the sensitivity of CRC cells to 5-FU by reducing the expression of thymidylate synthase, ERCC1, DNA topoisomerase 1 and BRCA1
BRCA1↓,
ROS↑, CA was also able to induce apoptosis in cancer cells by increasing intracellular ROS levels
BAX↑, A induces cell apoptosis by upregulating Bax expression, and downregulating Bcl-2 and X-linked inhibitor of apoptosis (XIAP) expression
Bcl-2↓,
XIAP↓,
MMP↓, CA can also induce apoptosis in leukemia K562 cells by reducing the mitochondrial transmembrane potential via mitochondrial-mediated pathways
STAT3↓, figure 2
mTOR↓,
NF-kB↓, ↓NF-κB
eff↑, CA-Cu-PDA was able to release copper ions and CA in tumor cells, and weakened the antioxidant system by binding to glutathione (GSH), which in turn produced additional ROS, thereby inducing enhanced oxidative stress effects
toxicity↓, Consistent with these findings, another study has demonstrated that CA does not exhibit genotoxic or carcinogenic effects on the body
cardioP↑, CA has demonstrated a capacity to alleviate cardiotoxicity induced by DOX
*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.
*AntiThr↑, dipyridamole enhances the anti-thrombotic effects of aspirin for the prevention of secondary strokes.
eff↑, We found that dipyridamole combined with aspirin had a better inhibitory effect on CRC than either monotherapy alone.
ER Stress↑, induction of an overwhelmed endoplasmic reticulum (ER) stress and subsequent pro-apoptotic unfolded protein response (UPR), which was different from the anti-platelet effect.
UPR↑,
*AntiAg↑,
*COX1↓, aspirin acts through inhibiting cyclooxygenase-1 (COX-1) in platelets.
Risk↓, Combined use of dipyridamole and aspirin associates with a low risk of CRC through a nationwide population-based cohort study
TumCG↓, The combination of dipyridamole with aspirin has an enhanced inhibitory effect on tumor growth in orthotopic CRC mouse model and AOM/DSS-induced CRC mouse model
Apoptosis↑, The combination of dipyridamole with aspirin inhibits CRC cell growth and promotes CRC cell apoptosis
HMG-CoA↓, Dipyridamole can also suppress the activity of SREBF2, a transcription factor regulating the expression of HMGCS1 to compromise the mevalonate (MVA) signaling pathway in inhibiting colon cancer
*Inflam↓, Dipyridamole has anti-inflammatory [40, 41] and anti-oxidant [42, 43] functions.
*antiOx↓,
*AntiAg↑, Dipyridamole has anti-platelet and anti-inflammatory effects.
*Inflam↓,
*AntiThr↑, Anti thrombotic, anti viral and anti inflammatory actions of this drug may be efficacious and safe in hospitalized subjects
*Dose↝, Dipyridamole-100mg taken 3 times a day by mouth for 7 days
*cardioP↑, describes the cardioprotective potential of dandelion products and preparations.
*Dose↝, Dandelion is a rich source of phenolic acids (chicoric acid, chlorogenic acid), flavonoids (luteolin derivatives, quercetin), and terpenes (sesquiterpene lactones).
*Dose↝, It is also a strong source of vitamins (A, C, E, K, and B) and minerals (calcium, sodium, magnesium, iron, copper, silicon, zinc, manganese)
*toxicity∅, Although dandelion is mainly known for its medicinal properties, it has for many years been successfully used worldwide in the food industry as an entirely non-toxic and edible plant
*toxicity↓, dose should not exceed 4 g or 12 g per day for the aerial parts of the plant or 1 g or 3 g per day for the root. The roots, leaves, and flowers may be eaten raw or cooked
*BP↓, Dandelion leaves are also believed to have a positive effect on the cardiovascular system due to their high potassium content (397 mg potassium/100 g): increased potassium intake with food (about 3500 mg/day for an adult) has been found to lower BP
*Inflam↓, sesquiterpene lactones, which have been found to have anti-inflammatory and antibacterial effects, as well as triterpenes or phytosterols, which possess anti-atherosclerotic properties
*Bacteria↓,
*Imm↑, roots are also rich in inulin, which has a probiotic, hypoglycemic, and immune-boosting effect
*lipid-P↓, extract was found to elevate total antioxidant capacity and decrease lipid peroxidation, a marker of oxidative stress, in the heart, liver, kidney, and brain, among others.
