5LO Cancer Research Results

5LO, 5-lipoxygenase (5-LO): Click to Expand ⟱
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5‑Lipoxygenase (5‑LO) is an enzyme that catalyzes the oxygenation of arachidonic acid to produce leukotrienes and other bioactive lipid mediators. It is a member of the lipoxygenase family and plays a key role in inflammatory responses.

5‑LO is overexpressed in various malignancies, particularly those with a strong inflammatory component.
Overexpression of 5‑LO is often detected in tumor cells as well as in stromal cells (e.g., tumor-associated macrophages) within the tumor microenvironment.
Elevated 5‑LO expression is frequently linked with increased tumor proliferation, enhanced angiogenesis, and higher metastatic potential—factors that often correlate with a poor prognosis.
Scientific Papers found: Click to Expand⟱
5365- AV,    Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications
- Review, Nor, NA - Review, IBD, NA - Review, Diabetic, NA
*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

3690- BM,    Neurocognitive Effect of Nootropic Drug Brahmi (Bacopa monnieri) in Alzheimer's Disease
- Review, AD, NA
*ROS↓, EBm promotes free radical scavenger mechanisms
*5LO↓, reduces lipoxygenase activity reducing lipid peroxidation, increases glutathione peroxidase and chelates iron.
*lipid-P↓,
*GPx↑,
*IronCh↑,
*neuroP↑, EBm was seen to protect the cholinergic neurons and reduce anticholinesterase activity comparable to donepezil, rivastigmine, and galantamine.
*AChE↓,
*memory↑, EBm improved the total memory score and maximum improvement was seen in logical memory and paired associate learning in humans and reversed phenytoin-induced memory impairment in experimental model.
*toxicity↓, Mild nausea and gastrointestinal upset are seen in humans.
*SOD↑, EBm was administered to the rats for 21 days. It showed increase in activity of enzymes SOD, CAT, and GPx in prefrontal cortex, hippocampus, and striatum. I
*Catalase↑,
*cognitive↑, administration in indicated doses may act as a remedy for age-associated memory and cognitive decline in AD.
*ChAT↑, OBX reduced cholinergic activity and hence also ChAT in hippocampus. Subsequent administration of EBm and tacrine to the substrate, however, reversed this effect
*Ach↑,
*BP↓, Brahmi decreased systolic and diastolic blood pressure without significantly affecting heart rate.

3518- Bor,    Boron Report
- Review, Var, NA - Review, AD, NA
Risk↓, Boron reduces prostate cancer incidence by up to 64%
serineP↓, Boric acid acts to inhibit serine proteases—it decreases PSA by 87% and reduces tumor size in a prostate cancer mouse model
PSA↓,
TumVol↓,
IGF-1↓, expression of IGF-1 (insulin-like growth factor type 1) was markedly reduced by boron treatment. Circulating blood levels of IGF-1 were not reduced in the treated mice, however.
*Mag↑, In situations of adequate calcium supply but deficient magnesium resources, boron appears to substitute or “pinch hit” for magnesium during the process of bone formation.
*Calcium↑, The effect of boron on raising plasma calcium levels may, in part, be due to its enhancing effect on vitamin D.1
*VitD↑,
*COX2↓, boron has been shown to inhibit cyclooxygenase (COX) and lipoxygenase (LOX).
*5LO↓,
*PGE2↓, leads to a decrease in prostaglandin E2 (PGE2)
*NF-kB↓, suppressing nuclear factor kappa beta (NfkappaB)
*cognitive↑, Since it is now commonly accepted that the routine use of NSAIDs significantly reduces the incidence of Alzheimer’s disease,31,32 it is not surprising that papers have been published on boron’s positive effect on cognitive function.

2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1/CCND1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
FOXM1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)

2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat- ing the caspase-dependent pathway in human pancreatic cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,

2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*Inflam↓,
*AChE↓, inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Choline↑,
*NRF2↑, BAs modulate key molecular targets and signalling pathways like 5-lipoxygenase/cyclooxygenase, Nrf2, NF-kB, cholinergic, amyloid-beta (Aβ), and neurofibrillary tangles formation (NFTs) that are involved in AD
*NF-kB↑,
*BBB↑, AKBA has efficiently abled to cross the blood brain barrier (BBB)
*BioAv↑, bioavailability of AKBA was significantly higher in case of sublingual route when compared to intranasal administration, as demonstrated by area under curves (AUCs) analysis
*Half-Life↓, half-life of the drug was about six hours and peak plasma levels of the drug reach 30 hrs after oral administration of 333 mg of BSE.
*Dose↝, drug needs to be administered at a dosing interval of 6 hrs
*PGE2↓, BAs possessed anti-inflammatory activity by inhibiting microsomal prostaglandin E2 synthase-1 (mPGES1)
*ROS↓, prevented oxidative stress-induced neuronal damage and cognitive impairment because of the antioxidant, anti-inflammatory and anti-glutamatergic effects
*cognitive↑,
*antiOx↑,
5LO↓, AKBA significantly reduced pro-inflammatory mediators such as 5-LOX, TNF-α, IL-6 levels and improve cognition
*TNF-α↓,
*IL6↓,
*HO-1↑, AKBA shows neuroprotective effects against ischaemic injury via nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) cascade activation

