condition found tbRes List
PBG, Propolis -bee glue: Click to Expand ⟱
Features: Compound
Brazilian Green Propolis often considered best
• Derived from Baccharis dracunulifolia, this type is rich in artepillin C.
• It has been widely researched for its anticancer, anti-inflammatory, and antioxidant properties.
-Propolis common researched flavonoids :chrysin, pinocembrin, galangin, pinobanksin(Pinocembrin)
-most representative phenolic acids were caffeic acid, p-coumaric acid, and ferulic acid, as well as their derivatives, DMCA and caffeic acid prenyl, benzyl, phenylethyl (CAPE), and cinnamyl esters
-One of the most studied active compounds of a poplar-type propolis is caffeic acid phenethyl ester (CAPE)
-caffeic acid phenethyl ester (CAPE), galangin, chrysin, nemorosone, propolin G, artepillin C, cardanol, pinocembrin, pinobanksin, chicoric acid, and phenolic acids (caffeic acid, ferulic acid, and coumaric acid), as well as luteolin, apigenin, myricetin, naringenin, kaempferol, quercetin, polysaccharides, tannins, terpenes, sterols, and aldehydes -content highly variable based on location and extraction
Two main factors of interest:
1. affects interstitual fluild pH
2. high concentration raises ROS (Reactive Oxygen Species), while low concentration may reduce ROS

- Artepillin-C (major phenolic compounds found in Brazilian green propolis (BGP))
- caffeic acid major source

Do not combine with 2DG

Pathways:
-Propolis compounds (e.g., artepillin C, caffeic acid phenethyl ester [CAPE]) can trigger apoptosis (programmed cell death) in cancer cells.
-Propolis has been shown to inhibit NF‑κB activation.
-Propolis extracts can cause cell cycle arrest at specific checkpoints (e.g., G0/G1 or G2/M phases).
-Enhance the body’s antitumor immune responses, for example by activating natural killer (NK) cells and modulating cytokine profiles.

-Note half-life no standard, high variablity of content.
BioAv poor water solubility, and low oral bioavailability.
Pathways:
- high concentration may induce ROS production, while low concentrations mya low it. This may apply to both normal and cancer cells. Normal Cells Example. (Also not sure if high level are acheivable in vivo due to bioavailability)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ -->
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓">NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓,
- Others: PI3K↓, AKT↓, STAT↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
1651- CA,  PBG,    Caffeic acid and its derivatives as potential modulators of oncogenic molecular pathways: New hope in the fight against cancer
- Review, Var, NA
Apoptosis↑,
TumCCA↓, CAPE (1-80 uM) can stimulate apoptosis and cell cycle arrest (G1 phase
TumCMig↓,
TumMeta↓,
ChemoSen↑,
eff↑, Nanoparticles promote therapeutic effect of CA and CAPE in reducing cancer cell malignancy.
eff↑, improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid
eff↓, Currently, solvent extraction is utilized by methanol and ethyl acetate combination at high temperatures. However, a low amount of CA is yielded via this pathway
eff↝, Decyl CA (DCA) is a novel derivative of CA but its role in affecting colorectal cancer has not been completely understood.
Dose∅, The CAPE administration (0-60 uM) induces both autophagy and apoptosis in C6 glioma cells.
AMPK↑, CAPE induces autophagy via AMPK upregulation.
p62↓, CAPE can induce autophagy via p62 down-regulation and LC3-II upregulation
LC3II↑,
Ca+2↑, CA (0-1000 uM) enhances Ca2+ accumulation in cells in a concentration-dependent manner
Bax:Bcl2↑, CA can promote Bax/Bcl-2 ratio i
CDK4↑, The administration of CAPE (1–80 μM) can stimulate apoptosis and cell cycle arrest (G1 phase) via upregulation of Bax, CDK4, CDK6 and Rb
CDK6↑,
RB1↑,
EMT↓, CAPE has demonstrated high potential in inhibiting EMT in nasopharyngeal caner via enhancing E-cadherin levels, and reducing vimentin and β-catenin levels.
E-cadherin↑,
Vim↓,
β-catenin/ZEB1↓,
NF-kB↓,
angioG↑, CAPE (0.01-1ug/ml) inhibited angiogenesis via VEGF down-regulation
VEGF↓,
TSP-1↑, and furthermore, CAPE is capable of increasing TSP-1 levels
MMP9↓, CAPE was found to reduce MMP-9 expression
MMP2↓, CAPE can also down-regulate MMP-2
ChemoSen↑, role of CA and its derivatives in enhancing therapy sensitivity of cancer cells.
eff↑, CA administration (100 uM) alone or its combination with metformin (10 mM) can induce AMPK signaling
ROS↑, CA can promote ROS levels to induce cell death in human squamous cell carcinoma
CSCs↓, CA can reduce self-renewal capacity of CSCs and their migratory ability in vitro and in vivo.
Fas↑, CAPE (0-100 uM) is capable of inducing Fas signaling to promote p53 expression, leading to apoptotic cell death via Bax and caspase activation
P53↑,
BAX↑,
Casp↑,
β-catenin/ZEB1↓, anti-tumor activity of CAPE is mediated via reducing β-catenin levels
NDRG1↑, CAPE (30 uM) can promote NDRG1 expression via MAPK activation and down-regulation of STAT3
STAT3↓,
MAPK↑, CAPE stimulates mitogen-activated protein kinase (MAPK) and ERK
ERK↑,
eff↑, Res, thymoquinone and CAPE mediate lung tumor cell death via Bax upregulation and Bcl-2 down-regulation.
eff↑, co-administration of CA (100 μM) and metformin (10 mM) is of interest in cervical squamous cell carcinoma therapy.
eff↑, in addition to CA, propolis contains other agents such as chrysin, p-coumaric acid and ferulic acid that are beneficial in tumor suppression.

