MCP1 Cancer Research Results

MCP1, CCL2,monocyte chemotactic protein-1: Click to Expand ⟱

Source:

Type:

MCP-1 (Monocyte Chemoattractant Protein-1, also known as CCL2)
MCP-1/CCL2 is a chemokine involved in recruiting monocytes, memory T cells, and dendritic cells to sites of inflammation.
– It plays a key role in mediating immune cell trafficking, inflammation, and tissue remodeling. MCP-1 is pivotal in inflammatory responses and can modulate immune cell infiltration into tissues.
– It also influences the polarization of macrophages, which may adopt pro-inflammatory (M1) or anti-inflammatory/pro-tumoral (M2) roles.

Many cancers (such as breast, prostate, ovarian, lung, and colon cancers) exhibit increased levels of MCP-1.
– Both tumor cells and associated stromal cells (e.g., cancer-associated fibroblasts, infiltrating immune cells) can produce MCP-1, contributing to an inflammatory milieu.

• Inducers of MCP-1:
– Hypoxia, oncogenic pathways, and cytokine-rich environments (e.g., IL-1β, TNF-α) can drive increased MCP-1 expression.
– This upregulation often correlates with an ongoing inflammatory response in the tumor microenvironment.

Scientific Papers found: Click to Expand⟱

3283-

ALA,

Alpha-lipoic acid inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in human aortic endothelial cells

in-vitro,

Nor,

*TNF-α↓, LA also strongly inhibited TNF-alpha-induced mRNA expression of monocyte chemoattractant protein-1
*NF-kB↓, LA dose-dependently inhibited TNF-alpha-induced IkappaB kinase activation, subsequent degradation of IkappaB, the cytoplasmic NF-kappaB inhibitor, and nuclear translocation of NF-kappaB.
*antiOx↑, LA in its free, non-protein-bound form has potent antioxidant and metal-chelating properties
*IronCh↑,
*GSSG↓, DHLA/LA couple may chemically reduce glutathione disulfide (GSSG) to GSH
*VCAM-1↓, E-selectin, VCAM-1, ICAM-1, and MCP-1 message levels decreased by 93%, 77%, 67%, and 100%, respectively, when HAEC were pretreated with 0.5mmol/l LA
*E-sel↓,
*ICAM-1↓,
*MCP1↓,
*NF-kB↓, Lipoic acid inhibits TNF-a-induced activation of NF-kB and degradation of IkBs
IKKα↓,

3667-

ART/DHA,

Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia

Review,

Sepsis,

40 μΜ)

mice

*cognitive↑, artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests
*neuroP↑, attenuated neuronal damage and microglial activation in the hippocampus.
*TNF-α↓, artemisinin (40 μΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6)
*IL6↓,
*NF-kB↓, artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway;
*AMPK↑,
*ROS↓, artemisinin protects neuronal HT-22 cells from oxidative injury by activating the Akt pathway
*Akt↑,
*MCP1↓, artemisinin reversed the LPS-induced increases in the chemokines MCP-1 and MIP-2
*MIP2↓,
*TGF-β↑, Artemisinin also significantly increased the mRNA and protein expression of TGF-β
*Inflam↓, The AMPKα1 pathway is involved in the anti-inflammatory effect of artemisinin

1074-

ART/DHA,

Artemisinin attenuates lipopolysaccharide-stimulated proinflammatory responses by inhibiting NF-κB pathway in microglia cells

in-vitro,

Nor,

BV2

BV-2 microglia

*TNF-α↓,
*IL6↓,
*MCP1↓,
*NO↓,
*iNOS↓,
*IκB↑,

3689-

Ash,

Ashwagandha attenuates TNF-α- and LPS-induced NF-κB activation and CCL2 and CCL5 gene expression in NRK-52E cells

in-vitro,

NA,

NRK52E

*RenoP↑, ashwaganda WSE as a valid candidate for evaluation of therapeutic potential for the treatment of chronic renal dysfunction.
*NF-kB↓, WSE completely prevented TNF-α-induced increases in CCL5, while attenuating the increase in CCL2 expression and NF-κB activation.
*MCP1↓,
*RANTES↓,

3174-

Ash,

Withaferin A Acts as a Novel Regulator of Liver X Receptor-α in HCC

in-vitro,

HCC,

HepG2

in-vitro,

HCC,

Hep3B

in-vitro,

HCC,

HUH7

NF-kB↓, We found that many of Nuclear factor kappa B (NF-κB), angiogenesis and inflammation associated proteins secretion is downregulated upon Withaferin A treatment.
angioG↓,
Inflam↓,
TumCP↓, uppressed the proliferation, migration, invasion, and anchorage-independent growth of these HCC cells.
TumCMig↓,
TumCI↓,
Sp1/3/4↓, Withaferin A inhibits NF-κB, Specificity protein 1 (Sp1) transcription factors, and downregulates Vascular Endothelial Growth Factor (VEGF) gene expression
VEGF↓,
angioG↓, Withaferin A (2.5 µM) treatment decreased the secretion of various angiogenesis-related markers, growth factors, and cytokines (Serpin F1(PEDF), uPA, PDGF-AA, Angiogenin, Endothelin-1, Macrophage migration inhibitory factor (MIF), PAI-1, MCP1, ICAM-1
uPA↓,
PDGF↓,
MCP1↓,
ICAM-1↓,
*NRF2↑, It also upregulates the Nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor and protects from Acetaminophen-induced hepatotoxicity and liver injury
*hepatoP↑,