1417- Bos,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
5LO↓,
COX2↓,
PGE2↓,

1421- Bos,    Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes
- in-vitro, AML, HL-60 - in-vitro, Nor, NA
ROS↑, AKBA and KBA strongly upregulated the formation of ROS, whereas β-BA and A-β-BA had only moderate effects
NADPH↝, AKBA-induced ROS formation involves NADPH oxidase, PI 3-K, and p42/44MAPK, and requires Ca2+
5LO↓, With respect to inhibition of 5-LO, 3-acetyl-11-keto-BA (AKBA) was the most potent BA, whereas BAs lacking an 11-keto-group were weak 5-LO inhibitor s
Ca+2↑, 11-keto-BAs potently stimulate the elevation of intracellular Ca2+ levels and activate p38 MAPK as well as p42MAPK
p38↑,
p42↑,

1422- Bos,    Boswellic acid exerts antitumor effects in colorectal cancer cells by modulating expression of the let-7 and miR-200 microRNA family
- in-vitro, CRC, NA - in-vivo, NA, NA
5LO↓, boswellic acids, is known to be a non-redox and non-competitive inhibitor of 5-lipoxygenase
TumCG↓,
Let-7↑,
miR-200b↑, AKBA significantly up-regulated expression of the let-7 and miR-200 families in various CRC cell lines
NF-kB↓,
cMyc↓,
cycD1/CCND1↓,
MMP9↓,
CXCR4↓,
VEGF↓,
Bcl-xL↓,
survivin↓,
IAP1↓,
XIAP↓,
TumCG↓,
CDK6↓,
Vim↓,
E-cadherin↑,

1416- Bos,    Anti-cancer properties of boswellic acids: mechanism of action as anti-cancerous agent
- Review, NA, NA
5LO↓,
TumCCA↑, G0/G1 phase
LC3B↓, reduced the expression of LC3A/B-I and LC3A/B-II,
PI3K↓,
Akt↓,
Glycolysis↓,
AMPK↑,
mTOR↓,
Let-7↑,
COX2↓, methanolic extract decreased the expression of cyclooxygenase-2 gene
VEGF↓,
CXCR4↓,
MMP2↓,
MMP9↓,
HIF-1↓,
angioG↓,
TumCP↓,
TumCMig↓,
NF-kB↓,

3791- CA,    Caffeic Acid and Diseases—Mechanisms of Action
- Review, AD, NA
*memory↑, Feeding hyperinsulinemic rats with caffeic acid (30 mg/kg b.w./day) for 30 weeks significantly improved their memory and learning impairments caused by a high-fat diet
*cognitive↑, caffeic acid (100 mg/kg for two weeks) significantly improved learning deficits and increased cognitive function
*p‑tau↓, pretreatment with caffeic acid (10 μg/mL) decreased the level of phosphorylated tau protein
*ROS↓, Caffeic acid (100 mg/kg for two weeks) also suppressed oxidative stress, inflammation, NF-κB-p65 protein expression, and caspase-3 activity
*Inflam↓,
*NF-kB↓,
*Casp3↓,
*lipid-P↓, caffeic acid (50 mg/kg/day) improved cognitive functions and inhibited lipid peroxidation and nitric oxide formation in the brain
*AChE↓, Caffeic acid (12 μg/mL) inhibited acetylcholinesterase and butyrylcholinesterase activity in the brain of untreated rats in vitro
*BChE↓,
*GSK‐3β↓, improves cognitive functions, probably by inhibiting NF-κB and GSK3β signaling and acetylcholinesterase and butyrylcholinesterase activity (
*5LO↓, we consider the inhibitory effect of caffeic acid on 5-lipoxygenase as another factor in protecting the brain against damage
*BDNF↓, Caffeic acid also increased the expression of brain-derived neurotrophic factor (BDNF) in stressed mice; the effect was mediated by 5-lipoxygenase inhibition
VEGF↓, the primary way how caffeic acid affects hepatocellular carcinoma in vitro is inhibiting VEGF expression
HSP70/HSPA5↓, affeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),

