IL1 Cancer Research Results

IL1, Interleukin-1: Click to Expand ⟱

Source:

Type:

Interleukin-1 (IL-1) has long been known to be a key mediator of immunity and inflammation. Its dysregulation has been implicated in recent years in tumorigenesis and tumor progression, and its upregulation is thought to be associated with many tumors.

Interleukin-1 (IL-1) is a pro-inflammatory cytokine that plays a crucial role in the immune response and inflammation. It exists in two main forms: IL-1α and IL-1β, both of which are produced by various cell types, including macrophages, monocytes, and dendritic cells. IL-1 is involved in a wide range of biological processes, including cell proliferation, differentiation, and apoptosis.

IL-1 is often overexpressed in various cancers, including breast cancer, colorectal cancer, lung cancer, and melanoma. Its expression can be influenced by the tumor microenvironment and the presence of inflammatory cells.
Elevated levels of IL-1 are frequently associated with tumor progression and metastasis.

IL-1 is considered a pro-tumorigenic cytokine in many contexts. It can promote tumor growth by enhancing cell proliferation, survival, and angiogenesis. IL-1β, in particular, has been shown to stimulate the proliferation of cancer cells and promote the formation of new blood vessels (angiogenesis).

Scientific Papers found: Click to Expand⟱

4447-

AgNPs,

Anti-inflammatory action of silver nanoparticles in vivo: systematic review and meta-analysis

Review,

Nor,

*Inflam↓, Qualitative analysis showed a reduction in pro-inflammatory proteins and in the COX-2 pathway.
*COX2↓,
*ROS↓, Its in vitro mechanism of action shows potential to eliminate free radicals
*Dose↝, The method of synthesizing nanoparticles (NPs) influences parameters such as size, shape, topography, stability, concentration, purity and release of Ag + ions, which in turn influences their anti-inflammatory activity
*eff↑, In vitro studies have compared the ingestion of AgNPs at low concentrations (0.012 % per kg) with gold standard drugs (glucocorticoids; 0.1 % per kg) and observed higher efficacy of NPs in promoting therapeutic effect
*toxicity↓, another study has shown that chronic in vivo application of AgNPs at the minimum concentration necessary to promote therapeutic effect does not cause toxic effects
*IL4↑, AgNPs and mitoxantrone increased levels of anti-inflammatory cytokines (IL4, IL5, IL10, IL13, and IFNα) and decreased pro-inflammatory cytokines (IL1, IL6, IL12, IL18, IFNY and TNFα).
*IL5↑,
*IL10↑,
*IL1↓,
*IL6↓,
*TNF-α↓,
*NF-kB↓, AgNPs selectively inhibit COX-2 and the NF-kB pathway.
*MDA↓, AgNPs reduce biomarkers of oxidative stress [55], such as malondialdehyde (MDA) and cell membrane peroxidation [19,31] and increase intracellular GSH
*GSH↑,

391-

AgNPs,

Silver nanoparticles inhibit VEGF-and IL-1β-induced vascular permeability via Src dependent pathway in porcine retinal endothelial cells

in-vitro,

Nor,

40 to 50 nm

*VEGF↓,
*IL1↓, IL-1β-induced permeability
toxicity↝, Since low concentrations of Ag-NP were found to be non-toxic
other↝, Our results indicate that Ag-NP have a therapeutic benefit in vascular permeability.

1159-

And,

Andrographolide, an Anti-Inflammatory Multitarget Drug: All Roads Lead to Cellular Metabolism

Review,

NA,

NRF2↑,
COX2↓,
IL6↓,
IL8↓,
IL1↓, IL-1β
iNOS↓,
MPO↓,
TNF-α↓,
VEGF↓,
Hif1a↓,
p‑AMPK↑,

556-

ART/DHA,

Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing

Review,

NA,

IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
KDR/FLK-1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,

2629-

Ba,

Baicalein, a Component of Scutellaria baicalensis, Attenuates Kidney Injury Induced by Myocardial Ischemia and Reperfusion

in-vivo,

Nor,

Rats, Myocardial ischemia and reperfusion, induced by a 40-minute occlusion and a 3-hour reperfusion of the left anterior descending coronary artery

*RenoP↑, Intravenous pretreatment with baicalein (in doses of 3, 10, or 30 mg/kg), however, significantly reduced the increases in the creatinine level, renal histological damage, and apoptosis induced by myocardial ischemia and reperfusion.
*Apoptosis↓,
*TNF-α↓, In addition, the increases in the serum levels of tumor necrosis factor-α, interleukin-1, and interleukin-6, and of tumor necrosis factor-α in the kidneys were significantly reduced
*IL1↓,
*Bcl-2↑, Western blot analysis revealed that baicalein significantly increased Bcl-2 and reduced Bax in the kidneys
*BAX↓,
*Akt↑, inhibition of apoptosis, possibly through the reduction of tumor necrosis factor-α production, the modulation of Bcl-2 and Bax, and the activation of Akt and extracellular signal-regulated kinases 1 and 2.