4303-

Ash,

Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review

Review,

AD,

*neuroP↑, neuroprotective, sedative and adaptogenic effects and effects on sleep.
*Sleep↑,
*Inflam↓, anti-inflammatory, antimicrobial, cardioprotective and anti-diabetic properties
*cardioP↑,
*cognitive↑, Significant improvements in cognitive function were observed as a result of the inhibition of amyloid β-42, and a reduction in pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and MCP-1, nitric oxide, and lipid peroxidation was also observed.
*Aβ↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MCP1↓,
*lipid-P↓,
*tau↓, reducing β-amyloid aggregation and inhibiting τ protein accumulation.
*ROS↓, withaferin A is responsible for inhibiting oxidative and pro-inflammatory chemicals and regulating heat shock proteins (HSPs), the expression of which increases when cells are exposed to stressors.
*BBB↑, ability of withanolide A to penetrate the blood-brain barrier (BBB) was demonstrated.
*AChE↓, potentially inhibiting acetylcholinesterase activity, which may have benefits in the treatment of canine cognitive dysfunction and Alzheimer’s disease
*GSH↑, increased glutathione concentration, increased glutathione S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase activities,
*GSTs↑,
*GSR↑,
*GPx↑,
*SOD↑,
*Catalase↑,
ChemoSen↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin
*Strength↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin

2481-

Ba,

Rad,

Radiotherapy Increases 12-LOX and CCL5 Levels in Esophageal Cancer Cells and Promotes Cancer Metastasis via THP-1-Derived Macrophages

in-vitro,

ESCC,

Eca109

0, 20, 40, or 80 µmol/L

in-vitro,

ESCC,

KYSE150

12LOX↓, increased by 12-LOX upregulation but was suppressed by the well-established 12-LOX inhibitor, baicalein
RadioS↑, In prostate cancer cells, 12-LOX inhibition has been shown to increase radiation sensitivity,
Dose↝, Additionally, 12-LOX expression was significantly inhibited at 40 µmol/L
RANTES↓, post-radiotherapy protein levels of CCL5 increased in Eca109 and Kyse150 cells but were inhibited by baicalein
MCP1↓, Baicalein, a recognized inhibitor of 12-LOX, successfully inhibited CCL2 and CCL5 expression, which was verified by RT-qPCR.

2614-

Ba,

Therapeutic potentials of baicalin and its aglycone, baicalein against inflammatory disorders

Review,

NA,

*toxicity↓, These flavonoids have almost no toxicity to human normal epithelial, peripheral and myeloid cells
*antiOx↑, antioxidant and anti-inflammatory activities are largely due to their abilities to scavenge the reactive oxygen species (ROS)
*Inflam↓,
*ROS↓,
*NF-kB↓, by attenuating the activity of NF-κB and suppressing the expression of several inflammatory cytokines and chemokines including monocyte chemotactic protein-1 (MCP-1)
*MCP1↓,
*hepatoP↑, Both baicalin and baicalein ... including antioxidant, anti-inflammatory, anticancer, anticardiovascular, antidiabetic, hepatoprotective, antiviral, anti-ulcerative colitis, antithrombotic, eye protective and neuroprotective activities
*neuroP↑,