5772- CAPE,    The Pluripotent Activities of Caffeic Acid Phenethyl Ester
- Review, Var, NA
*Bacteria↓, properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities.
*AntiCan↑,
*Imm↑,
*Wound Healing↑,
*NF-kB↓, including inhibition of the transcription factors NF-κB
*5LO↓, use of CAPE in diabetes therapy have shown that caffeic acid phenethyl ester inhibits the enzyme 5-lipoxygenase
*AntiDiabetic↑, Antidiabetic Properties
ChemoSen↑, CAPE treatment enhances the antitumor effect of cytostatic drugs, such as vinblastine, paclitacol, estramustine and docetaxel, used in the chemotherapy of prostate cancer [76,81,82].
selectivity↑, CAPE acts selectively on diseased cells, without adversely affecting normal cells [88]
chemoPv↑, CAPE may be useful as support for cancer therapy in terms of chemoprevention of non-cancerous cells

5757- CAPE,    Caffeic acid phenethyl ester (CAPE): pharmacodynamics and potential for therapeutic application
- Review, Nor, NA
*NF-kB↓, inhibition of the activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)
NF-kB↓, CAPE has been shown to block NF-κB activation in tumor
P53↑, CAPE enhances the expression of the tumor suppressor protein p53 in glioma cells
FOXO↑, CAPE also interferes with FOXO signaling by increasing the levels of the FOXO-1 downstream tumor suppressor in prostate cancer cells
Wnt↓, CAPE suppressed canonical Wnt signaling of prostate cancer cells, reducing their invasiveness
TumCI↓,
*HO-1↑, CAPE exerts its antioxidant effects through increased HO1 expression, mediated by Nrf-2
MMP9↓, CAPE has been shown to selectively inhibit human matrix metalloproteinase-9 (MMP-9) and matrix metalloproteinase-2 (MMP-2)
MMP2↓,
COX1↓, CAPE has been shown to inhibit the in vitro activity of the cyclooxygenases COX-1 and COX-2
COX2↓,
5LO↓, CAPE has also been shown to inhibit arachidonate 5-lipoxygenase (5-LOX)

5899- CAR,  TV,    Evaluation of the Interaction between Carvacrol and Thymol, Major Compounds of Ptychotis verticillata Essential Oil: Antioxidant, Anti-Inflammatory and Anticancer Activities against Breast Cancer Lines
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
eff↑, The thymol/carvacrol mixture demonstrated superior cytotoxicity (IC50 = 0.92–1.70 µg/mL) and increased selectivity compared to cisplatin,
selectivity↑, with high selectivity indices (144.88–267.71).
BioAv↝, The bioavailability score for both thymol and carvacrol is 0.55, indicating moderate bioavailability
BBB↑, The blood–brain barrier (BBB) permeability values are 1.82 for thymol and 1.99 for carvacrol, indicating that both compounds have moderate permeability across the BBB.
*toxicity↝, carvacrol may be slightly less toxic than thymol. Both compounds have a predicted toxicity class of 4, indicating moderate toxicity.
*antiOx↑, This remarkable synergy in antioxidant activity
COX2↓, carvacrol and thymol showed considerable outcomes, their mixture proved more effective in suppressing COX-2.
5LO↓, synergistic effect observed with the thymol/carvacrol mixture, particularly pronounced for 5-LOX and COX-2 inhibition

5926- CAR,    An Updated Review of Research into Carvacrol and Its Biological Activities
- Review, Nor, NA - Review, AD, NA - Review, asthmatic, NA
*Inflam↓, ic, analgesic, anti-inflammatory,antioxidant, and neuroprotective effects.
*antiOx↑,
*neuroP↑, Carvacrol has exhibited notable neuroprotective effects in experimental models of cognitiveimpairment and neurodegenerative diseases
*BioAv↑, advances in encapsulation andnanotechnology have enhanced its stability and bioavailability
*toxicity↓, Compared to phenol, carvacrol and thymol exhibitsignificantly lower toxicity. This makes carvacrol a safer alternative for various applications, frombiological agents to dietary supplements [
*Pain↓, Pain-Relieving Mechanisms of Car
*TRPV3↑, , carvacrol-induced TRPV3 activation enhances lipolysis in adipocytes via theNRF2/FSP1 a
*NRF2↑,
*Ca+2↑, TRPV3 activation in distal colon epithelial cells elevates intracellular Ca²⁺ levels and stimulates ATP release, implicating carvacrol in gut physiology and signaling
*ATP↑,
*5LO↓, s, including the inhibition of angiotensin-converting enzyme 2 (ACE2), lipoxygenase(LOX), and cyclooxygenase (COX) enzyme
*COX2↓,
PGE2↓, arvacrol’s anti-inflammatory effects involve theinhibition of prostaglandin E₂ (PGE₂) production via COX-2
*hepatoP↑, Carvacrol in Hepatic Protection as Natural Antioxidant
*AntiAg↑, Carvacrol has demonstrated significant antiplatelet activity, highlighting its potential therapeutic role in preventing thrombosis
*Diar↓, s essentialoil exhibited antidiarrheal effects in castor oil-induced diarrhea models, potentially mediated bymechanisms involving Kv channel activation and Ca²⁺ channel inhibition
*cardioP↑, em as promising nutraceutical candidates for alleviatingCVD-related complicat
*other↝, Carvacrol was evaluated for its therapeutic potential in managing erectile dysfunction (ED)associated with aging
*chemoPv↑, Chemopreventive Potential of Carvacrol in Detoxification pathways
*cognitive↑, carvacrol(0.5–2 mg/kg) and thymol significantly improved cognitive function in rats
*AChE↓, potent acetylcholinesterase inhibitory activity (IC₅₀: 158.94 μg/mL)
*GastroP↑, . Gastroprotective Effects of Carvacrol and Mechanism
*eff↑, . When combined with polysorbate 80 as a surfactant, carvacrol was efficiently deliveredto embryonic tissues, maintaining bioavailability during the peri-hatching phase
*BChE↓, acrol. The essential oil rich in carvacrol showedstrong inhibitory effects on AChE and butyrylcholinesterase (BChE) [
*CRP↓, d Phase II clinical trial, asthmatic patients whoreceived 1.2 mg/kg/day of carvacrol for two months showed significant improvements in pulmonaryfunction tests and a notable reduction in C-reactive protein levek