*AST↓, ; treatment was found to improve the lipid profile and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations in obese mice.
*ALAT↓,
*AntiAg↑, extracts E2 and E3 and fractions A, B, and C significantly inhibited ADP-activated platelet adhesion to fibrinogen, while flavonoid fractions A to C inhibited thrombin-activated platelet adhesion at both tested doses (10 and 50 μg/mL)
*ROS↓, (1) the inhibition of reactive oxygen species (ROS) production;
*AntiThr↑, antithrombotic effects.
*toxicity∅, Administration of Clovinol did not result in any toxicologically significant changes in clinical/behavioural observations, ophthalmic examinations, body weights, organ weights, feed consumption, urinalysis, hematology and clinical biochemistry parame
*Dose↑, no observed-adverse-effect level (NOAEL) as 1000 mg/kg b.wt./day
*Bacteria↓, Clove oil and its major component eugenol [70–85% (w/v)], exhibited several therapeutic effects including antibacterial, antifungal, analgesic, antispasmodic, anticarminative, antiseptic, and insecticidal effects
*Inflam↓, Major pharmacological activities of clove oil and eugenol include antioxidant, anti-inflammatory, antidiabetic, hypolipidemic, antinociceptive, hepatoprotective, antiviral and anticancer properties
*antiOx↑,
*AntiDiabetic↑,
*hepatoP↑,
*AntiCan↑,
*AntiThr↑, such as gallic acid, ellagic acid, tannins, flavonoids and their glycosides were reported to possess aphrodisiac, hypoglycemic, gastroprotective, anti-inflammatory and antithrombotic effects
*Dose↝, trans-anethole, estragole and fenchone have been reported as the major phytoconstituents of this species.
*Bacteria↓, antibacterial, antioxidant, antithrombotic and hepatoprotective activities, lending support to the rationale behind several of its therapeutic uses.
*hepatoP↑,
*antiOx↑, Phenolic compounds isolated from F. vulgare are considered to be responsible for its antioxidant activity while the volatile aroma compounds make it an excellent flavouring agent.
*AntiThr↑, The essential oil of F. vulgare and its main component, anethole has been shown to have a safe antithrombotic activity
*AntiDiabetic↑, Antidiabetic activity
*toxicity↝, Estragole (Methylchavicol) is one of the main components of the essential oil of F. vulgare. It has been reported that estragole is associated with the development of malignant tumours in rodents.
*antiOx↑, anti-oxidative, anti-inflammatory, anti-mutagenic and anti-carcinogenic properties coupled with their capacity to modulate key cellular enzyme function.
AntiCan↑,
*cardioP↑, Research on flavonoids received an added impulse with the discovery of the low cardiovascular mortality rate and also prevention of CHD.
*XO↓, They are also known to be potent inhibitors for several enzymes, such as xanthine oxidase (XO), cyclo-oxygenase (COX), lipoxygenase and phosphoinositide 3-kinase
*COX2/PTGS2↓,
*5LO↓,
*PI3K↓,
*AChE↓, A number of flavonoids have been reported for their anti-cholinesterase activity.
*Imm⇅, These effects indicate the immune-regulatory roles of flavonoids.
*BP↓, regular quercitin intake on blood pressure in overweight and obese patients with pre-hypertension and stage I hypertension was studied in seventy patients.
TumCCA↑, t pelingo juice induced cell accumulation in the G2/M phase of the cell cycle
*Aβ↓, certain flavonoids such as genistein, quercetin, taxifolin, kaemferol, luteolin, apigenin, daidzein, aminogeneistein, and α- and β-napthofalvone can affect Aβ production.
*BACE/β-secretase↓, direct inhibition of β active site cleavage enzyme-1 (BACE-1) activity
*NF-kB↓, inhibition of NF-κB activation by flavonoids
*ROS↓, flavones and catechins seem to be the most powerful flavonoids for protecting the body against reactive oxygen species.
*neuroP↑, like prevention of the neurodegeneration associated with AD and Parkinson's disease
*AntiAg↑, figure 3
*AntiThr↑,
*Inflam↓, May reduce immune cell mediated inflammation and oxidative stress, but has very low oral
bioavailability.