2674-

BBR,

Berberine: A novel therapeutic strategy for cancer

Review,

Var,

Review,

IBD,

Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

2686-

BBR,

Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs

Review,

Nor,

Inflam↓, BBR has documented to have anti-diabetic, anti-inflammatory and anti-microbial (both anti-bacterial and anti-fungal) properties.
IL6↓, BBRs can inhibit IL-6, TNF-alpha, monocyte chemo-attractant protein 1 (MCP1) and COX-2 production and expression.
MCP1↓,
COX2↓,
PGE2↓, BBRs can also effect prostaglandin E2 (PGE2)
MMP2↓, and decrease the expression of key genes involved in metastasis including: MMP2 and MMP9.
MMP9↓,
DNAdam↑, BBR induces double strand DNA breaks and has similar effects as ionizing radiation
eff↝, In some cell types, this response has been reported to be TP53-dependent
Telomerase↓, This positively-charged nitrogen may result in the strong complex formations between BBR and nucleic acids and induce telomerase inhibition and topoisomerase poisoning
Bcl-2↓, BBR have been shown to suppress BCL-2 and expression of other genes by interacting with the TATA-binding protein and the TATA-box in certain gene promoter regions
AMPK↑, BBR has been shown in some studies to localize to the mitochondria and inhibit the electron transport chain and activate AMPK.
ROS↑, targeting the activity of mTOR/S6 and the generation of ROS
MMP↓, BBR has been shown to decrease mitochondrial membrane potential and intracellular ATP levels.
ATP↓,
p‑mTORC1↓, BBR induces AMPK activation and inhibits mTORC1 phosphorylation by suppressing phosphorylation of S6K at Thr 389 and S6 at Ser 240/244
p‑S6K↓,
ERK↓, BBR also suppresses ERK activation in MIA-PaCa-2 cells in response to fetal bovine serum, insulin or neurotensin stimulation
PI3K↓, Activation of AMPK is associated with inhibition of the PI3K/PTEN/Akt/mTORC1 and Raf/MEK/ERK pathways which are associated with cellular proliferation.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt. In HCT116 cells, PTEN inhibits Akt signaling and proliferation.
Akt↓,
Raf↓,
MEK↓,
Dose↓, The effects of low doses of BBR (300 nM) on MIA-PaCa-2 cells were determined to be dependent on AMPK as knockdown of the alpha1 and alpha2 catalytic subunits of AMPK prevented the inhibitory effects of BBR on mTORC1 and ERK activities and DNA synthes
Dose↑, In contrast, higher doses of BBR inhibited mTORC1 and ERK activities and DNA synthesis by AMPK-independent mechanisms [223,224].
selectivity↑, BBR has been shown to have minimal effects on “normal cells” but has anti-proliferative effects on cancer cells (e.g., breast, liver, CRC cells) [225–227].
TumCCA↑, BBR induces G1 phase arrest in pancreatic cancer cells, while other drugs such as gemcitabine induce S-phase arrest
eff↑, BBR was determined to enhance the effects of epirubicin (EPI) on T24 bladder cancer cells
EGFR↓, In some glioblastoma cells, BBR has been shown to inhibit EGFR signaling by suppression of the Raf/MEK/ERK pathway but not AKT signaling
Glycolysis↓, accompanied by impaired glycolytic capacity.
Dose?, The IC50 for BBR was determined to be 134 micrograms/ml.
p27↑, Increased p27Kip1 and decreased CDK2, CDK4, Cyclin D and Cyclin E were observed.
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↓,
Bax:Bcl2↑, Increased BAX/BCL2 ratio was observed.
Casp3↑, The mitochondrial membrane potential was disrupted and activated caspase 3 and caspases 9 were observed
Casp9↑,
VEGFR2↓, BBR treatment decreased VEGFR, Akt and ERK1,2 activation and the expression of MMP2 and MMP9 [235].
ChemoSen↑, BBR has been shown to increase the anti-tumor effects of tamoxifen (TAM) in both drug-sensitive MCF-7 and drug-resistant MCF-7/TAM cells.
eff↑, The combination of BBR and CUR has been shown to be effective in suppressing the growth of certain breast cancer cell lines.
eff↑, BBR has been shown to synergize with the HSP-90 inhibitor NVP-AUY922 in inducing death of human CRC.
PGE2↓, BBR inhibits COX2 and PEG2 in CRC.
JAK2↓, BBR prevented the invasion and metastasis of CRC cells via inhibiting the COX2/PGE2 and JAK2/STAT3 signaling pathways.
STAT3↓,
CXCR4↓, BBR has been observed to inhibit the expression of the chemokine receptors (CXCR4 and CCR7) at the mRNA level in esophageal cancer cells.
CCR7↓,
uPA↓, BBR has also been shown to induce plasminogen activator inhibitor-1 (PAI-1) and suppress uPA in HCC cells which suppressed their invasiveness and motility.
CSCs↓, BBR has been shown to inhibit stemness, EMT and induce neuronal differentiation in neuroblastoma cells. BBR inhibited the expression of many genes associated with neuronal differentiation
EMT↓,
Diff↓,
CD133↓, BBR also suppressed the expression of many genes associated with cancer stemness such as beta-catenin, CD133, NESTIN, N-MYC, NOTCH and SOX2
Nestin↓,
n-MYC↓,
NOTCH↓,
SOX2↓,
Hif1a↓, BBR inhibited HIF-1alpha and VEGF expression in prostate cancer cells and increased their radio-sensitivity in in vitro as well as in animal studies [290].
VEGF↓,
RadioS↑,

2760-

BetA,

A Review on Preparation of Betulinic Acid and Its Biological Activities

Review,

Var,

Review,

Stroke,

AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I

2767-

Bos,

The potential role of boswellic acids in cancer prevention and treatment

Review,

Var,

*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-ÎºB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/Î²-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-Î²-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-Î² and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/Î²-catenin and NF-ÎºB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-Î± and IL-1Î² in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (PhytosomeÂ®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

5951-

Cela,

Celastrol Suppresses Tumor Cell Growth through Targeting an AR-ERG-NF-κB Pathway in TMPRSS2/ERG Fusion Gene Expressing Prostate Cancer

vitro+vivo,

Pca,

treat mice bearing subcutaneous VCaP xenograft tumors.