5925- CAR,    Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,

6084- CHOC,    Cocoa Polyphenols and Their Potential Benefits for Human Health
- Review, Nor, NA - Review, Stroke, NA - Review, IBD, NA
*lipid-P↓, inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.
*ROS↓,
*Inflam↓, decreasing platelet function and inflammation along with diastolic and systolic arterial pressures, which, taken together, may reduce the risk of cardiovascular mortality.
*BP↓,
*cardioP↑, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*chemoPv↑, They also have antiproliferative, antimutagenic, and chemoprotective effects, in addition to their anticariogenic effects.
*BioAv⇅, great controversy surrounding the bioavailability of phenolics in general and of cocoa derivatives in particular.
*antiOx↑, Cocoa has more phenolics and higher antioxidant capacity than green tea, black tea, or red wine
*Risk↓, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*5LO↓, cocoa polyphenols decrease the plasma concentration of proinflammatory cysteinyl leukotrienes through inhibition of 5-LOX, as demonstrated by Sies et al.
*AntiAg↑, Moreover, cocoa decreases not only platelet aggregation, but also adhesion. 234 mg cocoa phenolics a day for 28 days
*Imm↑, Kenny et al. [21] demonstrated that cocoa oligomers are potent stimulators of both the innate immune system and early events in adaptive immunity.
*NF-kB↓, nd their dimeric forms were found to inhibit the NF-κB activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in T cells,
*other↓, in vivo and in vitro models have provided evidence that pure polyphenols and natural polyphenol plant extracts can modulate intestinal inflammation.
CYP1A1↓, polyphenol cocoa extract leads to the induction of CYP1A1 in breast cancer cells.
COX2↓, hey also inhibited the expression of COX-2,
*Obesity↓, Ferrazzano et al. hypothesized that the polyphenols contained in cocoa may have antiobesity effects due to their ability to suppress fatty acid synthesis while stimulating cell energy expenditure in the mitochondria
*cognitive↑, Moreover, cocoa consumption may also have beneficial effects on satiety, cognitive function, and mood [93].

1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, Curcumin downregulates the cyclooxygenase-2 (COX-2) pathway, reducing the production of prostaglandins associated with inflammation
*Inflam↓,
*5LO↓, directly inhibits lipoxygenase (LOX)
*NO↓,
*NF-kB↓,
*TNF-α↓,
*IL1↓,
*IL2↑,
*IL6↓,
*IL8↓,
*IL12↓,
*MCP1↓,
*PGE2↓,
*MMP2↓,
*MMP3↓,
*MMP9↓,
*NLRP3↓,
*ROS↓, arthritis(basically normal cell)

3589- PI,    Anti-inflammatory and antiarthritic effects of piperine in human interleukin 1β-stimulated fibroblast-like synoviocytes and in rat arthritis models
- in-vivo, Arthritis, NA
*IL6↓, Piperine inhibited the expression of IL6 and MMP13 and reduced the production of PGE2 in a dose dependant manner at concentrations of 10 to 100 μg/ml.
*MMP13↓,
*PGE2↓, In particular, the production of PGE2 was significantly inhibited even at 10 μg/ml of piperine.
*AP-1↓, Piperine inhibited the migration of activator protein 1 (AP-1)
*Inflam↓, piperine significantly reduced the inflammatory area in the ankle joints
*5LO↓, piper species have shown in vitro inhibitory activity against the enzymes responsible for leukotriene and prostaglandin biosynthesis, 5-lipoxygenase and COX-1, respectively
*COX1↓,
*COX2↓, Piperine also inhibited both the protein and mRNA expression levels of IL6 and COX-2.
*ERK↓, suggested that piperine inhibition of the ERK1/2 signaling pathway blocked the migration of AP-1 into the nucleus.
*BioEnh↑, Piperine is also known to enhance the bioavailability of some drugs by inhibiting drug metabolism or by increasing absorption