*ROS↓,
*BioAv↓,
*GutMicro↑, May exert beneficial effects through modulation of the intestine/microbiome
*neuroP↑, Neuroprotective Benefit: Can protect against onset of inflammatory and oxidative damage by
mitigating immune cell activation in animal models.
*glucose↝, May help regulate glucose homeostasis, have anti-thrombotic effects, and improve tolerability of chemotherapy, but benefits are limited by poor oral bioavailability.
*AntiThr↑,
*chemoP↑,
*Half-Life↝, Half-life: Varies with preparation (~1-3 hours in rats)
*BBB∅, BBB: Not penetrant
*AntiAge↑, Diets rich in fucoidan associated with increased lifespan and lower cancer incidence.
Risk↑,
*Dose↝, 0, 3, 6, and 9 h after ingestion of 3 g of fucoidan.
*BioAv↝, 332.3 ± 357.6 μg/gCr in subjects living in Okinawa prefecture, compared with 240.1 ± 302.4 μg/gCr in subjects living outside Okinawa
*eff↝, Okinawa prefecture than in those living outside Okinawa prefecture, the habit of eating mozuku was speculated to be a factor in the absorption of fucoidan
*Inflam↓, Fucodan exhibits many different biological properties, including anti-inflammatory, anticoagulant, antithrombotic, antiadhesive, antiangiogenic, antiviral, antitumor and antioxidant activities
*AntiThr↑,
angioG↓,
*AntiViral↑,
*AntiTum↑,
*antiOx↓,
*BioAv↝, The rate of absorption through the small intestine was highly variable among the participants.
TumCCA↑, Among the anticancer mechanisms of fucoidan are cell cycle arrest, apoptosis evocation, and stimulation of cytotoxic natural killer cells and macrophages.
Apoptosis↑,
NK cell↑,
chemoP↑, Fucoidan also protects against toxicity associated with chemotherapeutic drugs and radiation-induced damage.
TumCG↓, fucoidan slows tumor growth, kills cancer cells, and interacts with cancer chemotherapy drugs.
*Inflam↓, fucoidan has countless superior biological activities, which include anti-inflammatory, antioxidant, anticlotting, antithrombotic, antiviral, anti-angiogenesis, and anti-Helicobacter pylori activities
*antiOx↑,
*AntiThr↑,
*AntiViral↑,
angioG↓,
ChemoSen↑, Furthermore, LMWF complexed with tamoxifen, cisplatin, or paclitaxel shows cell growth inhibition, cellular apoptosis, and arrest of the cell cycle in the human breast cancer cell line MCF-7/ MDA-MB-231.
ROS↑, The study revealed that in breast cancer cells, phosphorylation of different proteins, elevation the reactive oxygen species (ROS) levels, and reduced glutathione (GSH) levels were all crucial in cancer cell apoptosis
GSH↓,
mtDam↓, reatment with fucoidan leads to increased levels of ROS in cells, along with mitochondrial damage and mitochondrial membrane potential (MMP) depolarization.
MMP↓,
DNMT3B↓, inhibition of its downstream target DNA methyltransferase 3B (DNMT3B) by the administration of a fixed dose of fucoidan
TumCG↓, Oral administration of fucoidan (5 mg/kg) effectively inhibited tumor growth in mice grown with B16 melanoma cells.