NF-kB↓, Celastrol is a well known NF-kB inhibitor, and thus may inhibit T/E fusion expressing PCa cell growth.
AR↓, targeting three critical signaling pathways: AR, ERG and NF-kB in these cells
MCP1↓, Celastrol can Inhibit CCL2 Expression at Both the RNA and Protein Level
Akt↓, Multiple molecular targets of Celastrol have been identified including AKT, Hsp90 and others
HSP90↓,
TumCG↓, Studies have shown Celastrol can inhibit PCa tumor growth in vivo

1418-

CUR,

Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis

Review,

Arthritis,

*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)

3795-

CUR,

Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence

Review,

AD,

*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.

2819-

CUR,

Chemo,

Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury

Review,

Var,

*hepatoP↑, Several studies have shown that curcumin could prevent and/or palliate chemotherapy-induced liver injury
*Inflam↓, mainly due to its anti-inflammatory, antioxidant, antifibrotic and hypolipidemic properties.
*antiOx↑,
*lipid-P↓, Curcumin can lower lipid peroxidation by increasing the content of GSH, a major endogenous antioxidant,
*GSH↑,
*SOD↑, as well as by enhancing the activity of endogenous antioxidant enzymes, such as SOD, CAT, GPx and GST
*Catalase↑,
*GPx↑,
*GSTs↑,
*ROS↓, elimination of ROS
*ALAT↓, attenuated the increase in serum levels of TNF-α as well as several liver enzymes, including ALT, AST, alkaline phosphatase and MDA which are markers of liver damage caused by MTX or cisplatin.
*AST↓,
*MDA↓,
*NRF2↑, Curcumin also attenuated DILI through activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway
*COX2↑, Curcumin can also inhibit the expression of cyclooxygenase-2 (COX-2)
*NF-kB↓, NF-κB inhibition, which decreased the downstream induction of COX-2, ICAM-1 and MCP-1 pro-inflammatory regulators
*ICAM-1↓,
*MCP1↓,
*HO-1↑, increase in HO-1 and NQO1 expression
CXCc↓, Downregulation of pro-inflammatory chemokines, (CXCL1, CXCL2, and MCP-1)

1976-

EGCG,

Epigallocatechin-3-gallate exhibits anti-tumor effect by perturbing redox homeostasis, modulating the release of pro-inflammatory mediators and decreasing the invasiveness of glioblastoma cells

in-vitro,

GBM,

U87MG

50-100uM

ROS↑, Polyphenol epigallocatechin-3-gallate (EGCG) induced apoptosis in glioma cells by elevating oxidative stress through increased reactive oxygen species (ROS) generation. Signs of apoptosis included altered mitochondrial membrane potential and elevated
MMP↓, altered mitochondrial membrane potential
Casp3↑, elevated expression of caspase-3 (5fold) and cytochrome c
Cyt‑c↑,
Trx1↓, The increase in ROS was concomitant with the decrease in expression of thioredoxin (TRX-1)
Ceru↓, and ceruloplasmin (CP)
IL6↓, EGCG downregulated the levels of pro-inflammatory cytokine interleukin (IL)-6 and chemokines IL-8, monocyte-chemoattractant protein (MCP)-1 and RANTES
IL8↓,
MCP1↓,
RANTES?,
uPA↝, 40-50% decrease in uPa activity was observed in glioma cells upon treatment with 50 and 100 uM of EGCG
ROS↑, ROS production, a significant 1.7- and 2-fold (p<0.05) increase in ROS production was observed in cells treated with 50 and 100 uM EGCG respectively,

3768-

H2,

Effects of Hydrogen Gas Inhalation on Community-Dwelling Adults of Various Ages: A Single-Arm, Open-Label, Prospective Clinical Trial

Trial,

AD,

*ROS↓, Investigation of oxidative stress markers such as reactive oxygen species and nitric oxide showed that their levels decreased post-treatment.
*NO↓,
*BACE↓, BACE-1), amyloid beta (Aβ), r (BDNF), (VEGF-A), T-tau, monocyte chemotactic protein-1 (MCP-1), and inflammatory cytokines (interleukin-6), showed that their cognitive condition significantly improved after treatment, in most cases.
*BDNF↑, see figure 5
*VEGF↑,
*p‑tau↓, t-tau and p-tau levels reduced dramatically in different ages within 4 weeks of treatment;
*MCP1↓, MCP-1 (p < 0.001) (Figure 7A), IL-6 (p < 0.05) (Figure 7B), and VEGF-A (Figure 7C) levels significantly decreased
*IL6↓,
*cognitive↑, H2 gas inhalation may be a good candidate for improving AD with cognitive dysfunction
*toxicity∅, H2 gas inhalation treatment did not cause any adverse effects, indicating that it was safe.

228-

MFrot,

MF,

Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17

NA,

MS,

*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.