2781- CHr,  PBG,    Chrysin a promising anticancer agent: recent perspectives
- Review, Var, NA
PI3K↓, It can block Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling in different animals against various cancers
Akt↓,
mTOR↓,
MMP9↑, Chrysin strongly suppresses Matrix metalloproteinase-9 (MMP-9), Urokinase plasminogen activator (uPA) and Vascular endothelial growth factor (VEGF), i.e. factors that can cause cancer
uPA↓,
VEGF↓,
AR↓, Chrysin has the ability to suppress the androgen receptor (AR), a protein necessary for prostate cancer development and metastasis
Casp↑, starts the caspase cascade and blocks protein synthesis to kill lung cancer cells
TumMeta↓, Chrysin significantly decreased lung cancer metastasis i
TumCCA↑, Chrysin induces apoptosis and stops colon cancer cells in the G2/M cell cycle phase
angioG↓, Chrysin prevents tumor growth and cancer spread by blocking blood vessel expansion
BioAv↓, Chrysin’s solubility, accessibility and bioavailability may limit its medical use.
*hepatoP↑, As chrysin reduced oxidative stress and lipid peroxidation in rat liver cells exposed to a toxic chemical agent.
*neuroP↑, Protecting the brain against oxidative stress (GPx) may be aided by increasing levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*ROS↓, A decrease in oxidative stress and an increase in antioxidant capacity may result from chrysin’s anti-inflammatory properties
*Inflam↓,
*Catalase↑, Supplementation with chrysin increased the activity of antioxidant enzymes like SOD and catalase and reduced the levels of oxidative stress markers like malondialdehyde (MDA) in the colon tissue of the rats.
*MDA↓, Antioxidant enzyme activity (SOD, CAT) and oxidative stress marker (MDA) levels were both enhanced by chrysin supplementation in mouse liver tissue
ROS↓, reduction of reactive oxygen species (ROS) and oxidative stress markers in the cancer cells further indicated the antioxidant activity of chrysin
BBB↑, After crossing the blood-brain barrier, it has been shown to accumulate there
Half-Life↓, The half-life of chrysin in rats is predicted to be close to 2 hours.
BioAv↑, Taking chrysin with food may increase the effectiveness of the supplement: increased by a factor of 1.8 when taken with a high-fat meal
ROS↑, In contrast to 5-FU/oxaliplatin, chrysin increases the production of reactive oxygen species (ROS), which in turn causes autophagy by stopping Akt and mTOR from doing their jobs
eff↑, mixture of chrysin and cisplatin caused the SCC-25 and CAL-27 cell lines to make more oxygen free radicals. After treatment with chrysin, cisplatin, or both, the amount of reactive oxygen species (ROS) was found to have gone up.
ROS↑, When reactive oxygen species (ROS) and calcium levels in the cytoplasm rise because of chrysin, OC cells die.
ROS↑, chrysin is the cause of death in both types of prostate cancer cells. It does this by depolarizing mitochondrial membrane potential (MMP), making reactive oxygen species (ROS), and starting lipid peroxidation.
lipid-P↑,
ER Stress↑, when chrysin is present in DU145 and PC-3 cells, the expression of a group of proteins that control ER stress goes up
NOTCH1↑, Chrysin increased the production of Notch 1 and hairy/enhancer of split 1 at the protein and mRNA levels, which stopped cells from dividing
NRF2↓, Not only did chrysin stop Nrf2 and the genes it controls from working, but it also caused MCF-7 breast cancer cells to die via apoptosis.
p‑FAK↓, After 48 hours of treatment with chrysin at amounts between 5 and 15 millimoles, p-FAK and RhoA were greatly lowered
Rho↓,
PCNA↓, Lung histology and immunoblotting studies of PCNA, COX-2, and NF-B showed that adding chrysin stopped the production of these proteins and maintained the balance of cells
COX2↓,
NF-kB↓,
PDK1↓, After the chrysin was injected, the genes PDK1, PDK3, and GLUT1 that are involved in glycolysis had less expression
PDK3↑,
GLUT1↓,
Glycolysis↓, chrysin stops glycolysis
mt-ATP↓, chrysin inhibits complex II and ATPases in the mitochondria of cancer cells
Ki-67↓, the amounts of Ki-67, which is a sign of growth, and c-Myc in the tumor tissues went down
cMyc↓,
ROCK1↓, (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) were much lower.
TOP1↓, DNA topoisomerases and histone deacetylase were inhibited, along with the synthesis of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and (IL-1 beta), while the activity of protective signaling pathways was increased
TNF-α↓,
IL1β↓,
CycB↓, Chrysin suppressed cyclin B1 and CDK2 production in order to stop cancerous growth.
CDK2↓,
EMT↓, chrysin treatment can also stop EMT
STAT3↓, chrysin block the STAT3 and NF-B pathways, but it also greatly reduced PD-L1 production both in vivo and in vitro.
PD-L1↓,
IL2↑, chrysin increases both the rate of T cell growth and the amount of IL-2

1644- HCAs,  PBG,    Artepillin C (3,5-diprenyl-4-hydroxycinnamic acid) sensitizes LNCaP prostate cancer cells to TRAIL-induced apoptosis
- in-vitro, Pca, LNCaP
NF-kB↓,
TRAILR↑, Artepillin C increased the expression of TRAIL-R2 and decreased the activity of NF-κB
Casp8↑, Co-treatment with TRAIL and artepillin C induced the significant activation of caspase-8 and caspase-3, as well as the disruption of ΔΨm
Casp3↑,
MMP↓,
Dose?, co-treatment of LNCaP cells with 100 ng/ml TRAIL and 50–100 μM artepillin C for 24 h the cytotoxicity ranged from 59.3±1.6 to 66.3±2.3%.