Dose↝, fucoidan (5 mg/kg) effectively inhibited tumor growth in mice
Dose↝, Twenty patients with advanced cancer were selected for the study, in which oral fucoidan (4 g daily) was administered for at least four weeks. After two consecutive weeks of ingestion, there was a significant reduction in the levels of key proinflamm
QoL∅, but no significant change was observed in patients’ quality of life, including the experience of fatigue
fatigue∅,
Dose↝, 300 mg fucoidan is safe and well tolerated by humans
antiOx↑, anti-oxidant, antiviral, immunoregulatory, anti-coagulant, anti-thrombotic, anti-lipidemic, anti-diabetic, anti-tumor, anti-metastatic, and anti-angiogenic properties
AntiViral↑,
Imm↝,
*AntiThr↑,
*AntiDiabetic↑,
AntiTum↑,
TumMeta↑,
angioG↓,
Hif1a↓, ↓ HIF-1α and VEGF in hypoxic-like conditions
VEGF↓,
MMPs↓, ↓ MMPs
EMT↓, ↓ EMT (↓ N-cadherin; ↑ E-cadherin)
N-cadherin↓,
E-cadherin↑,
TIMP1↑, ↑ TIMP
PI3K↓, ↓ PI3K/Akt/mTOR
Akt↓,
mTOR↓,
MMP2↓, ↓ MMP-2, 9
ChemoSen↑, available findings indicate that oral intake of fucoidan as dietary supplement in combination with conventional adjuvant chemotherapy can prolong survival time, decrease some adverse effects (e.g., fatigue)
OS↑,
fatigue↓,
CD31/PECAM-1↓, fig 2
Apoptosis↑, honokiol induced apoptosis of RKO cells in a time- and dose-dependent manner
Casp↑, At 5-10 ug/mL for 48 h, honokiol induced apoptosis through activating Caspase cascades.
Dose↝, honokiol could be absorbed quickly by intraperitoneal injection, and maintained in plasma for more than 10 h.
OS↑, honokiol displayed anticancer activity by inhibiting tumor growth and prolonging the lifespan of tumor bearing mice.
*Inflam↓, honokiol has been found having a variety of pharmacological effects, such as anti-inflammatory[2], antithrombotic[3], anti-arrhythmic[4], antioxidative[5] and anxiolytic effects
*AntiThr↑,
*antiOx↑,
*Half-Life↝, intraperitoneal injection of 250 mg/kg to BALB/c mice.absorption half-life of 10.121 ± 2.761 min, and an elimination half-life of 5.218 ± 0. 461 h
TumCG↓, nhibition of solid tumor growth in nude mice bearing RKO cells
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection
*Inflam↓, exhibits a multitude of biological functions including anti-inflammatory, antidepressant, antioxidative, vascular protective effects and neuroprotective effects,
*antiOx↑,
*neuroP↑,
*lipid-P↓, Anti-oxidant Saccharomyces Cerevisiae 5, 20 mg/L Decreased LPO and the level of ROS
*ROS↓,
*IL1β↓, HT22 cells 20 μM Alleviates the level of IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax, and caspase-3; increases the expression of CAT, SOD, GSH, Bcl-2, BDNF, TrkB, and NGF.
*IL6↓,
*IL8↓,
*TNF-α↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Catalase↑,
*SOD↑,
*GSH↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*BDNF↑, Male Albino Swiss mice 0.94 mg/kg, 3.75 mg/kg Mediated by monoaminergic system and the upregulation of BDNF level
*NF-kB↓, Inhibited the activation of NF-κB, lessened the expression of iNOS,
*AChE↓, ICR mice 2.5 mg/kg Inhibited AchE activity
*H2S↑, SD rats 1, 10, 100 μM Upregulation of H2S,
Casp3↑, Anti-lung cancer A549 cells, Balb/c-nude mice 15, 20, 25 μM in vitro 15, 20, 25 mg/kg in vivo Activation of caspase-3 to motivate apoptosis and inactivation of NF-κB to inhibit inflammatory
Apoptosis↑,
NF-kB↓,
AMPK↑, A549 cells 10, 50, 100 μM Upregulation of AMPK signal pathway and HO-1 expression to suppressed the survival and proliferation of A549 cells
HO-1↑,
MAPK↑, A549 cells, H466 cells, C57BL/6J mice – Upregulated the expression of p38 MAPK, caspase 3, caspase 9, cleaved caspase 3, cleaved caspase 9 and Bax, downregulated the expression of Cu/Zn SOD, CAT, Nrf2, NQO1, HO-1 and Bcl-2
cl‑Casp3↑,
cl‑Casp9↑,
BAX↑,
SOD?,
Catalase↓,
NRF2↓,
NQO1↓,
HO-1↓,
Bcl-2↓,
TumCCA↑, A549 cells 10, 20, 50, 100, 200, 400 μg/mL Inhibited the process of G1/S phase to inhibit proliferation
FOXO1↑, NCI-H1975 cells, PC-9 cells, Nude male mice 30, 60, 90, 120, 150 μM in vitro, 25 mg/kg in vivo Upregulation of FoxO1
TumAuto↑, A549 cells 0.5, 1, 2 mM Induced autophagy through inhibiting the Akt/mTOR/p70S6K signal pathway
Akt↓,
mTOR↓,
P70S6K↓,
BMP7/OP1↓, HepG2 cells 5, 10, 20, 40, 80 μM Inhibiting the BMP-7
*cardioP↑, Cardiovascular Protective Effect
*hepatoP↑, Hepatoprotective
*antiCG↑, The report indicates hyperoside possesses antithrombotic activities and offer bases for development of a novel anticoagulant
*AntiThr↑,
*Diar↓, Antidiarrheal Activity
*AntiFungal↑, Antifungal Activity
*CYP2D6↓, hyperoside is a potent selective CYP2D6 inhibitor in HLMs, and might cause herb-drug interactions when co-administrated with CYP2D substrates.