4036-

NAD,

VitB3,

NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency

in-vivo,

AD,

mouse

*Inflam↓, NAD+ supplementation with nicotinamide riboside significantly normalized neuroinflammation, synaptic transmission, phosphorylated Tau, and DNA damage as well as improved learning and memory and motor function.
*p‑tau↓, NR Decreases Tau Phosphorylation but Not Aβ Accumulation in AD and AD/Polβ Mice.
*DNAdam↓,
*memory↑,
*motorD↑,
*cognitive↑, NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice.
*BBB↑, NR enters the brain and boosts cellular NAD+ levels when administered orally.
IL1β↓, AD/Polβ mice had elevated levels of proinflammatory cytokines and chemokines, including IL-1α, TNFα, MCP-1, IL-1β, MIP-1α, and RANTES, and decreased levels of antiinflammatory cytokines such as IL-10 (Fig. 3G and Fig. S4A). NR treatment normalized
*TNF-α↓,
*MCP1↓,
*RANTES↓,
*ROS↓, NR treatment of AD fibroblasts resulted in decreased levels of mitochondrial ROS compared with vehicle-treated cells
*SIRT3↑, NR Treatment Decreases DNA Damage and Apoptosis Through SIRT3 and SIRT6.
*SIRT6↑,

3249-

PBG,

Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence

Review,

Var,

*Inflam↓, ropolis was consistently demonstrated to reduce the expression of inflammatory and oxidative markers such as malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), nitric oxide (NO), and inducible nitric oxide synthase (iNOS)
*ROS↓,
*MDA↓,
*TNF-α↓,
*NO↓,
*iNOS↓,
*SOD↑, while increasing and maintaining antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)
*GPx↑,
*GSR↓,
*GSH↑,
*neuroP↑, neuroprotective effect of propolis was also demonstrated in terms of alleviating symptoms associated with aneurysm, ischemia, ischemia-reperfusion and traumatic brain injuries.
*IL6↓, Propolis reduced the expression of interleukin-6 (IL-6), TNF-α, matrix metalloproteinase-2 (MMP-2), MMP-9, monocyte chemotactic protein-1 (MCP-1), and iNOS
*MMP2↓,
*MMP9↓,
*MCP1↓,
*HSP70/HSPA5↑, while increasing the expression of protective proteins such as heat shock protein-70 (hsp70)
*motorD↑, significantly ameliorate the impairment of sensory–motor and other physical indices in animals subjected to these injuries
*Pain↓, Unsurprisingly, propolis was shown to be effective in attenuating symptoms of neuroinflammation, pain, and oxidative stress.
*VCAM-1↓, consistently shown to reduce inflammation markers such as vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappa B (NF-kB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK)-
*NF-kB↓,
*MAPK↓,
*JNK↓,
*IL1β↓, It also reduced the expression of reactive oxygen species (ROS) and pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α
*AChE↓, propolis inhibited the activity of both acetylcholinesterase and butyrylcholinesterase in a dose-dependent manner
*toxicity∅, Kalia et al. (2014) observed no cytotoxicity in organs, including the brain of normal mice fed up to 1000 mg propolis extract/ kg body weight.
cognitive↑, figure 4

3000-

PL,

Biological and physical approaches on the role of piplartine (piperlongumine) in cancer

in-vitro,

Nor,

HUVECs

in-vitro,

Laryn,

HEp2

Inflam↓, anti-inflammatory and antitumor activity.
AntiTum↑,
*α-tubulin↓, PL inhibits α-tubulin expression
selectivity↑, PL appeared to have no effect on the migration and invasion ability of normal or neoplastic cells
HIF2a↓, Other groups have expanded the knowledge of the biological properties of PL and suggested, inter alia, that PL inhibits hypoxia inducible factor-2 (HIF-2) transcription
MCP1↓, reduced the MCP-1 levels,

3927-

PTS,

Effects of Pterostilbene on Cardiovascular Health and Disease

Review,

AD,

Review,

Stroke,

*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke

3343-

QC,

Quercetin, a Flavonoid with Great Pharmacological Capacity

Review,

Var,

Review,

AD,

Review,

Arthritis,

*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

3068-

RES,

Resveratrol decreases the expression of genes involved in inflammation through transcriptional regulation

in-vitro,

lymphoma,

U937

p65↓, In our study, RESV treatment significantly decreased p65 expression and reduced the activities of the antioxidant enzymes SOD2, PRX2, CAT, and TRX.
SOD2↓,
Prx↓,
Catalase↓,
Trx↓,
TNF-α↓, (i.e., TNF-α, IL-8, and MCP-1), whereas a reduction in the protein levels of these cytokines was observed in the presence of RESV.
IL8↓,
MCP1↓,
SIRT1↑, a trend of increased SIRT1 activity in the presence of RESV was observed, which may be due to the low dose of RESV used

3012-

RosA,

Rad,

Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROSMYPT1TGFβ1 Signaling Via miR-19b-3p

in-vitro,

Nor,

IMR90

*Inflam↓, RA reduced X-ray-induced the expression of inflammatory related factors, and the level of reactive oxygen species.
*ROS↓,
*p‑NF-kB↓, RA down-regulated the phosphorylation of nuclear factor kappa-B (NF-κB).
*Rho↓, RA attenuated RhoA/Rock signaling through upregulating miR-19b-3p, leading to the inhibition of fibrosis
*ROCK1↓,
*radioP↑, RA attenuated radiation- induced damage by its capacity to relieve inflammation and regulate inflammatory factors.
*MCP1↓, RA treatment reduced RNA levels of NF-kB target gene, including MCP-1, RANTES, and ICAM-1
*RANTES↓,
*ICAM-1↓,
*PGC1A↑, Western blot analysis showed that RA promoted the expression of PGC-1a and reduced the expression of NOX-4, this evidence further suggested that RA inhibits the generation of ROS
*NOX4↓,
*Dose↝, RA exerted strongly protective effects in the X-ray-induced inflammation at doses of 60 mg/kg, and treat- ment with a higher dose (120 mg/kg) do not enhance its anti- inflammatory effect.