1681- PBG,    Propolis: Its Role and Efficacy in Human Health and Diseases
- Review, Nor, NA
*Inflam↓,
*AntiCan↑,
*antiOx↑,
*hyperG↓, flavanone glycoside found in propolis, has been reported to have insulin-like and lipid-reducing properties that reduce both insulin resistance and hyperglycemia
*BG↓, These flavonoids, including apigenin, naringin, chrysin, galangin, kaempferol, luteolin, genistein, and quercetin help to reduce blood glucose concentration
*HbA1c↓, propolis showed significant effects, reducing the blood glucose levels, serum insulin, and serum glycosylated haemoglobin (HbA1c) levels of T2DM patients
*NF-kB↓, propolis can also suppress inflammatory cascades by blocking the NF-κB pathway and reducing ROS by enhancing antioxidants
*ROS↓,
*TGF-β↑, formation of the transforming growth factor-β1 (TGF-β1) of the cells are promoted by the caffeic acid, CAPE, hesperidin, and quercetin of propolis
*selectivity↑, CAPE is a very significant compound of propolis that has anti-inflammatory properties and also acts as the selective inhibitor of NF-κB activation

3259- PBG,    Propolis and its therapeutic effects on renal diseases: A review
- Review, Nor, NA
*Inflam↓, Several mechanisms are involved in the anti-inflammatory effects of propolis including the inhibition of cyclooxygenase (COX) and prostaglandin biosynthesis, free radical scavenging, inhibition of nitric oxide synthesis, the reduction of inflammatory
*COX2↓,
*ROS↓,
*NO↓,
*NF-kB↓, anticancer activity of propolis is ascribed to its ability to inhibit the localization of NF-κB and regulate gene expression
TumCP↓, artepillin C had inhibitory effects on the proliferation of cancer cells and induced instant apoptosis in mice tumor cells.
angioG↓, caffeic acid inhibits the angiogenesis of human kidney tumors implanted in nude mice.
VEGF↓, The decrease in VEGF and diminishment of tumor development are attributed to the inhibition of STAT phosphorylation and reduction of HIF-1-mediated expression of VEGF
STAT↓,
Hif1a↓,
RenoP↑, restored renal tubular function via down-regulation of the Toll-like receptor 4/nuclear factor-kappa B axis, decreasing inflammatory cytokine levels, and macrophage infiltration in renal tissues
TLR4↓,
*MDA↓, rat model of diabetes, propolis decreased malondialdehyde (MDA) and elevated the activity of anti-oxidants such as glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)
*GSH↑,
*SOD↑,
*Catalase↑,
*toxicity∅, Propolis is safe for patients with renal disease and no adverse effects are reported

1682- PBG,    Honey, Propolis, and Royal Jelly: A Comprehensive Review of Their Biological Actions and Health Benefits
- Review, Var, NA
i-LDH↓, cytotoxic activities of Tualang honey in human breast cancer cells were demonstrated by elevated secretion of lactate dehydrogenase (LDH)
Akt↓, figure 2
MAPK↓, figure 2
NF-kB↓, figure 2
IL1β↓, figure 2
IL6↓, figure 2
TNF-α↓, figure 2
iNOS↓, figure 2
COX2↓, figure 2
ROS↓, figure 2
Bcl-2↓, figure 2
PARP↓, figure 2
P53↑, figure 2
BAX↑, figure 2
Casp3↑, figure 2
TumCCA↑, Several components of honey such as chrysin, quercetin, and kaempferol have been shown to arrest cell cycle at various phases such as G0/G1, G1, and G2/M
Cyt‑c↑, hese stimuli cause several proteins located within the intermembrane space (IMS) of the mitochondria, such as cytochrome c, to be released
MMP↓, Honey induces MOMP in cancer cell lines by decreasing the mitochondrial membrane potential
eff↑, amplifying the apoptotic effect of tamoxifen by intensified depolarization of the mitochondrial membrane.