*PDGFR-BB↓, In diabetic rats’ model, hyperoside inhibited the platelet-derived growth factor-BB (PDGF-BB)/platelet-derived growth factor-B receptor (PDGFR-β) ligand binding
*PDGFRB↓,
*toxicity↓, In research conducted in Wistar rats, the researchers demonstrated that in a long-term oral administration lasted for 6 months, hyperoside has a good safety. And the possible target organ of toxicity is kidney and the damage is reversible
*Half-Life↑, hyperoside also showed a long half-life for 4 hours and the safety experiments also proves that it has good safety.
*cardioP↑, Consumption of soy products have been linked to reduction in incidence or severity of chronic diseases such as cardiovascular, breast and prostate cancers, menopausal symptoms, bone loss, etc.
Risk↓, The antioxidant powers of isoflavones can reduce the long-term risk of cancer by preventing free radical damage to DNA. n Asian populations, where soy intake is high, the researchers found an inverse association between soy food intake and breast can
*BMD↑, isoflavones on BMD concluded that six month intake of soy isoflavones was adequate to exert a beneficial effect on it, especially of the lumber spine.
*eff↑, Maximal health benefits are most likely to be derived by consuming small amounts of isoflavone-rich foods throughout the day.
*antiOx↑, isoflavones have potent antioxidant properties, comparable to that of the well-known antioxidant vitamin E
*lipid-P↓, . The inhibition of lipid peroxidation, particularly of low density lipoprotein (LDL) by isoflavones may be an important mechanism by which they positively influence lipid profiles.
*LDL↓,
AntiThr↑, consumption of antioxidant/polyphenol rich foods might impart antithrombotic and cardiovascular protective effects via their inhibition of platelet hyperactivation or aggregation
AntiAg↑, Also, dietary isoflavones or polyphenols rich foods may substitute or complements currently used anti-platelet drugs in sedentary, obese, pre-diabetic or diabetic population
PSA↓, isoflavone supplementation appeared to slow the rising serum prostate specific antigen (PSA) concentration associated with prostate tumor growth of prostate cancer patients. However short-term intake of soy isoflavones did not affect PSA
TumCCA↑, Food intake rich with soy isoflavones may induce growth arrest and apoptosis of PCa
cognitive↑, healthy postmenopausal women with variable age groups receiving isoflavone tablets showed an increase in cognitive functions like working and visual memory
memory↑,
*Dose↝, 30 patients with tinnitus were treated with sulodexide (250 LSU BID, in the morning and in the evening) and melatonin (3 mg in the evening before going to sleep) for 80 days.
*Tinn↓, Tinnitus Handicap Inventory (THI) and acufenometry showed a significative improvement of tinnitus after treatment with sulodexide and melatonin.
*AntiThr↑, sulodexide, a natural glycosaminoglycan with antithrombotic, profibrinolytic and vascular anti-inflammatory properties used in the treatment of many vascular diseases
*AntiThr↑, Rutin@AgNPs is a potential anticoagulant for antithrombotic therapy
*AntiAg↑, rutin effectively targets the PDI and inhibits its activity, thus the platelet accumulation and fibrin generation can be blocked
*antiOx↑, rutin is a kind of flavonoid, which contains antioxidation and anti-inflammatory activities.