1432-

SFN,

Evaluation of biodistribution of sulforaphane after administration of oral broccoli sprout extract in melanoma patients with multiple atypical nevi

Human,

Melanoma,

50-200uM

Seventeen patients who each had at least 2 atypical nevi and a prior history of melanoma were randomly allocated to 50, 100, or 200 µmol oral BSE-SFN daily for 28 days.

other↑, Median skin sulforaphane levels on day 28 were 0.0 ng/g, 3.1 ng/g, and 34.1 ng/g for 50, 100, and 200 µmol, respectively
decorin↑,
*toxicity↓, Oral BSE-SFN is well-tolerated at daily doses up to 200 µmol and achieves dose-dependent levels in plasma and skin.
IP-10/CXCL-10↓,
MCP1↓,
CXCL9↓,
MIP-1β↓,
IFN-γ↓,

4498-

SSE,

Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases

Review,

Var,

Review,

AD,

Review,

IBD,

*Imm↑, Selenium is essential for the maintenance of the immune system, conversion of thyroid hormones, protection against the harmful action of heavy metals and xenobiotics as well as for the reduction of the risk of chronic diseases
*GutMicro↑, Selenium is able to balance the microbial flora avoiding health damage associated with dysbiosis.
*BioAv↑, highlighting their role in improving the bioavailability of selenocompounds
*Risk↓, Selenium deficiency may result in a phenotype of gut microbiota that is more susceptible to cancer, thyroid dysfunctions, inflammatory bowel disease, and cardiovascular disorders.
*Dose↝, highest sources of Se with concentrations that range from 1.80 to 320.80 μg Se/g
Risk↓, serum Se greater than or equal to 135 μg/L were associated with reduced cancer mortality
*CRP↓, Se supplementation decreases the serum levels of C-reactive protein and increases the levels of GPX, suggesting a positive effect on reduction of inflammation and oxidative stress in cardiovascular diseases
*GPx↓,
*Inflam↓,
*selenoP↑, SELENOP may be involved in some brain disorders, in particular in Alzheimer's disease, providing Se for brain tissue to produce selenoproteins.
*Dose↝, 100, 200, or 300 μg Se/day as Se-enriched yeast or placebo yeast. The results of this study warn that a 300-μg/day dose of Se (as Se yeast) taken for 5 years in a country with moderately low Se status can increase all-cause mortality by 10 years late
*ROS↓, Animals treated with SeCys and selenocystine showed a reduction in the concentration of ROS and malondialdehyde (MDA), as well as an increase in intestinal activity of SOD and GPX, which seems to indicate a protective effect against damage to the gut
*MDA↓,
*SOD↑,
*GPx↑,
*IL1↓, In addition, the levels of IL-1, MCP, IL-6, and TNF-α were significantly reduced in the group treated with SeCys
*MCP1↓,
*IL6↓,
*TNF-α↓,
Risk↓, higher SELENOP concentrations were inversely associated with colorectal cancer risk
*neuroP↑, Due to the antioxidant property of Se, some selenoproteins play a neuroprotective role
*memory↑, Long-term dietary supplementation (3 months) with Se-enriched yeast (Se-yeast) in triple transgenic mouse model of Alzheimer disease (AD), significantly improved spatial learning, retention of neuronal memory and activity

2103-

TQ,

Anti-inflammatory effects of the Nigella sativa seed extract, thymoquinone, in pancreatic cancer cells

in-vitro,

PC,

Hs766t

25–75 µM

in-vitro,

PC,

MIA PaCa-2

MCP1↓, Tq dose- and time-dependently significantly reduced PDA cell synthesis of MCP-1, TNF-α, interleukin (IL)-1β and Cox-2.
TNF-α↓,
IL1β↓,
COX2↓,
NF-kB↓, Tq also inhibited the constitutive and TNF-α-mediated activation of NF-κB in PDA cells and reduced the transport of NF-κB from the cytosol to the nucleus.
HDAC↓, Tq also increased p21 WAF1 expression, inhibited histone deacetylase (HDAC) activity, and induced histone hyperacetylation
P21↑,

3410-

TQ,

Anti-inflammatory effects of thymoquinone and its protective effects against several diseases