1684- PBG,    Antitumor Activity of Chinese Propolis in Human Breast Cancer MCF-7 and MDA-MB-231 Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, HUVECs
Apoptosis?, treatment of EECP for 24 and 48 h induced both cells apoptosis obviously
ANXA7↑, EECP significantly increased ANXA7 expression and ROS level, and NF-κB p65 level
ROS↑,
NF-kB↓, EECP significantly upregulated the expression of ANXA7 and downregulated NF-?B p65 level in a dose-dependent manner
MMP↓, mitochondrial membrane potential were depressed by EECP dramatically
selectivity↑, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs)

1685- PBG,    Antitumor Activity of Chinese Propolis in Human Breast Cancer MCF-7 and MDA-MB-231 Cells
- in-vitro, BC, MCF-7
ANXA7↑, Exposure to EECP significantly increased ANXA7 expression and ROS level
ROS↑,
NF-kB↓, NF-κB p65 level and mitochondrial membrane potential were depressed by EECP dramatically.
MMP↓,
selectivity↑, Interestingly, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs)
Dose⇅, propolis plays a dual role on ROS depending on concentrations: at high concentration, it exerts a prooxidant effect; at low concentration, it can also act as an antioxidant by scavenging free radicals.
ROS⇅,

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, NA
*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

3250- PBG,    Allergic Inflammation: Effect of Propolis and Its Flavonoids
- Review, NA, NA
*SOD↑, increase in antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase, peroxiredoxin, and heme oxygenase-1
*GPx↑,
*Catalase↑,
*Prx↑,
*HO-1↑,
*Inflam↓, anti-inflammatory properties of propolis may be based on the following mechanisms:
*TNF-α↓, (1) suppression of the release of inflammatory cytokines, such as TNF-α and IL-1β;
*IL1β↓,
*IL4↑, (2) increase in production of anti-inflammatory cytokines such as IL-4 and IL-10;
*IL10↑,
*TLR4↓, (3) prevention of TLR4 activation;
*LOX1↓, (4) suppression of LOX, COX-1 and COX-2 gene expression
*COX1↓,
*COX2↓,
*NF-kB↓, (5) suppression of NF-κB and AP-1 activities;
*AP-1↓,
*ROS↓, CAPE treatment reduced ROS levels in the airway microenvironmen
*GSH↑, GSH level increased after CAPE treatment in an animal allergic asthma model
*TGF-β↓, significantly limiting secretion of eotaxin-1, TGF-β1, TNF-α, IL-4, IL-13, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-9, and alpha-smooth muscle actin expression
*IL8↓,
*MMP9↓,
*α-SMA↓,
*MDA↓, (MDA) production and protein carbonyl (PC) levels significantly decreased

3251- PBG,    The Antioxidant and Anti-Inflammatory Effects of Flavonoids from Propolis via Nrf2 and NF-κB Pathways
- Review, AD, NA - Review, Diabetic, NA - Review, Var, NA - in-vitro, Nor, H9c2
*antiOx↑, In this study, the antioxidant and anti-inflammatory effects of the main flavonoids of propolis (chrysin, pinocembrin, galangin, and pinobanksin) and propolis extract were researched.
*Inflam↓,
*ROS↓, ROS levels were decreased; SOD and CAT activities were increased; and the expression of HO-1 protein was increased by chrysin.
*SOD↑,
*Catalase↑,
*HO-1↑,
*NO↓, The results demonstrated that NO (Nitric Oxide), NOS (Nitric Oxide Synthase), and the activation of the NF-κB signaling pathway were inhibited in a dose-dependent manner
*NOS2↓,
*NF-kB↓,
*NRF2↑, it is possible that phytochemicals activate the Nrf2 pathway and inhibited the NF-κB (Nuclear factor kappa B) pathway.
*hepatoP↑, propolis has antioxidant, anti-inflammatory, anti-cancer, anti-bacterial, and hepatoprotective properties.
*MDA↓, chrysin reduced the cytotoxicity, MDA levels, and lysosomal and mitochondrial damage induced by AlP in a dose-dependent manner and increased the GSH activity induced by AlP i
*mtDam↓,
*GSH↑,
*p65↓, Similarly, galangin at 15, 30, and 60 mg/kg inhibited the expression of NF-κB p65, NOS, TNF-α, and IL-1β in a dose-dependent manner
*TNF-α↓,
*IL1β↓,
*NRF2↑, Nrf2 translocation from the cytoplasm to the nucleus was up-regulated (chrysin range of 5 μM–10 μM, pinocembrin range of 5 μM–40 μM, and propolis-extract range of 5 μg/mL–40 μg/mL)
*NRF2↓, and then down-regulated (chrysin range of 15 μM–25 μM, pinocembrin range of 40 μM–60 μM, and propolis-extract range of 40 μg/mL–100 μg/mL) following treatments with chrysin, pinocembrin, and propolis extract
*ROS⇅, Secondly, chrysin, pinocembrin, galangin, pinobanksin, and propolis extract exhibited antioxidant and pro-oxidant effects in a dose-dependent manner.
*BioAv↓, bioavailability values of galangin and chrysin in propolis extracts were determined in a study, and they were at 7.8% and 7.5%, respectively
*BioAv↑, Moreover, propolis extract has a higher bioavailability than single-flavonoid standards

3252- PBG,    Propolis Extract and Its Bioactive Compounds—From Traditional to Modern Extraction Technologies
- Review, NA, NA
*Inflam↓, extracts act by suppressing similar targets, from pro-inflammatory TNF/NF-κB to the pro-proliferative MAPK/ERK pathway.
*TNF-α↓,
*NF-kB↓,
*MAPK↓,
*ERK↓,
*antiOx↑, they activate similar antioxidant mechanisms of action, like Nrf2-ARE intracellular antioxidant pathway,
*NRF2↑,
*cardioP↑, pinocembrin was shown to be cardioprotective by enhancing glycolysis in the myocardium, which is an essential mechanism of action against ischemic injury of the heart
*Glycolysis↑,
*Ca+2↓, Reducing the content of Ca2+ in mitochondria prevents mitochondrial membrane swelling,
*HO-1↑, CAPE is beneficial as an antioxidant and the inductor of heme oxygenase-1 (HO), Nrf2-regulated gene
*NRF2↑,
*neuroP↑, HO-1 induction results in cardioprotective effects in diabetes [80], neuroprotective in microglial cells