3595- PI,    Black pepper and health claims: a comprehensive treatise
- Review, Var, NA - Review, AD, NA
*antiOx↑, Black pepper (Piper Nigrum L.) is an important healthy food owing to its antioxidant, antimicrobial potential and gastro-protective modules
*ROS↓, The free-radical scavenging activity of black pepper and its active ingredients might be helpful in chemoprevention and controlling progression of tumor growth.
*chemoP↑,
TumCG↓,
*cognitive↑, piperine assist in cognitive brain functioning, boost nutrient's absorption and improve gastrointestinal functionality
*MMPs↓, They postulated that inhibition of interlukon, matrix metalloproteinase, prostaglandin E2, and activator protein 1 are possible routes for their said properties
*PGE2↓,
*AP-1↓,
*5LO↓, Piperine along with some other components can inhibit the expression of enzymes like 5-lipoxygenase and COX-1 that are responsible for leukotriene and prostaglandin biosynthesis.
*COX1↓,
*other↑, It is widely accepted that black pepper is instrumental to prevent and cure gastrointestinal problems. The black pepper enhances the production of hydrochloric acid from stomach thus improving digestion through stimulation of histamine H2 recepto
*other↑, black pepper has diaphoretic (promotes sweating), and diuretic (promotes urination) properties
*other↑, Moreover, it protects intestinal membranes from gastric secretions and ROS damage owing to antioxidant potential.
*SOD↑, black pepper significantly enhanced the activities of antioxidant enzymes, that is, SOD, CAT, GR, and GST.
*Catalase↑,
*GSTs↑,
*GSR↑,
*other↑, black pepper and its active ingredients improve expression of some digestive enzymes along with increase in the secretion of saliva
*Weight↓, piperine intake may decrease body weight
*BioEnh↑, The black pepper and piperine improve the bioavailability of many drugs.
*BioAv↑, Piperine also boosts the bioavailability of important phyto- chemicals contained in other foods, for example, bioactive com- ponents present in curcumin and green tea
*eff↑, The combination of piperine (2.5 mg/kg, i.p., 21 days) with curcumin (20 and 40 mg/kg, i.p., 21 days) showed improved anti-immobility, neurotransmitter enhancing, and monoamine oxidase inhibitory (MAO-A) effects of curcumin
*CYP3A2↓, combination of curcumin and piperine is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa (Volak et al., 2008)
*neuroP↑, Neuroprotective Potential of Black Pepper
*BP↓, Piperine (20 mg/kg/day) decreased the blood pressure caused by the blockage of voltage-dependent calcium channels
*other↑, black pepper oil is one of the strongest appetizer; inhalation stimulates the swallowing in post stroke patients with dysphagia.

4296- QC,    A Flavonoid on the Brain: Quercetin as a Potential Therapeutic Agent in Central Nervous System Disorders
- Review, AD, NA
*Inflam↓, Commonly recognized as an anti-inflammatory agent, quercetin not only limits capillary vessel permeability by inhibiting hyaluronidase but also blocks cyclooxygenases and lipoxygenases.
*COX2↓,
*5LO↓,
*antiOx↑, well-known antioxidant (recognized as one of the most potent antioxidant flavonoids, considered to be stronger than vitamin C or tocopherols
*BioAv↝, Quercetin-Loaded Nanocarriers—New Delivery to Better Availability
*GPx↑, Que at two higher doses improved the antioxidant enzymes (glutathione peroxidase, superoxide dismutase (SOD), Na+/K+-ATPase) supplies and elevated the levels of ACh
*SOD↑,
*Ach↑,
*4-HNE↓, whereas the levels of peroxidation product, 4-HNE, were reduced in the striatum
*CREB↑, A recent study showed a positive influence on the expression of the hippocampal FoxG1/CREB/BDNF signaling pathway [93]
*BDNF↑,
*ROS↓, quercetin exerted antioxidant (reducing ROS, increasing SOD, GST, GSH activity) as well as anti-inflammatory activity (suppressing IL-1β, IL-6, TNF-α, COX-2, microglial activation) [
*GSH↑,
*IL1β↓,
*IL6↓,
*TNF-α↓,