Review,

Arthritis,

*Inflam↓, anti-inflammatory, anti-oxidant, and anti-apoptotic properties in several disorders such as asthma, hypertension, diabetes, inflammation, bronchitis, headache, eczema, fever, dizziness and influenza
*antiOx↑, anti-inflammatory and anti-oxidant effects via several molecular pathways
*COX2↓, TQ has been shown to suppress COX2 expression and the ensuing generation of prostaglandins
*NRF2↑, TQ also attenuates inflammation via the Nrf2 pathway [28]. Heme-oxygenase 1 (HO-1) has been shown to be stimulated by TQ
*HO-1↑,
*IL1β↓, oral TQ treatment caused a decrease in several pro-inflammatory regulators, such as interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor (TNFα), interferon γ (IFNγ) and prostaglandin E2 PGE(2)
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
*PGE2↓,
*cardioP↑, Cardioprotective activity of TQ through anti-inflammation
*Catalase↑, LPS diminished anti-oxidant enzymes including catalase (CAT) and superoxide dismutase (SOD) and the total thiol group. TQ treatment reduced these effects, restoring many of the LPS effects to basal levels
*SOD↑,
*Thiols↑,
*neuroP↑, Neuroprotective activity of TQ through anti-inflammation
*IL12↓, TQ diminished the levels of several cytokines such as IL-6, IL-1β, IL-12p40/70, chemokine C-C motif ligand 12 (CCL12)/monocyte chemotactic protein 5 (MCP-5), CCL2/MCP-1, granulocyte colony-stimulating factor (GCSF), and C-X-C motif chemokine 10 (Cxcl
*MCP1↓,
*CXCc↓,
*ROS↓, consistent with TQ’s efficacy in reducing ROS generation and the ensuing inflammation

3404-

TQ,

The Neuroprotective Effects of Thymoquinone: A Review

Review,

Var,

Review,

AD,

Review,

Park,

Review,

Stroke,

*Inflam↓, anti-inflammatory, antioxidant, antimicrobial, antiparasitic, anticancer, hypoglycemic, antihypertensive, and antiasthmatic effects.
AntiCan↑,
*TNF-α↓, TQ treatment (2.5, 5, and 10 μM) inhibited the release of TNF-α, IL-6, and IL-1β.
*IL6↓,
*IL1β↓,
*NF-kB↓, TQ treatment (2.5, 5 and 10 μM) inhibited NF-κB-dependent neuroinflammation in BV2 microglia via decreasing iNOS protein levels, κB inhibitor phosphorylation, and binding of NF-κB to the DNA
*iNOS↓,
*NRF2↑, activation of the Nrf2/ARE signaling pathway by TQ resulted in the inhibition of NF-κB-mediated neuroinflammation.
*neuroP↑, TQ has neuroprotection potential against Aβ1-42 in rat hippocampal by ameliorating oxidative stress.
*MMP↑, Thymoquinone ameliorated Aβ1-42-induced neurotoxicity and prevented the mitochondrial membrane potential depolarization and finally reduced the oxidative stress.
*ROS↓,
*MDA↓, Thymoquinone decreased the neuronal cell death in the hippocampal CA1 region and MDA level and increased glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities after forebrain ischemia.
*GSH↑,
*Catalase↑,
*SOD↑,
*IL12↓, Thymoquinone exhibited anti-inflammatory effects by decreasing several cytokines, including TNF-α, NF-κB, IL-6, IL-1β, IL-12p40/70, (CCL12)/MCP-5, (CCL2)/MCP-1, GCSF, and Cxcl 10/IP-10 of, NO, PGE2, and iNOS.
*MCP1↓,
*IP-10/CXCL-10↓,
*PGE2↓,

3425-

TQ,

Advances in research on the relationship between thymoquinone and pancreatic cancer

Apoptosis↑, TQ can inhibit cell proliferation, promote cancer cell apoptosis, inhibit cell invasion and metastasis, enhance chemotherapeutic sensitivity, inhibit angiogenesis, and exert anti-inflammatory effects.
TumCP↓,
TumCI↓,
TumMeta↓,
ChemoSen↑,
angioG↓,
Inflam↓,
NF-kB↓, These anticancer effects predominantly involve the nuclear factor (NF)-κB, phosphoinositide 3 kinase (PI3K)/Akt, Notch, transforming growth factor (TGF)-β, c-Jun N-terminal kinase (JNK)
PI3K↓,
Akt↓,
TGF-β↓,
Jun↓,
p38↑, and p38 mitogen-activated protein kinase (MAPK) signaling pathways as well as the regulation of the cell cycle, matrix metallopeptidase (MMP)-9 expression, and pyruvate kinase isozyme type M2 (PKM2) activity.
MAPK↑, activation of the JNK and p38 MAPK
MMP9↓,
PKM2↓, decrease in PKM2 activity
ROS↑, ROS-mediated activation
JNK↑, activation of the JNK and p38 MAPK
MUC4↓, downregulation of MUC4;
TGF-β↑, TQ led to the activation of the TGF-β pathway and subsequent downregulation of MUC4
Dose↝, Q acts as an antioxidant (free radical scavenger) at low concentrations and as a pro-oxidant at high concentrations.
FAK↓, TQ can inhibit several key molecules such as FAK, Akt, NF-κB, and MMP-9 and that these molecules interact in a cascade to affect the metastasis of pancreatic cancer
NOTCH↓, TQ involved in increasing chemosensitivity consist of blocking the Notch1/PTEN, PI3K/Akt/mTOR, and NF-κB signaling pathways, reducing PKM2 expression, and inhibiting the Warburg effect.
PTEN↑, it also restored the PTEN protein that had been inhibited by GEM
mTOR↓,
Warburg↓, reducing PKM2 expression, and inhibiting the Warburg effect.
XIAP↓,
COX2↓,
Casp9↑,
Ki-67↓,
CD34↓,
VEGF↓,
MCP1↓,
survivin↓,
Cyt‑c↑,
Casp3↑,
H4↑,
HDAC↓,