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

1092-

BBR,

Berberine as a Potential Anticancer Agent: A Comprehensive Review

Review,

NA,

0.2-0.5uM

U87 and U251 human glioblastoma cell lines in BALB/c nude mice (IC50 of 42 and 32 μmol/L, respectively).

Apoptosis↑,
TumCCA↑,
TumAuto↑,
TumCI↓,
IL1↓, IL-1α, IL-1β
IL6↓,
TNF-α↓,
LDH↓, BBR also increases the release of Lactic Acid Dehydrogenase (LDH) in the MDA epithelial human breast cancer cell line (MDA-cells)
P2X7↓,
proCasp1↓,
Casp1↓,
ASC↓,

718-

Bor,

Boric Acid Exhibits Anticancer Properties in Human Endometrial Cancer Ishikawa Cells

in-vitro,

NA,

40 mM

Ishikawa cells

OSI↑, decreased in healthy cells ****
TNF-α↓,
IL1↓, IL-1β
Casp3↑,
Apoptosis↑,
TOS↑, increased in Ishikawa cells but decreased in healthy cells ****

726-

Bor,

Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still Open

Review,

NA,

NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,

2768-

Bos,

Boswellic acids as promising agents for the management of brain diseases

Review,

Var,

Review,

AD,

Review,

Park,

*neuroP↑, BAs-induced neuroprotection is proposed to be associated with the ability to reduce neurotoxic aggregates, decrease oxidative stress, and improve cognitive dysfunction.
*ROS↓,
*cognitive↓,
TumCP↓, BAs have been suggested as potential agents for the treatment of brain tumors due to their potential to attenuate cell proliferation, migration, metastasis, angiogenesis, and promote apoptosis during both in vitro and in vivo studies
TumCMig↓,
TumMeta↓,
angioG↓,
Apoptosis↑,
*Inflam↓, The anti-inflammatory activities of BAs have been investigated in many preclinical and clinical trials
IL1↓, BAs inhibit the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-4, IL-6, and tumor necrosis factor-α (TNF-α) in several experimental studies.
IL2↓,
IL4↓,
IL6↓,
TNF-α↓,
P53↑, AKBA has been reported to induce apoptosis in pancreatic and gastric cancers, through tumor suppressor protein 53 (p53)-independent pathway, while reducing expression of protein kinase (PK) B and NF-kb
Akt↓,
NF-kB↓,
DNAdam↑, DNA fragmentation, and activation of caspase cascade
Casp↑,
COX2↓, regulated genes such as cyclooxygenase-2 (COX-2), matrix metallopeptidase-9 (MMP-9), C-X-C motif chemokine receptor 4 (CXCR4), and vascular endothelial growth factor (VEGF)
MMP9↓,
CXCR4↓,
VEGF↓,
*SOD↑, BAs against oxidative injury has been shown in several cell lines and animal models [12], [13], [21]. BAs exert protective effects through the normalization of antioxidant enzyme levels, such as superoxide dismutase (SOD), catalase, and glutathione p
*Catalase↑,
*GPx↑,
*NRF2↑, Moreover, it can activate nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant response element-regulated pathways

3635-

Cro,

A Review of Potential Efficacy of Saffron (Crocus sativus L.) in Cognitive Dysfunction and Seizures

Review,

NA,

*memory↑, value of saffron and its’ components, alone, or in combination with the other pharmaceuticals, for improving learning and memory abilities and controlling seizures
*cognitive↑, use of saffron in cognitive disturbance and epilepsy
*BioAv↑, Crocin is converted to crocetin by gastrointestinal cells (Hosseini et al., 2018), and is then absorbed and distributed to body tissues including the central nervous system
*ROS↓, -pretreated rats, cognitive performance was restored through attenuation of oxidative stress
*IL1↓, Crocin suppressed formation of advanced glycation products and brain inflammatory mediators [interleukin (IL)-1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB].
*TNF-α↓,
*NF-kB↓,
*neuroP↑, neuroprotective effects against oxidative stress was suggested to be related to increases in phosphoinositide 3-kinase/Akt and mitogen-activated protein kinases/extracellular signal-regulated kinases
*lipid-P↓, Reduced lipid peroxidation and DNA injury and restored thiol redox and antioxidant status
*Thiols↑,
*antiOx↑,
*AChE↓, restoring oxidative damage biomarkers including glutathion and lipid peroxidation as well as modulating the activities of acetylcholinesterase (AChE) and monoamine oxidase (MAO)
*MAOA↝,
*SIRT1↑, up-regulate the SIRT1/PGC-1α pathway.
*PGC-1α↑,
*Ach↑, increases synaptic acetylcholine levels

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)