3354- QC,    Quercetin: Its Main Pharmacological Activity and Potential Application in Clinical Medicine
- Review, Var, NA
*ROS↓, quercetin is the most effective free radical scavenger in the flavonoid family
*IronCh↓, Chelating metal ions: related studies have confirmed that quercetin can induce Cu2+ and Fe2+ to play an antioxidant role through catechol in its structure.
*lipid-P↓, quercetin could inhibit Fe2+-induced lipid peroxidation by binding Fe2+ a
*GSH↑, regulation of glutathione levels to enhance antioxidant capacity.
*NRF2↑, quercetin upregulates the expression of Nrf2 and nuclear transfer by activating the intracellular p38 MAPK pathway, increasing the level of intracellular GSH
TumCCA↑, human leukaemia U937 cells, quercetin induces cell cycle arrest at G2 (late DNA synthesis phase)
ER Stress↑, quercetin can induce ER stress and promote the release of p53, thereby inhibiting the activities of CDK2, cyclin A, and cyclin B, thereby causing MCF-7 breast cancer cells to stagnate in the S phase.
P53↑,
CDK2↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycE/CCNE↓, downregulation of cyclins E and D, PNCA, and Cdk-2 protein expression and increased expressions of p21 and p27
cycD1/CCND1↓,
PCNA↓,
P21↑,
p27↑,
PI3K↓, quercetin inhibited the PI3K/AKT/mTOR and STAT3 pathways in PEL, which downregulated the expression of survival cell proteins such as c-FLIP, cyclin D1, and cMyc.
Akt↓,
mTOR↓,
STAT3↓, in excess of 20 μM by inhibiting STAT3 signalling
cFLIP↓,
cMyc↓,
survivin↓, Lung cancer [27] ↓ Survivin ↑DR5
DR5↓,
*Inflam↓, Quercetin has been confirmed to be a long-acting anti-inflammatory substance in flavonoids
*IL6↓, inhibit IL-8 is stronger and can inhibit IL-6 and increase cytosolic calcium levels
*IL8↓,
COX2↓, inhibit the enzymes that produce inflammation (cyclooxygenase (COX) and lipoxygenase (LOX))
5LO↓,
*cardioP↑, The protective mechanism of quercetin on the cardiovascular system
*FASN↓, 25 μM, within 30 minutes could inhibit the synthesis of fatty acids.
*AntiAg↑, quercetin helps reduce lipid peroxidation, platelet aggregation, and capillary permeability
*MDA↓, quercetin can decrease the levels of malondialdehyde (MDA)

3055- RES,    Resveratrol and Tumor Microenvironment: Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
BioAv↓, Resveratrol is poorly bioavailable, and that considered the major hindrance to exert its therapeutic effect, especially for cancer management
BioAv↓, at lower doses (25 mg per healthy subject) demonstrate that the mean proportion of free resveratrol in plasma was 1.7–1.9% with a mean plasma concentration of free resveratrol around 20 nM
Dose↑, Boocock and his colleagues studied the pharmacokinetic of resveratrol; in vitro data showed that minimum of 5 µmol/L resveratrol is essential for the chemopreventive effects to be elicited
eff↑, Despite the low bioavailability of resveratrol, it shows efficacy in vivo. This may be due to the conversion of both glucuronides and sulfate back to resveratrol in target organs such as the liver
eff↑, repeated administration of high doses of resveratrol generates a higher plasma concentration of parent and a much higher concentration of sulfate and glucuronide conjugates in the plasma
Dose↑, The doses tested in this study were 0.5, 1.0, 2.5 or 5.0 g daily for 29 days. No toxicity was detected, but moderate gastrointestinal symptoms were reported for 2.5 and 5.0 g doses
BioAv↑, the co-administration of piperine with resveratrol was used to enhance resveratrol bioavailability
ROS↑, Recent studies have shown that resveratrol increases ROS generation and decreases mitochondrial membrane potential
MMP↓,
P21↑, treatment decreased the viability of melanoma cells by activating the expression of both p21 and p27, which promoted cell cycle arrest.
p27↑,
TumCCA↑,
ChemoSen↑, Additionally, the use of resveratrol with cisplatin in malignant human mesothelioma cells (MSTO-211H and H-2452 cells) synergistically induces cell death by increasing the intracellular ROS level [64].
COX2↓, covers the down-regulation of the products of the following genes, COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA [93].
5LO↓,
VEGF↓,
IL1↓,
IL6↓,
IL8↓,
AR↓,
PSA↓,
MAPK↓, by preventing also the activation of the MAPK and PI3K/Akt signaling pathways, it suppresses HIF-1a and VEGF release in ovarian cancer cells of humans
Hif1a↓,
Glycolysis↓, Resveratrol was found to effectively impede the activation, invasion, migration and glycolysis of PSCs induced by reactive oxygen species (ROS) by down-regulating the expression of microRNA 21 (miR-21)
miR-21↓,
PTEN↑, also by increasing the phosphatise and tensin homolog (PTEN) protein levels
Half-Life↝, 25 mg/70 kg resveratrol administered to healthy human participants, the compound predominantly appeared in the form of glucuronide and sulfate conjugates in serum and urine and reached its peak concentrations in serum about 30 min after ingestion
*IGF-1↓, Brown and colleagues noted how a major decline in circulating insulin-like growth factor (IGF)-I as well as IGF-binding proteins (IGFBP-3) among healthy individuals can be credited to the intake of resveratrol
*IGFBP3↑,
Half-Life↓, Microactive® and Resveratrol SR and manufactured by Bioactives. This compound is capable of sustained release for over 12 h to increase intestinal residence time.