*Inflam↓,
Showing Research Papers: 1 to 23 of 23
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 23
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
BMP7/OP1↓, 1, MTA1↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↓, 2, GSH↓, 2, HO-1↓, 1, HO-1↑, 1, NQO1↓, 1, NRF2↓, 1, ROS↓, 1, ROS↑, 2, SOD?, 1, SOD↓, 1, TAC↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 3, mtDam↓, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, HMG-CoA↓, 1, LDH↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 5, Apoptosis↑, 6, BAD↑, 1, Bak↑, 1, BAX↑, 3, Bcl-2↓, 4, Bcl-xL↓, 1, Casp↑, 1, Casp3↑, 3, cl‑Casp3↑, 1, Casp8↑, 1, cl‑Casp9↑, 1, Cyt‑c↑, 2, Fas↑, 1, JNK↓, 1, MAPK↓, 1, MAPK↑, 1, p27/CDKN1B↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 2, cJun↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
BRCA1↓, 1, DNMT3B↓, 1, P53↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 1, CDK4↓, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
cFos↓, 1, EMT↓, 1, ERK↓, 1, FOXO1↑, 1, mTOR↓, 4, P70S6K↓, 2, PI3K↓, 3, STAT↓, 1, STAT3↓, 1, TOP1↓, 1, TumCG↓, 4,
Migration(tgid=13) ⓘ
AntiAg↑, 1, AP-1↓, 1, CD31/PECAM-1↓, 1, E-cadherin↑, 2, LRP1↓, 1, MMP2↓, 4, MMP9↓, 2, MMPs↓, 1, N-cadherin↓, 1, TIMP1↑, 2, TIMP2↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 2, TumMeta↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 4, Hif1a↓, 1, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CXCR4↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 1, IL8↓, 1, Imm↝, 1, JAK↓, 1, NF-kB↓, 4, NK cell↑, 1, PD-L1↓, 1, PSA↓, 1, TLR4↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 3, Dose↝, 5, eff↓, 1, eff↑, 5,
Clinical Biomarkers(tgid=22) ⓘ
BRCA1↓, 1, IL6↓, 1, LDH↓, 1, PD-L1↓, 1, PSA↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, AntiTum↑, 1, cardioP↑, 1, chemoP↑, 2, chemoPv↑, 1, cognitive↑, 1, fatigue↓, 1, fatigue∅, 1, memory↑, 1, OS↑, 2, QoL∅, 1, Risk↓, 2, Risk↑, 1, toxicity↓, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 118
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, antiCG↑, 1, antiD↓, 1, CYP2D6↓, 1, Stroke↓, 1, Tinn↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 2, antiOx↑, 11, Catalase↑, 1, GSH↑, 2, GSTs↑, 1, lipid-P↓, 3, MDA↓, 1, ROS↓, 4, SOD↑, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 2, BUN↓, 1, glucose↝, 1, H2S↑, 1, LDL↓, 1,
Cell Death(tgid=5) ⓘ
BAX↓, 1, Casp3↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 21, other↝, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
PDGFRB↓, 1, PI3K↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, AntiAg↑, 9, PAI-1/SERPINE1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↑, 1, NO↑, 1, PDGFR-BB↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB∅, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↓, 1, COX2/PTGS2↓, 1, IL1β↓, 1, IL6↓, 1, IL8↓, 1, Imm↑, 2, Imm⇅, 1, Inflam↓, 11, NF-kB↓, 3, TNF-α↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 2, BDNF↑, 2, NGF↑, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1, XO↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 4, Dose↑, 1, Dose↝, 7, eff↑, 2, eff↝, 1, Half-Life↑, 1, Half-Life↝, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 2, AST↓, 2, BloodF↑, 1, BMD↑, 1, BP↓, 2, GutMicro↑, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↓, 1, AntiDiabetic↑, 4, AntiTum↑, 1, cardioP↑, 5, chemoP↑, 1, hepatoP↑, 5, neuroP?, 1, neuroP↑, 5, RenoP↑, 1, toxicity↓, 2, toxicity↝, 1, toxicity∅, 2, Wound Healing↑, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 3, Bacteria↓, 5, Diar↓, 1, Sepsis↓, 1,
Total Targets: 86
Scientific Paper Hit Count for: AntiThr, antithrombotic
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#:1388 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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