3588-

CUR,

The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies

Review,

AD,

*cognitive↝, Clinical studies are mixed regarding curcumin’s effects on cognitive deficits.
*BioAv↑, Ways to improve curcumin’s bioavailability are required.
*Inflam↓, anti-inflammatory activity can be attributed to the suppression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes via down-regulation of nuclear factor kappa B (NF-κB)
*COX2↓,
*iNOS↓,
*NF-kB↓,
*TNF-α↓, nhibition of several inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-a) or interleukin (IL) -1, -2, -6, -8, and -12 (
*IL1↓,
*IL2↓,
*IL6↓,
*IL8↓,
*IL12↓,
*ROS↓, Curcumin’s ability to scavenge free radicals, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), provides its antioxidant capacity
*RNS↓,
*antiOx↑,
*BBB↑, Multiple studies in rodents and humans have shown that curcumin crosses the blood brain barrier (BBB)
*BioAv↓, drawback is the low bioavailability due to poor solubility, low absorption, rapid metabolism, and rapid excretion
*cognitive↑, The researchers detected a significant cognitive improvement at both doses compared to the untreated group, while a significant dose-response effect was found throughout time with higher doses of curcumin producing greater cognitive improvement
*memory↑, supplementation may improve memory and result in a number of biochemical alternations leading to suppressed tau aggregation
*tau↓,
*eff↑, Combined curcumin and piperine showed superiority, in a dose dependent manner,

13-

CUR,

Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action

Review,

BC,

P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

465-

CUR,

Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues

vitro+vivo,

Liver,

HepG2

1.2, 2.4, 4.8 and 9.6 µg/mL, 24 and 48 h; 120 and 240 mg/kg/day, 15 days

vitro+vivo,

Liver,

HUH7

vitro+vivo,

Liver,

MHCC-97H

TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

4650-

CUR,

Curcumin and cancer stem cells: curcumin has asymmetrical effects on cancer and normal stem cells

Review,

Var,

SCD1↓, Curcumin has been shown to have numerous cytotoxic effects on cancer stem cells (CSCs).
IL6↓, This is due to its suppression of the release of cytokines, particularly interleukin (IL)-6, IL-8 and IL-1
IL8↓,
IL1↓,
*selectivity↑, curcumin has little toxicity against normal stem cells (NSCs).
Wnt↝, effects at multiple sites along CSC pathways, such as Wnt, Notch, Hedgehog and FAK.
NOTCH↝,
HH↝,
FAK↝,

3227-

EGCG,

Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury

NA,

Nor,

*Rho↓, EGCG treatment is able to reduce the expression of RhoA in the injured spinal cord
*IL1↓, EGCG treatment reduces the expression of pro-inflammatory cytokines (e.g., IL-1, IL-6, TNF-alpha) and modulates the expression of a transcription factor (NF-κB) and a small GTPase (RhoA) in the spinal cord
*IL6↓,
*TNF-α↓,

854-

Gra,

AgNPs,

Green Synthesis of Silver Nanoparticles Using Annona muricata Extract as an Inducer of Apoptosis in Cancer Cells and Inhibitor for NLRP3 Inflammasome via Enhanced Autophagy

vitro+vivo,

AML,

THP1

17.34 µg/mL

in-vitro,

AML,

AMJ13

vitro+vivo,

lymphoma,

HBL

TumCP↓, THP-1 and AMJ-13
TumAuto↑,
IL1↓, IL-1b
NLRP3↓,
Apoptosis↑,
mtDam↑,
P53↑,
LDH↓, ability of AgNPs in increasing of LDH release.