3257- PBG,    The Potential Use of Propolis as a Primary or an Adjunctive Therapy in Respiratory Tract-Related Diseases and Disorders: A Systematic Scoping Review
- Review, Var, NA
CDK4↓, CAPE also induces G1 phase cell arrest by lowering the expression of CDK4, CDK6, Rb, and p-Rb. M
CDK6↓,
pRB↓,
ROS↓, Artepillin C, a bioactive component of Brazilian green propolis, reduces oxidative damage markers, namely 4-HNE-modified proteins, 8-OHdG, malonaldehyde, and thiobarbituric acid reactive substances in lung tissues with pulmonary adenocarcinoma
TumCCA↑, Propolin, a novel component of prenylflavanones in Taiwanese propolis, was demonstrated to have anti-cancer properties. Propolin H induces cell arrest at G1 phase and upregulates the expression of p21
P21↑,
PI3K↓, Propolin C also inhibits PI3K/Akt and ERK-mediated epithelial-to-mesenchymal transition by upregulating E-cadherin (epithelial cell marker) and downregulating vimentin
Akt↓,
EMT↓,
E-cadherin↑,
Vim↓,
*COX2↓, bioactive compounds such as CAPE, galangin significantly reduce the activity of lung cyclooxygenase (COX) and myeloperoxidase (MPO), and malonaldehyde (MDA), TNF-α, and IL-6 levels, while increasing the activity of catalase (CAT) and SOD
*MPO↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*Catalase↑,
*SOD↑,
*AST↓, Chrysin also reduces the expression of oxidative and inflammatory markers such as aspartate transaminase (AST), alanine aminotransferase (ALT), IL-1β, IL-10, TNF-α, and MDA levels and increases the antioxidant parameters such as SOD, CAT, and GPx
*ALAT↓,
*IL1β↓,
*IL10↓,
*GPx↓,
*TLR4↓, propolis also inhibits the expression of Toll-like receptor 4 (TLR4), macrophage infiltration, MPO activity, and apoptosis of lung tissues in septic animals
*Sepsis↓,
*IFN-γ↑, CAPE also significantly increases IFN-γ
*GSH↑, propolis significantly increased the level of GSH and the histological appearances of propolis-treated bleomycin-induced pulmonary fibrosis rats.
*NRF2↑, CAPE significantly increases the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)
*α-SMA↓, propolis significantly inhibits the expression of α- SMA, collagen fibers, and TGF-1β.
*TGF-β↓,
*IL5↓, Propolis also inhibits the expression of inflammatory cytokines and chemokines such as TNF-α, IL-5, IL-6, IL-8, IL-10, NF-kB, IFN-γ, PGF2a, and PGE2.
*IL6↓,
*IL8↓,
*PGE2↓,
*NF-kB↓,
*MMP9↓, downregulating the expression of TGF-1β, ICAM-1, α-SMA, MMP-9, IgE, and IgG1.

1231- PBG,    Caffeic acid phenethyl ester inhibits MDA-MB-231 cell proliferation in inflammatory microenvironment by suppressing glycolysis and lipid metabolism
- in-vitro, BC, MDA-MB-231
TumCP↓,
TumCMig↓,
TumCI↓,
MMP↓,
TLR4↓,
TNF-α↓,
NF-kB↓,
IL1β↓,
IL6↓,
IRAK4↓,
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓,
PKM2↓,
LDHA↓,
ACC↓,
FASN↓,
eff↓, After adding the glycolysis inhibitor 2-deoxy-D-glucose (2-DG), the inhibitory effects of CAPE on cell viability and migration were not significant when compared with the LPS group.