3331- SIL,    The clinical anti-inflammatory effects and underlying mechanisms of silymarin
- Review, NA, NA
*Inflam↓, anti-inflammatory mechanisms of silymarin,
*NF-kB↓, inhibition of the NF-kB and NLRP3 signaling pathways and the suppression of COX-2 and inducible nitric oxide synthase (iNOS) expression
*NLRP3↓,
*COX2↓,
*iNOS↓,
*neuroP↑, silymarin offers neuroprotection by inhibiting the phosphorylation of ERK1/2, JNK, and p38 MAPK and reducing the expression of the epidermal growth factor receptor and glial fibrillary acidic protein
*p‑ERK↓,
*p38↓,
*MAPK↓,
*EGFR↓,
*ROS↓, By the way, silymarin was reported to curb the formation of oxygen radicals and lipid peroxides.
*lipid-P?,
*5LO↓, Its anti-inflammatory effects were shown by inhibiting 5-LOX activity and obstructing the lipid peroxidation pathway to prevent the generation of ROS involved in inflammatory responses.

3427- TQ,    Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets
ROS⇅, It appears that the cellular and/or physiological context(s) determines whether TQ acts as a pro-oxidant or an anti-ox- idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in different cancer cells have been observed with 5-fluorouracil in gastric cancer and colorectal cancer models

3429- TQ,    Thymoquinone exerts potent growth-suppressive activity on leukemia through DNA hypermethylation reversal in leukemia cells
- in-vitro, AML, NA - in-vivo, NA, NA
DNMT1↓, Further, exposure of leukemia cell lines and patient primary cells to TQ resulted in DNMT1 downregulation, mechanistically, through dissociation of Sp1/NFkB complex from DNMT1 promoter.
Sp1/3/4↓,
NF-kB↓,
Apoptosis↑, led to a reduction of DNA methylation, a decrease of colony formation and an increase of cell apoptosis via the activation of caspases.
Casp↑,
Bcl-xL↓, been shown to downregulate the expression of Bcl-xL [18], COX-2 [19], iNOS [20], 5-LOX [21], TNF [22] and cyclin D1 [16]
COX2↓,
iNOS↓,
5LO↓,
TNF-α↓,
cycD1/CCND1↓,
BioAv↝, The stability data revealed that the compound was stable at −20°C under dim light condition, but not at 25°C and 37°C. Thus, TQ is more stable in the dark and at cold temperature.
TumCG↓, TQ administration attenuates leukemia growth in mice


Showing Research Papers: 1 to 26 of 26

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

CYP1A1↓, 1,   ROS↓, 1,   ROS↑, 4,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC2↓, 1,   CDC25↓, 2,   MMP↓, 1,   p42↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   AMPK↑, 2,   ATG7↑, 1,   cMyc↓, 2,   Glycolysis↓, 2,   NADPH↝, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 1,   Apoptosis↑, 2,   Bcl-2↓, 1,   Bcl-xL↓, 2,   BID↓, 1,   Casp↑, 2,   Casp3↑, 3,   Casp8↑, 2,   Casp9↑, 2,   cFLIP↓, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↓, 1,   DR5↑, 2,   Fas↑, 1,   IAP1↓, 1,   ICAD↓, 1,   iNOS↓, 2,   JNK↑, 2,   MAPK↓, 2,   MAPK↑, 1,   Mcl-1↓, 1,   Myc↓, 1,   p27↑, 3,   p38↑, 2,   survivin↓, 4,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

SOX9↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↓, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B↓, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

CYP1B1↑, 1,   DNAdam↑, 1,   DNMT1↓, 2,   p16↑, 1,   P53↑, 3,   cl‑PARP↑, 2,   PCNA↓, 1,   UHRF1↓, 1,  

Cell Cycle & Senescence ⓘ

p‑CDK1↓, 1,   CDK2↓, 2,   CDK4↓, 1,   cycA1/CCNA1↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 6,   cycE/CCNE↓, 1,   E2Fs↓, 1,   P21↑, 5,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   CSCs↓, 1,   ERK↓, 2,   p‑ERK↓, 1,   FOXM1↓, 1,   FOXO↑, 2,   GSK‐3β↓, 2,   HDAC1↓, 1,   IGF-1↓, 1,   Let-7↑, 2,   mTOR↓, 4,   NOTCH↓, 1,   P70S6K↓, 1,   PI3K↓, 4,   PTEN↑, 1,   STAT3↓, 3,   TOP2↓, 1,   TumCG↓, 5,   Wnt↓, 3,  