2916-

LT,

Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies

Review,

Var,

Review,

AD,

Review,

Park,

proCasp9↓, , by inactivating proteins; such as procaspase‐9, CDC2 and cyclin B or upregulation of caspase‐9 and caspase‐3, cytochrome C, cyclin A, CDK2, and APAF‐1, in turn inducing cell cycle
CDC2↓,
CycB/CCNB1↓,
Casp9↑,
Casp3↑,
Cyt‑c↑,
cycA1/CCNA1↑,
CDK2↓, inhibit CDK2 activity
APAF1↑,
TumCCA↑,
P53↑, enhances phosphorylation of p53 and expression level of p53‐targeted downstream gene.
BAX↑, Increasing BAX protein expression; decreasing VEGF and Bcl‐2 expression it can initiate cell cycle arrest and apoptosis.
VEGF↓,
Bcl-2↓,
Apoptosis↑,
p‑Akt↓, reduce expression levels of p‐Akt, p‐EGFR, p‐Erk1/2, and p‐STAT3.
p‑EGFR↓,
p‑ERK↓,
p‑STAT3↓,
cardioP↑, Luteolin plays positive role against cardiovascular disorders by improving cardiac function
Catalase↓, It can reduce activity levels of catalase, superoxide dismutase, and GS4
SOD↓,
*BioAv↓, bioavailability of luteolin is very low. Due to the momentous first pass effect, only 4.10% was found to be available from dosage of 50 mg/kg intake of luteolin
*antiOx↑, luteolin classically exhibits antioxidant features
*ROS↓, The antioxidant potential of luteolin and its glycosides is mainly due to scavenging activity against reactive oxygen species (ROS) and nitrogen species
*NO↓,
*GSTs↑, Luteolin may also have a role in protection and enhancement of endogenous antioxidants such as glutathione‐S‐transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT)
*GSR↑,
*SOD↑,
*Catalase↑,
*lipid-P↓, Luteolin supplementation significantly suppressed the lipid peroxidation
PI3K↓, inhibits PI3K/Akt signaling pathway to induce apoptosis
Akt↓,
CDK2↓, inhibit CDK2 activity
BNIP3↑, upregulation of BNIP3 gene
hTERT/TERT↓, Suppress hTERT in MDA‐MB‐231 breast cancer cel
DR5↑, Boost DR5 expression
Beclin-1↑, Activate beclin 1
TNF-α↓, Block TNF‐α, NF‐κB, IL‐1, IL‐6,
NF-kB↓,
IL1↓,
IL6↓,
EMT↓, Suppress EMT essentially notable in cancer metastasis
FAK↓, Block EGFR‐signaling pathway and FAK activity
E-cadherin↑, increasing E‐cadherin expression by inhibiting mdm2
MDM2↓,
NOTCH↓, Inhibit NOTCH signaling
MAPK↑, Activate MAPK to inhibit tumor growt
Vim↓, downregulation of vimentin, N‐cadherin, Snail, and induction of E‐cadherin expressions
N-cadherin↓,
Snail↓,
MMP2↓, negatively regulated MMP2 and TWIST1
Twist↓,
MMP9↓, Inhibit matrix metalloproteinase‐9 expressions;
ROS↑, Induce apoptosis, reactive oxygen development, promotion of mitochondrial autophagy, loss of mitochondrial membrane potential
MMP↓,
*AChE↓, Reduce AchE activity to slow down inception of Alzheimer's disease‐like symptoms
*MMP↑, Reverse mitochondrial membrane potential dissipation
*Aβ↓, Inhibit Aβ25‐35
*neuroP↑, reduces neuronal apoptosis; inhibits Aβ generation
Trx1↑, luteolin against human bladder cancer cell line T24 was due to induction cell‐cycle arrest at G2/M, downregulation of p‐S6, suppression of cell survival, upregulation of p21 and TRX1, reduction in ROS levels.
ROS↓,
*NRF2↑, Luteolin reduced renal injury by inhibiting XO activity, modulating uric acid transporters, as well as activating Nrf2 HO‐1/NQO1 antioxidant pathways and renal SIRT1/6 cascade.
NRF2↓, Luteolin exerted anticancer effects in HT29 cells as it inhibits nuclear factor‐erythroid‐2‐related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway
*BBB↑, Luteolin can be used to treat brain cancer due to ability of this molecule to easily cross the blood–brain barrier
ChemoSen↑, In ovarian cancer cells, luteolin chemosensitizes the cells through repressing the epithelial‐mesenchymal transition markers
GutMicro↑, Luteolin was also observed to modulate gut microbiota which reduce the number of tumors in case of colorectal cancer by enhancing the number of health‐related microbiota and reduced the microbiota related to inflammation

3264-

Lyco,

Pharmacological potentials of lycopene against aging and aging‐related disorders: A review

Review,

Var,

Review,

AD,

Review,

Stroke,

*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.

4780-

Lyco,

Potential inhibitory effect of lycopene on prostate cancer

Review,

Pca,

TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level

4782-

Lyco,

New Insights into Molecular Mechanism behind Anti-Cancer Activities of Lycopene

Review,

Var,

AntiCan↑, From an anti-cancer perspective, lycopene is often associated with reduced risk of prostate cancer and people often look for it as a dietary supplement which may help to prevent cancer.
TumCP↓, Lycopene was known to be able to suppress cancerous cell proliferation, migration, invasion and adhesion activity in cell culture studies.
TumCMig↓,
TumCI↓,
TumCA↓,
ROS↓, Such suppression was often observed with changes of cancer-related gene expression and relief of oxidative stress
MMP2↓, In general, lycopene could suppress the expression of MMP-2, MMP-7, MMP-9, Sp1, IGF-1R, VEGF while increasing E-cadherin stabilization, connexin 43, nm23-H1, TIMP-1 and TIMP-2 levels
MMP7↓,
MMP9↓,
VEGF↓,
E-cadherin↑,
TIMP1↑,
TIMP2↑,
BioAv↝, it is recommended to avoid consumption of lycopene concurrently with high dietary fiber intake as several types of dietary fiber were found to be able to reduce the bioavailability of lycopene
*IL12↓, lycopene could suppress proinflammatory cytokines such as IL-12, TNF-α, IL-1, IL-1β, IL-6
*TNF-α↓,
*IL1↓,
*IL1β↓,
*IL6↓,
COX2↓, Sprague Dawley rat model, lycopene treatment after induction by azoxymethane caused suppression of aberrant crypt foci, preneoplastic lesion and biomarkers such as COX-2 and iNOS expression
iNOS↓,
*radioP↑, lycopene before induction of DNA damage via X-irradiation as lycopene treatment after irradiation failed to show such DNA protective effect
NF-kB↓, anti-cancer effect of lycopene was also observed in pancreatic cancer cells (PANC-1 cell line) whereby significant reduction of ROS, NF-κB and anti-apoptotic biomarkers (cIAP1, cIAP2 and survivin) was detected while an increment of caspase-3 and Bax:
survivin↓,
Casp3↑,
Bax:Bcl2↑,