1668- PBG,    Propolis: A Detailed Insight of Its Anticancer Molecular Mechanisms
- Review, Var, NA
antiOx↑, Propolis has well-known therapeutic actions including antioxidative, antimicrobial, anti-inflammatory, and anticancer properties.
Inflam↓,
AntiCan↑,
TumCP↓, primarily by inhibiting cancer cell proliferation, inducing apoptosis
Apoptosis↑,
eff↝, Depending on the bee species, geographic location, plant species, and weather conditions, the chemical makeup of propolis fluctuates significantly
MMPs↓, via inhibiting the metastatic protein expression such as MMPs (matrix metalloproteinases)
TNF-α↓, inhibit inflammatory mediators including tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-1/2 (COX ½), lipoxygenase (LOX), prostaglandins (PGs), and interleukin 1- β (IL1-β)
iNOS↓,
COX2↓,
IL1β↑,
*BioAv↓, Despite the low bioavailability of Artepillin C, a compound with a wide variety of physiological activities
BAX↑, Egyptian propolis extract revealed high apoptotic effects through an increase in BAX (pro-apoptotic protein), caspase-3, and cytochrome-c expression levels, and by a reduction in B-cell lymphoma2 (BCL2)
Casp3↑,
Cyt‑c↑,
Bcl-2↓,
eff↑, enhanced the G0/G1 cell cycle arrest induced by methotrexate
selectivity↑, Thailand propolis on normal and cancerous cells carried out by Umthong et al. found significant differences with the propolis showing cytotoxicity against cancerous but not normal cells.
P53↑, significant increases in the levels of p53 in cells treated with propolis extracts.
ROS↑, propolis induced apoptosis in the SW620 human colorectal cancer cell line through mitochondrial dysfunction caused by high production of reactive oxygen species (ROS) and caspase activation
Casp↑,
eff↑, Galangin- and chrysin-induced apoptosis and mitochondrial membrane potential loss in B16-F1 and A375 melanoma cell lines
ERK↓, Galangin- and chrysin-induced apoptosis and mitochondrial membrane potential loss in B16-F1 and A375 melanoma cell lines
Dose∅, propolis extracts at concentrations of 50 μg/mL significantly increased the levels of TRAIL in cervical tumor cell lines
TRAIL↑,
NF-kB↑, p53, NF-κB, and ROS. These molecules were found to be elevated following exposure of the cells to the alcoholic extract of the propolis
ROS↑,
Dose↑, high concentrations, propolis increased the amounts of integrin β4, ROS, and p53
MMP↓, high expression levels of these molecules, in turn, drove a decrease in mitochondrial membrane potential
DNAdam↑, propolis extract induced DNA fragmentation
TumAuto↑, CAPE, were found to induce autophagy in a breast cancer cell line (MDA-MB-231) through upregulating LC3-II and downregulating p62,
LC3II↑,
p62↓,
EGF↓, downregulation of EGF, HIF-1α, and VEGF
Hif1a↓,
VEGF↓,
TLR4↓, downregulating Toll-like receptor 4 (TLR-4), glycogen synthase kinase 3 beta (GSK3 β), and NF-κB signaling pathways
GSK‐3β↓,
NF-kB↓,
Telomerase↓, Propolis was shown to inhibit the telomerase reverse transcriptase activity in leukemia cells.
ChemoSen↑, Propolis has been shown to increase the activity of existing chemotherapeutic agents and inhibit some of their side effects
ChemoSideEff↓,

1660- PBG,    Emerging Adjuvant Therapy for Cancer: Propolis and its Constituents
- Review, Var, NA
MMPs↓, inhibition of matrix metalloproteinases, anti-angiogenesis
angioG↓,
TumMeta↓, prevention of metastasis, cell-cycle arrest
TumCCA↑,
Apoptosis↑,
ChemoSideEff↓, moderation of the chemotherapy-induced deleterious side effects
eff∅, components conferring antitumor potentials have been identified as caffeic acid phenethyl ester, chrysin, artepillin C, nemorosone, galangin, cardanol, etc
HDAC↓, Taiwanese green propolis extract was used to develop an anticancer agent NBM-HD-3, a histone deacetylase inhibitor (HDACis).
PTEN↑, found to increase phosphatase and tensin homolog (PTEN) and protein kinase B (Akt) protein levelssignificantly, while decreasing phospho-PTEN and phospho-Akt levels markedly
p‑PTEN↓,
p‑Akt↓,
Casp3↑, Propolis induced apoptosis and caspase 3 cleavage, increased phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2), protein kinase B/Akt1 and focal adhesion kinase (FAK).
p‑ERK↑,
p‑FAK↑,
Dose?, When administered orally for 20 weeks at a dose of 100-300 mg/kg, the protective role against the lingual carcinogenesis was observed
Akt↓, treatment reduced the protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1
GSK‐3β↓,
FOXO3↓,
eff↑, Co-treatment with CAPE and 5-fluorouracil exhibited additive anti-proliferation of TW2.6 cells.
IL2↑, Propolis administration stimulated IL-2 and IL-10 production
IL10↑,
NF-kB↓, reduces the expression of growth and transcription factors, including NF-κB.
VEGF↓, CAPE dose-dependently suppresses vascular endothelial growth factor (VEGF) formation by MDA-231 cells,
mtDam↑, Brazilian red propolis significantly reduced the cancer cell viability through the induction of mitochondrial dysfunction, caspase-3 activity and DNA fragmentation.
ER Stress↑, the action was believed to be due to endoplasmic reticulum stress-related signalling induction of CCAAT/enhancer-binding protein homologous protein (CHOP)
AST↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALAT↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALP↓, Rats,(250 mg/kg) thrice a week for 3 weeks
COX2↓, Rats,(250 mg/kg) thrice a week for 3 weeks, Expression of COX-2 and NF-kB p65 was significantly lowered
eff↑, co-treatment of cancer cells with 100 ng/mL TRAIL and 50 μg/mL propolis extract increased the percentage of apoptotic cells to about 66% and caused a significant disruption of membrane potential in LNCaP cells (
Bax:Bcl2↑, decreased Bcl-2/Bax ratio

1661- PBG,    Propolis: a natural compound with potential as an adjuvant in cancer therapy - a review of signaling pathways
- Review, Var, NA
JNK↓, downregulating pathways involving Jun-N terminal kinase, ERK1/2, Akt and NF-ƘB
ERK↓,
Akt↓,
NF-kB↓,
FAK↓, inhibiting Wtn2 and FAK, and MAPK and PI3K/AKT signaling pathways
MAPK↓,
PI3K↓,
Akt↓,
P21↑, propolis-induced up-regulation of p21 and p27
p27↑,
TRAIL↑, effects of propolis are mediated through upregulation of TRAIL, Bax, p53, and downregulation of the ERK1/2 signaling
BAX↑,
P53↑,
ERK↓,
ChemoSen↑, effective adjuvant therapy aimed at reducing related side effects associated with chemotherapy and radiotherapy
RadioS↑,
Glycolysis↓, Chinese poplar propolis decreased aerobic glycolysis by reducing the levels of crucial enzymes such as phosphofructokinase (PFK), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
HK2↓,
PKM2↓,
LDHA↓,
PFK↓,