Migration ⓘ

5LO↓, 11,   AP-1↓, 1,   Ca+2↑, 1,   cal2↓, 1,   DLC1↑, 1,   E-cadherin↑, 1,   ITGA5↓, 1,   miR-200b↑, 1,   MMP1↓, 1,   MMP2↓, 4,   MMP7↓, 1,   MMP9↓, 6,   MMPs↓, 1,   N-cadherin↓, 1,   serineP↓, 1,   Slug↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   Twist↓, 1,   Vim↓, 2,   Zeb1↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 8,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 9,   CXCL1↓, 1,   CXCR4↓, 4,   IL1↓, 2,   IL10↓, 1,   IL12↓, 1,   IL2↑, 1,   IL6↓, 2,   IL8↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 6,   NK cell↑, 1,   p65↓, 1,   PGE2↓, 2,   PSA↓, 2,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 3,   CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 2,   ChemoSen↑, 5,   Dose↑, 2,   eff↑, 3,   Half-Life↓, 1,   Half-Life↝, 1,   selectivity↑, 2,   TET2↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 3,   FOXM1↓, 1,   GutMicro↑, 1,   IL6↓, 2,   Myc↓, 1,   PSA↓, 2,  

Functional Outcomes ⓘ

AntiTum↑, 1,   chemoPv↑, 1,   radioP↑, 1,   Risk↓, 1,   TumVol↓, 1,  
Total Targets: 165

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

4-HNE↓, 1,   antiOx↑, 8,   Catalase↑, 5,   Ferroptosis↓, 1,   GPx↑, 3,   GPx4↑, 1,   GSH↑, 4,   GSR↑, 1,   GSTs↑, 1,   HO-1↑, 3,   lipid-P?, 1,   lipid-P↓, 6,   MDA↓, 3,   NRF2↑, 5,   ROS↓, 12,   SOD↑, 7,   TAC↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↓, 1,   IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   CREB↑, 1,   CYP3A2↓, 1,   FASN↓, 1,   LDH↑, 1,  

Cell Death ⓘ

Casp3↓, 1,   Ferroptosis↓, 1,   iNOS↓, 2,   p‑JNK↓, 1,   MAPK↓, 1,   p38↓, 2,  

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 2,   other↓, 2,   other↑, 6,   other↝, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Choline↑, 1,   ERK↓, 1,   p‑ERK↓, 1,   GSK‐3β↓, 1,   IGF-1↓, 1,   IGFBP3↑, 1,   TRPM7↓, 1,  

Migration ⓘ

5LO↓, 15,   AntiAg↑, 3,   AP-1↓, 2,   Ca+2↑, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP3↓, 2,   MMP9↓, 1,   MMPs↓, 1,   PKCδ↑, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   NO↓, 2,   NO↑, 1,  

Barriers & Transport ⓘ

BBB↑, 2,   GastroP↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 3,   COX2↓, 10,   CRP↓, 2,   IL1↓, 1,   IL10↑, 1,   IL12↓, 1,   IL1β↓, 4,   IL2↑, 1,   IL6↓, 8,   IL8↓, 2,   Imm↑, 4,   Inflam↓, 11,   MCP1↓, 1,   NF-kB↓, 8,   NF-kB↑, 1,   PGE2↓, 6,   PGE2↑, 1,   Th1 response↓, 1,   Th2↑, 2,   TLR4↓, 1,   TNF-α↓, 7,   VitD↑, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 5,   BChE↓, 2,   BDNF↓, 1,   BDNF↑, 2,   ChAT↑, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 3,   BioAv⇅, 1,   BioAv↝, 1,   BioEnh↑, 2,   Dose↝, 2,   eff↑, 3,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 3,   Calcium↑, 1,   CRP↓, 2,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 8,   LDH↑, 1,   Mag↑, 1,   VitD↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 2,   cardioP↑, 4,   chemoP↑, 1,   chemoPv↑, 2,   cognitive↑, 9,   hepatoP↑, 2,   memory↑, 3,   neuroP↑, 7,   Obesity↓, 1,   Pain↓, 1,   Risk↓, 1,   toxicity↓, 2,   toxicity↝, 1,   Weight↓, 1,   Wound Healing↑, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Diar↓, 1,  
Total Targets: 125

Scientific Paper Hit Count for: 5LO, 5-lipoxygenase (5-LO)
7 Boswellia (frankincense)
3 Carvacrol
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Piperine
2 Quercetin
2 Thymoquinone
1 Aloe anthraquinones
1 Bacopa monnieri
1 Boron
1 Caffeic acid
1 Thymol-Thymus vulgaris
1 Chocolate
1 Curcumin
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
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#:1090  State#:%  Dir#:1
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