4784-

Lyco,

Protective effects of lycopene in cancer, cardiovascular, and neurodegenerative diseases: An update on epidemiological and mechanistic perspectives

Review,

Diabetic,

Review,

CardioV,

*antiOx↑, Owing to its potent antioxidant properties, lycopene can potentially alleviate enhanced levels of proinflammatory mediators (e.g., proinflammatory cytokines IL-8, -6, and -1, and oxidized phospholipids) and prevent NF-κB activation
*IL8↓,
*IL6↓,
*IL1↓,
*NF-kB↓,
Inflam↓, graphical abstract
cycD1/CCND1↓,
MMP2↓,
MMP9↓,
Bcl-2↓,
NF-kB↓,
*Nrf1↑, normal cells
*antiOx↑,
*BDNF↑,
*neuroP↑,
*cardioP↑,
ROS↑, i) enhanced oxidative stress due to prooxidant activities of lycopene under circumstances of tumor cell
Dose↝, There are no known adverse effects from low (12 mg/day) to very high (150 mg/day) intake of dietary or formulated lycopene in a healthy population

2246-

MF,

The Use of Pulsed Electromagnetic Field to Modulate Inflammation and Improve Tissue Regeneration: A Review

in-vitro,

Nor,

5.1hz, 0.04mT, 5 min

PEMF treatment for 15 min at 15 Hz and 2 mT sine wave

*Inflam↓, Our studies included herein confirm anti-inflammatory effects of PEMF on MSCs and MΦ
*IL1↓, PEMF significantly decreased the production of proinflammatory signaling in IL-1b, IL-6, and IL-17A cytokines (Figs. 1 and 2) in the MSCs.
*IL6↓,
IL17↓,
*TNF-α↓, After exposure to PEMF, outcomes show decreases in the proinflammatory cytokines secretion (IL-1b, IL-6, and TNF-α) and increase/stabilization of IL-10 in THP-1s (

204-

MFrot,

MF,

Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization

in-vivo,

AD,

 0.2T, 4Hz

 reduced aluminum deposition in the brains of AD mice

*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

3847-

MSM,

Methylsulfonylmethane: Applications and Safety of a Novel Dietary Supplement

Review,

Arthritis,

*Inflam↓, common use as an anti-inflammatory agent
*Pain↓, A variety of health-specific outcome measures are improved with MSM supplementation, including inflammation, joint/muscle pain, oxidative stress, and antioxidant capacity.
*ROS↓,
*antiOx↑,
*Dose↝, MSM is well-tolerated by most individuals at dosages of up to four grams daily, with few known and mild side effects
*Half-Life↝, Pharmacokinetic studies indicate that MSM is rapidly absorbed in rats [63,64] and humans [65], taking 2.1 h and <1 h, respectively.
*NF-kB↓, The inhibitory effect of MSM on NF-κB results in the downregulation of mRNA for interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) in vitro
*IL1↓,
*IL6↓,
*TNF-α↓,
*iNOS↓, MSM can also diminish the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) through suppression of NF-κB;
*COX2↓,
*NLRP3↓, MSM negatively affects the expression of the NLRP3 inflammasome by downregulating the NF-κB production of the NLRP3 inflammasome transcript and/or by blocking the activation signal in the form of mitochondrial generated reactive oxygen species (ROS)
*NRF2↑, MSM influences the activation of at least four types of transcription factors: NF-κB, signal transducers and activators of transcription (STAT), p53, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).
*STAT↓, MSM has been shown to repress the expression or activities of STAT transcription factors in a number of cancer cell lines in vitro
*Cartilage↑, , in vitro studies suggest that MSM protects cartilage through its suppressive effects on IL-1β and TNF-α
*eff↑, Supplementation with glucosamine, chondroitin sulfate, MSM, guava leaf extract, and Vitamin D improved physical function in patients with knee osteoarthritis based on the Japanese Knee OA Measure
*eff↑, MSM in combination with boswellic acid was also shown to improve knee joint function as assessed through the Lequesne Index
*GSH↑, MSM is able to restore the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio to normal levels, decrease NO production, and reduce neuronal ROS production following HIV-1 Tat exposure
*uricA↓, Humans studies show promise for MSM as an antioxidant with similar results noted, including reductions in MDA [19,167,168], protein carbonyls (PC) [167,168], and uric acid [168] and increases in GSH [167] and TEAC [159,161,168].
tumCV↓, MSM independently has been shown to be cytotoxic to cancer cells by inhibiting cell viability through the induction of cell cycle arrest [119,122,123], necrosis [119], or apoptosis
TumCCA↑,
necrosis↑,
Apoptosis↑,
VEGF↓, reduced expression of oncogenic proteins such as vascular endothelial growth factor (VEGF) [99,100,101,123], heat shock protein (HSP)90α [100], and insulin-like growth factor-1 receptor (IGF-1R)
HSP90↓,
IGF-1?,

3055-

RES,

Resveratrol and Tumor Microenvironment: Mechanistic Basis and Therapeutic Targets

Review,

Var,

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.