1662- PBG,    The immunomodulatory and anticancer properties of propolis
- Review, Var, NA
IL6↓, suppressing the proinflammatory cytokines IL-6 and IL-12 but overexpressing the immune-tolerant cytokine IL-10.
IL12↓,
IL10↑,
CSCs↓, Propolis may Decrease Cancer Stem Cells Population
PAK1↓, artepillin C, a major component in Brazilian green propolis extract, can completely suppress the growth of human neurofibromatosis-associated tumor xenografts in mice through the blocking of oncogenic PAK1 signaling
VEGF↓, royal jelly and Chinese red propolis suppressed both VEGF-induced HUVEC proliferation and migration,
MMP2↓, CAPE from propolis could effectively suppress the adhesion and invasion potential of human hepatocellular carcinoma cells (SK-Hep1) by totally abolishing the expression of MMP-2 and MMP-9.
MMP9↓,
NF-kB↓, It was postulated that such action was related to the inhibition of the NFκB pathway
Hif1a↓, Brazilian green propolis and found that some compounds significantly inhibited the expression of the HIF-1α protein and HIF-1 downstream target genes such as glucose transporter 1, hexokinase 2, and VEGF-A
ChemoSen↑, the group with combined usage of paclitaxel and propolis achieved the lowest tumor weight compared to those with paclitaxel alone, propolis alone, or untreated controls
RadioS↑, complementary therapy to mainstream anticancer chemotherapies or radiotherapies.

1663- PBG,    Propolis and Their Active Constituents for Chronic Diseases
- Review, Var, NA
NF-kB↓, CAPE (a bioactive constituent of propolis) was reported to have anticancer properties by inhibiting NF-κB, caspase and Fas signaling activation in MCF-7 cells
Casp↓,
Fas↓,
DNAdam↑, DNA fragmentation, CCAAT/enhancer binding protein homologous protein expression and caspase-3 activity
Casp3↑,
P53↝, Chinese propolis (EECP) and its bioactive constituents mainly persist due to regulation of the annexin A7 and p53 proteins, mitochondrial membrane potential and ROSs, as well as that inhibition of NF-κB causes apoptosis in cancer cells
MMP↝,
ROS↑, Herrera et al. and reported on the MDA-MB 231 tumor cell line, and the inhibitory effect of propolis was proposed to occur through the induction of mitochondrial dysfunction, resulting in ROS-associated necrosis
mtDam↑,
Dose?, A concentration of 100 μg/mL was able to attain 71% cytotoxicity
angioG↓, negative effect on angiogenesis, proliferation and migration of tumor cells. A concentration of 25–200 μg/mL noticeably inhibited the metastasis of breast cancer
TumCP↓,
TumCMig↓,
BAX↑,
selectivity↑, Negligible effect in fibroblasts
MMP↓, Cuban: Disturbed the mitochondrial potential, lactate dehydrogenase released, production of ROS and cell migration
LDH↓,
IL6↓, Chinese: Decreased cell tube generation, IL-6, IL-1β, TNF-α-like inflammatory mediators, glycolytic enzymes and mitochondrial potential. Promoted ROS generation
IL1β↓,
TNF-α↓,