4861-

Uro,

Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions

in-vivo,

AD,

mice were treated with UA (200 mg/kg/day) by oral gavage for 5 months, ending at 17 months

three mouse models of AD

*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1↓,
*MIP‑1α↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment

Showing Research Papers: 1 to 33 of 33

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 33

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Sepsis↓, 1,
Total Targets: 187

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 8, Catalase↑, 8, GPx↓, 1, GPx↑, 5, GSH↑, 7, GSR↓, 1, GSR↑, 1, GSSG↓, 1, GSTs↑, 2, HO-1↑, 4, lipid-P↓, 4, MDA↓, 4, MPO↓, 1, NOX4↓, 1, NQO1↑, 1, Nrf1↑, 1, NRF2↑, 7, ROS↓, 18, selenoP↑, 1, SIRT3↑, 1, SOD↑, 10, Thiols↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2, AMPK↑, 2, LDH↓, 1, LDL↓, 2, NADPH↓, 2, PGC1A↑, 1, PPARα↑, 1, SIRT1↓, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↑, 1, iNOS↓, 3, JNK↓, 1, MAPK↓, 1, MAPK↑, 1, MAPK↝, 1,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 2, SIRT6↑, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2, mTOR↓, 1,

Migration ⓘ

5LO↓, 1, Ca+2↝, 1, CDK5↓, 1, E-sel↓, 2, MMP2↓, 2, MMP3↓, 1, MMP9↓, 2, MMPs↓, 1, Rho↓, 1, ROCK1↓, 1, TGF-β↑, 1, Treg lymp↓, 1, TXNIP↓, 1, VCAM-1↓, 2, α-SMA↓, 1, α-tubulin↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, NO↓, 4, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 3,

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1, COX2↓, 5, COX2↑, 1, CRP↓, 1, CTSZ↓, 1, CXCc↓, 2, ICAM-1↓, 3, IFN-γ↓, 2, IL1↓, 2, IL10↓, 1, IL10↑, 1, IL12↓, 3, IL17↓, 3, IL1α↓, 1, IL1β↓, 7, IL2↓, 1, IL2↑, 1, IL23↓, 1, IL4↓, 1, IL6↓, 9, IL8↓, 2, Imm↑, 1, Inflam↓, 15, IP-10/CXCL-10↓, 1, IκB↑, 1, MCP1↓, 20, MIP‑1α↓, 2, MIP2↓, 1, NF-kB↓, 12, p‑NF-kB↓, 1, PGE2↓, 3, RANTES↓, 3, TNF-α↓, 15,

Synaptic & Neurotransmission ⓘ

AChE↓, 3, BDNF↑, 2, tau↓, 2, p‑tau↓, 4,

Protein Aggregation ⓘ

Aβ↓, 4, BACE↓, 2, NLRP3↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 2, Dose↝, 4, eff↓, 1, Half-Life↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 2, AST↓, 2, BP↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 9, LDH↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, cardioP↑, 3, cognitive↑, 4, hepatoP↑, 4, memory↑, 4, motorD↑, 3, neuroP↑, 9, OS↑, 1, Pain↓, 2, radioP↑, 1, RenoP↑, 2, Risk↓, 1, Sleep↑, 1, Strength↑, 2, toxicity↓, 4, toxicity∅, 2,
Total Targets: 132

Scientific Paper Hit Count for: MCP1, CCL2,monocyte chemotactic protein-1

4 Thymoquinone
3 Ashwagandha(Withaferin A)
3 Curcumin
2 Artemisinin
2 Baicalein
2 Radiotherapy/Radiation
2 Berberine
1 Alpha-Lipoic-Acid
1 Betulinic acid
1 Boswellia (frankincense)
1 Celastrol
1 Chemotherapy
1 EGCG (Epigallocatechin Gallate)
1 Hydrogen Gas
1 Magnetic Field Rotating
1 Magnetic Fields
1 nicotinamide adenine dinucleotide
1 Vitamin B3,Niacin
1 Propolis -bee glue
1 Piperlongumine
1 Pterostilbene
1 Quercetin
1 Resveratrol
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Selenite (Sodium)
1 Urolithin

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#:990  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

MCP1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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