5044-

SAS,

xCT inhibitor sulfasalazine depletes paclitaxel-resistant tumor cells through ferroptosis in uterine serous carcinoma

in-vitro,

Var,

xCT↓, Thus, the present study investigated the effect of the xCT inhibitor, sulfasalazine (SAS) on cytotoxicity in paclitaxel-sensitive and -resistant USC cell lines.
Ferroptosis↑, SAS-mediated cell death was induced through ferroptosis
ROS↑, ROS production was increased in paclitaxel-resistant but not in -sensitive cells, even at low SAS concentration
IL1↓, inhibit leukocyte motility and interleukin (IL)-1 and IL-2 production (18), and inhibit nuclear factor κ B (NFκB)
IL2↓,
NF-kB↓,
GSH↓, SAS has also been reported to effectively induce GSH depletion (90%) and arrest growth
TumCG↓,
ChemoSen↑, and to enhance sensitivity to chemotherapeutic agents in pancreatic, prostate and mammary cancer

3648-

SIL,

Silymarin/Silybin and Chronic Liver Disease: A Marriage of Many Years

Review,

NA,

*antiOx↑, antioxidant, anti-inflammatory and antifibrotic power
*Inflam↓,
*lipid-P↓, reduce both lipid peroxidation and cellular necrosis.
*necrosis↓,
*hepatoP↑, silybin use in chronic liver diseases, cirrhosis and hepatocellular carcinoma.
*IL1↓, figure 1
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
MAPK↓,
Apoptosis↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
*PPARγ↑,
*GLUT4↑,
*HSPs↓,
*HSP27↑,
*Trx↑,
*SIRT1↑,
*ALAT↓, as well as prevent ALT increase, Glutathione (GSH) decrease, lipid peroxidation and TNF-α increase
*GSH↑,
*lipid-P↓,
*TNF-α↓,
TumCG↓, silybin significantly reduces HuH7, HepG2, Hep3B, and PLC/PRF/5 human hepatoma cells growth by increasing cyclin-dependent kinase inhibitor p21 and p27/cyclin-dependent kinase (CDK) 4 complexes, by reducing retinoblastoma protein (Rb)-phosphorylatio
P21↑,
CDK4↑,

3290-

SIL,

A review of therapeutic potentials of milk thistle (Silybum marianum L.) and its main constituent, silymarin, on cancer, and their related patents

Analysis,

Var,

hepatoP↑, well as hepatoprotective agents.
chemoP↑, silymarin could be beneficial to oncology patients, especially for the treatment of the side effects of anticancer chemotherapeutics.
*lipid-P↓, Silymarin has been shown to significantly reduce lipid peroxidation and exhibit anti-oxidant, antihypertensive, antidiabetic, and hepatoprotective effects
*antiOx↑,
tumCV↓, reduces the viability, adhesion, and migration of tumor cells by induction of apoptosis and formation of reactive oxygen species (ROS), reducing glutathione levels, B-cell lymphoma 2 (Bcl-2), survivin, cyclin D1, Notch 1 intracellular domain (NICD),
TumCMig↓,
Apoptosis↑,
ROS↑,
GSH↓,
Bcl-2↓,
survivin↓,
cycD1/CCND1↓,
NOTCH1↓,
BAX↑, as well as enhancing the amount of Bcl-2-associated X protein (Bax) level (
NF-kB↓, The suppression of NK-κB-regulated gene products (e.g., cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF), and interleukin-1 (IL-1)) mediates the anti-inflammatory effect of silymarin
COX2↓,
LOX1↓,
iNOS↓,
TNF-α↓,
IL1↓,
Inflam↓,
*toxicity↓, Silymarin is also safe for humans, hence at therapeutic doses patients demonstrated no negative effects at the high dose of 700 mg, three times a day, for 24 weeks
CXCR4↓, fig 2
EGFR↓,
ERK↓,
MMP↓, reduction in mitochondrial transmembrane potential due to an increase in cytosolic cytochrome complex (Cyt c) levels.
Cyt‑c↑,
TumCCA↑, Moreover, silymarin increased the percentage of cells in the gap 0/gap 1 (G0/G1) phase and decreased the percentage of cells in the synthesis (S)-phase,
RB1↑, concomitant up-regulation of retinoblastoma protein (Rb), p53, cyclin-dependent kinase inhibitor 1 (p21Cip1), and cyclin-dependent kinase inhibitor 1B (p27Kip1)
P53↑,
P21↑,
p27↑,
cycE/CCNE↓, and down-regulation of cyclin D1, cyclin E, cyclin-dependent kinase 4 (CDK4), and phospho-Rb
CDK4↓,
p‑pRB↓,
Hif1a↓, silibinin inhibited proliferation of Hep3B cells due to simultaneous induction of apoptosis and prevented the accumulation
cMyc↓, Silibinin also reduces cellular myelocytomatosis oncogene (c-MYC) expression, a key regulator of cancer metabolism in pancreatic cancer cells
IL1β↓, Silymarin can also inhibit the production of inflammatory cytokines, such as interleukin-1beta (IL-1β), interferon-gamma (IFNγ),
IFN-γ↓,
PCNA↓, ilymarin suppresses the high proliferative activity of cells started with a carcinogen so that it significantly inhibits proliferating cell nuclear antigen (PCNA) and cyclin D1 labeling indices
PSA↓, In another patent, S. marianum has been used as an estrogen receptor β-agonist and an inhibitor of PSA for treating prostate cancer
CYP1A1↓, Silymarin prevents the expression of CYP1A1 and COX-2

3282-

SIL,

Role of Silymarin in Cancer Treatment: Facts, Hypotheses, and Questions

Review,

NA,

hepatoP↑, This group of flavonoids has been extensively studied and they have been used as hepato-protective substances
AntiCan↑, however, silymarin compounds have clear anticancer effects
TumCMig↓, decreasing migration through multiple targeting, decreasing hypoxia inducible factor-1α expression, i
Hif1a↓, In prostate cancer cells silibinin inhibited HIF-1α translation
selectivity↑, antitumoral activity of silymarin compounds is limited to malignant cells while the nonmalignant cells seem not to be affected
toxicity∅, long history of silymarin use in human diseases without toxicity after prolonged administration.
*antiOx↑, as an antioxidant, by scavenging prooxidant free radicals
*Inflam↓, antiinflammatory effects similar to those of indomethacin,
TumCCA↑, MDA-MB 486 breast cancer cells, G1 arrest was found due to increased p21 and decreased CDKs activity
P21↑,
CDK4↓,
NF-kB↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
ERK↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
PSA↓, Treating prostate carcinoma cells with silymarin the levels of PSA were significantly decreased and cell growth was inhibited through decreased CDK activity and induction of Cip1/p21 and Kip1/p27. 1
TumCG↓,
p27↑,
COX2↓, such as anti-COX2 and anti-IL-1α activity, 140 antiangiogenic effects through inhibition of VEGF secretion, upregulation of Insulin like Growth Factor Binding Protein 3 (IGFBP3), 141 and inhibition of androgen receptors.
IL1↓,
VEGF↓,
IGFBP3↑,
AR↓,
STAT3↓, downregulation of the STAT3 pathway which was seen in many cell models.
Telomerase↓, silymarin has the ability to decrease telomerase activity in prostate cancer cells
Cyt‑c↑, mitochondrial cytochrome C release-caspase activation.
Casp↑,
eff↝, Malignant p53 negative cells show only minimal apoptosis when treated with silymarin. Therefore, one conclusion is that silymarin may be useful in tumors with conserved p53.
HDAC↓, inhibit histone deacetylase activity;
HATs↑, increase histone acetyltransferase activity
Zeb1↓, reduce expression of the transcription factor ZEB1
E-cadherin↑, increase expression of E-cadherin;
miR-203↑, increase expression of miR-203
NHE1↓, reduce activation of sodium hydrogen isoform 1 exchanger (NHE1)
MMP2↓, target β catenin and reduce the levels of MMP2 and MMP9
MMP9↓,
PGE2↓, reduce activation of prostaglandin E2
Vim↓, suppress vimentin expression
Wnt↓, inhibit Wnt signaling
angioG↓, Silymarin inhibits angiogenesis.
VEGF↓, VEGF downregulation
*TIMP1↓, Silymarin has the capacity to decrease TIMP1 expression166–168 in mice.
EMT↓, found that silibinin had no effect on EMT. However, the opposite was found in other malignant tissues160–162 where it showed inhibitory effects.
TGF-β↓, Silibinin reduces the expression of TGF β2 in different tumors such as triple negative breast, 174 prostate, and colorectal cancers.
CD44↓, Silibinin decreased CD44 expression and the activation of EGFR (epidermal growth factor receptor)
EGFR↓,
PDGF↓, silibinin had the ability to downregulate PDFG in fibroblasts, thus decreasing proliferation.
*IL8↓, Flavonoids, in general, reduce levels of IL-8. Curcumin, 200 apigenin, 201 and silybin showed the ability to decrease IL-8 levels
SREBP1↓, Silymarin inhibited STAT3 phosphorylation and decreased the expression of intranuclear sterol regulatory element binding protein 1 (SREBP1), decreasing lipid synthesis.
MMP↓, reduced membrane potential and ATP content
ATP↓,
uPA↓, silibinin decreased MMP2, MMP9, and urokinase plasminogen activator receptor level (uPAR) in neuroblastoma cells. uPAR is also a marker of cell invasion.
PD-L1↓, Silibinin inhibits PD-L1 by impeding STAT5 binding in NSCLC.
NOTCH↓, Silybin inhibited Notch signaling in hepatocellular carcinoma cells showing antitumoral effects
*SIRT1↑, Silymarin can also increase SIRT1 expression in other tissues, such as hippocampus, 221 articular chondrocytes, 222 and heart muscle
SIRT1↓, Silymarin seems to act differently in tumors: in lung cancer cells SIRT downregulated SIRT1 and exerted multiple antitumor effects such as reduced adhesion and migration and increased apoptosis.
CA↓, Silymarin has the ability to inhibit CA isoforms CA I and CA II.
Ca+2↑, ilymarin increases mitochondrial release of Ca++ and lowers mitochondrial membrane potential in cancer cell
chemoP↑, Silymarin: Decreasing Side Effects and Toxicity of Chemotherapeutic Drugs
cardioP↑, There is also evidence that it protects the heart from doxorubicin toxicity, however, it is less potent than quercetin in this effect.
Dose↝, oral administration of 240 mg of silybin to 6 healthy volunteers the following results were obtained 377 : maximum\,plasmaconcentration0.34±0.16⁢𝜇⁢g/m⁢L
Half-Life↝, and time to maximum plasma concentration 1.32 ± 0.45 h. Absorption half life 0.17 ± 0.09 h, elimination half life 6.32 ± 3.94 h
BioAv↓, silymarin is not soluble in water and oral administration shows poor absorption in the alimentary tract (approximately 1% in rats,
BioAv↓, Our conclusion is that, from a bioavailability standpoint, it is much easier to achieve migration inhibition, than proliferative reduction.
BioAv↓, Combination with succinate: is available on the market under the trade mark Legalon® (bis hemisuccinate silybin). Combination with phosphatidylcholine:
toxicity↝, 13 g daily per os divided into 3 doses was well tolerated. The most frequent adverse event was asymptomatic liver toxicity.
Half-Life↓, It may be necessary to administer 800 mg 4 times a day because the half-life is short.
ROS↓, its ability as an antioxidant reduces ROS production
FAK↓, Silibinin decreased human osteosarcoma cell invasion through Erk inhibition of a FAK/ERK/uPA/MMP2 pathway

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

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

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:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 12, Catalase↑, 4, GPx↓, 1, GPx↑, 3, GSH↑, 4, GSR↑, 1, GSTs↑, 2, HO-1↑, 1, lipid-P↓, 6, MDA↓, 3, NOX4↓, 1, Nrf1↑, 1, NRF2↑, 5, RNS↓, 1, ROS↓, 11, selenoP↑, 1, SOD↑, 4, TAC↑, 1, Thiols↑, 1, Trx↑, 1, uricA↓, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, CRM↑, 1, PPARγ↑, 1, SIRT1↑, 3,

Cell Death ⓘ

Akt↑, 1, Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, iNOS↓, 4, JNK↓, 1, p‑JNK↓, 1, MAPK↓, 1, necrosis↓, 1, p‑p38↓, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1,

Protein Folding & ER Stress ⓘ

HSP27↑, 1, HSPs↓, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 2, IGF-1↓, 1, IGFBP3↑, 1, STAT↓, 1, STAT3↓, 1,

Migration ⓘ

5LO↓, 1, ARG↑, 1, Ca+2↝, 1, Cartilage↑, 1, MMP2↓, 1, MMP3↓, 1, MMP9↓, 1, Rho↓, 1, TGF-β1↑, 1, TIMP1↓, 1, VCAM-1↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 4, VEGF↓, 1,

Barriers & Transport ⓘ

BBB↑, 2, GLUT4↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 4, CRP↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, p‑IKKα↓, 1, IL1↓, 16, IL10↑, 2, IL12↓, 3, IL1β↓, 2, IL2↓, 1, IL2↑, 1, IL4↑, 2, IL5↑, 1, IL6↓, 13, IL8↓, 6, Imm↑, 1, Inflam↓, 11, p‑IκB↓, 1, MCP1↓, 2, MyD88↓, 1, NF-kB↓, 9, p‑p65↓, 1, PGE2↓, 1, TLR2↓, 1, TLR4↓, 2, TNF-α↓, 15,

Synaptic & Neurotransmission ⓘ

AChE↓, 2, BDNF↑, 2, MAOA↝, 1, tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 2, NLRP3↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 3, Dose↝, 4, eff↑, 4, Half-Life↝, 1, selectivity↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, BP↓, 1, creat↓, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 13,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 1, cognitive↓, 1, cognitive↑, 3, cognitive↝, 1, hepatoP↑, 1, memory↑, 4, neuroP↑, 8, Pain↓, 1, radioP↑, 1, RenoP↑, 2, Risk↓, 1, toxicity↓, 2,
Total Targets: 117

Scientific Paper Hit Count for: IL1, Interleukin-1

5 Curcumin
4 Lycopene
3 Silver-NanoParticles
3 Silymarin (Milk Thistle) silibinin
2 Berberine
2 Boron
2 Magnetic Fields
1 Andrographis
1 Artemisinin
1 Baicalein
1 Boswellia (frankincense)
1 Crocetin
1 EGCG (Epigallocatechin Gallate)
1 Graviola
1 Luteolin
1 Magnetic Field Rotating
1 Methylsulfonylmethane
1 Resveratrol
1 Sulfasalazine
1 Selenite (Sodium)
1 Thymoquinone

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

IL1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

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 ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

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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