1664- PBG,    Anticancer Activity of Propolis and Its Compounds
- Review, Var, NA
Apoptosis↑,
TumCMig↓,
TumCCA↑,
TumCP↓,
angioG↓,
P21↑, upregulating p21 and p27 expression
p27↑,
CDK1↓, thanol-extracted Cameroonian propolis increased the amount of DU145 and PC3 cells in G0/G1 phase, down-regulated cell cycle proteins (CDK1, pCDK1, and their related cyclins A and B)
p‑CDK1↓,
cycA1↓,
CycB↓,
P70S6K↓, Caffeic acid phenylethyl ester has been shown to inhibit the S6 beta-1 ribosomal protein kinase (p70S6K),
CLDN2↓, inhibition of NF-κB may be involved in the decrease of claudin-2 mRNA level
HK2↓, Chinese poplar propolis has been shown to significantly reduce the level of glycolysis at the stage of action of hexokinase 2 (HK2), phosphofructokinase (PFK), muscle isozyme pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
PFK↓,
PKM2↓,
LDHA↓,
TLR4↓, hinese propolis, as well as CAPE, inhibits breast cancer cell proliferation in the inflammatory microenvironment by inhibiting the Toll-like receptor 4 (TLR4) signal pathway
H3↓, Brazilian red propolis bioactive isoflavonoid, down-regulates the alpha-tubulin, tubulin in microtubules, and histone H3 genes
α-tubulin↓,
ROS↑, CAPE also affects the apoptotic intrinsic pathway by increasing ROS production
Akt↓, CAPE induces apoptosis by decreasing the levels of proteins related to carcinogenesis, including Akt, GSK3b, FOXO1, FOXO3a, NF-kB, Skp2 and cyclin D1
GSK‐3β↓,
FOXO3↓,
NF-kB↓,
cycD1↓,
MMP↓, It was found that chrysin caused a loss of mitochondria membrane potential (MMP) while increasing the production of reactive oxygen species (ROS), cytoplasmic Ca2+ levels, and lipid peroxidation
ROS↑,
i-Ca+2↑,
lipid-P↑,
ER Stress↑, Chrysin also induced endoplasmic reticulum (ER) stress by activating unfolded protein response proteins (UPR) such as PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and 78 kDa glucose-regulated protein (GRP78)
UPR↑,
PERK↑,
eIF2α↑,
GRP78/BiP↑,
BAX↑, CAPE activated Bax protein
PUMA↑, CAPE also significantly increased PUMA expression
ROS↑, Northeast China causes cell apoptosis in human gastric cancer cells with increased production of reactive oxygen species (ROS) and reduced mitochondrial membrane potential.
MMP↓,
Cyt‑c↑, release of cytochrome C from mitochondria to the cytoplasm is observed, as well as the activation of cleaved caspases (8, 9, and 3) and PARP
cl‑Casp8↑,
cl‑Casp8↑,
cl‑Casp3↑,
cl‑PARP↑,
eff↑, administration of Iranian propolis extract in combination with 5-fluorouracil (5-FU) significantly reduced the number of azaxymethane-induced aberrant crypt foci compared to 5-FU or propolis alone.
eff↑, Propolis may also have a positive effect on the efficacy of photodynamic therapy (PDT). enhances the intracellular accumulation of protoporphyrin IX (PpIX) in human epidermoid carcinoma cells
RadioS↑, breast cancer patients undergoing radiotherapy and supplemented with propolis had a statistically significant longer median disease-free survival time than the control group
ChemoSen↑, confirmed that propolis mouthwash is effective and safe in the treatment of chemo- or radiotherapy-induced oral mucositis in cancer patients.
eff↑, Quercetin, ferulic acid, and CAPE may also influence the MDR of cancer cells by inhibiting P-gp expression

1667- PBG,    Ethanolic extract of Brazilian green propolis sensitizes prostate cancer cells to TRAIL-induced apoptosis
- in-vitro, Pca, LNCaP
NF-kB↓, Brazilian EEP decreased the expression of NF-κB, in contrast to TRAIL, which induced the activation of NF-κB
Apoptosis↑, co-treatment of prostate cancer cells with 100 ng/ml TRAIL and 50 µg/ml EEP increased the percentage of apoptotic cells to 65.8 ± 1.2%
MMP↓, caused a significant disruption of ∆Ψm in LNCaP cells

1672- PBG,    The Potential Use of Propolis as an Adjunctive Therapy in Breast Cancers
- Review, BC, NA
ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.

1673- PBG,    An Insight into Anticancer Effect of Propolis and Its Constituents: A Review of Molecular Mechanisms
- Review, Var, NA
TumCP↓, propolis-treated cells showed inhibition of cell proliferation and induction of apoptosis
Apoptosis↑,
TumCCA↑, cell cycle arrest potential against cancer cell lines
MALAT1↓, CAPE blocks the expression of the MALT1 gene to decrease the cell proliferation, invasion, and tumor growth of prostate carcinoma cells via the p53 and NF-κB signaling pathways
P53↑,
RadioS↑, Propolis capsules (400 mg, 3 times daily) is consumed for 10 days before radiotherapy, 10 days during radiation treatment, and 10 days after irradiation
OS↑, Patients who used propolis supplements had a considerably longer median disease-free lifetime.
ROS↑, Chinese propolis extract (EECP) significantly increased annexin A7 expression, ROS, NF-κB, and p65 expressions and dramatically altered the potential of mitochondrial membrane
NF-kB↓, Chrysin treatment in U937 cells (histiocytic lymphoma cells) showed induction of apoptosis by suppressing the PI3K/Akt signaling and inactivation of nuclear factor kappa B (NF-?B)/inhibitor of apoptosis (IAP)
p65↑,
MMP↓,
ROS↑, 25 to 100 μg/ml of Chinese propolis-treated cells showed increased ROS generation
MMP9↓, Cuban propolis (83 μg/ml) suppresses cell migration and invasion by inhibiting MMP-9 activity, β-catenin, vimentin expression, and decreased E-cadherin expression in human colorectal cancer
β-catenin/ZEB1↓,
Vim↓,
E-cadherin↓,
VEGF↓, Chinese red propolis and CAPE displayed a solid inhibitory effect in VEGF-mediated angiogenesis
EMT↓, Chinese propolis (12.5 μg/ml) inhibited Panc-1 cell migration by modulating the epithelial-mesenchymal transition


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 23

Results for Effect on Cancer/Diseased Cells:
ACC↓,1,   Akt↓,7,   p‑Akt↓,1,   ALAT↓,1,   ALP↓,1,   AMPK↑,1,   angioG↓,5,   angioG↑,1,   AntiCan↑,2,   antiOx↑,1,   ANXA7↑,2,   Apoptosis?,2,   Apoptosis↑,6,   AR↓,1,   AST↓,1,   ATP↓,1,   mt-ATP↓,1,   BAX↓,1,   BAX↑,6,   Bax:Bcl2↑,2,   BBB↑,1,   Bcl-2↓,2,   BioAv↓,1,   BioAv↑,1,   Ca+2↑,1,   i-Ca+2↑,1,   Casp↓,1,   Casp↑,3,   Casp3↓,1,   Casp3↑,5,   cl‑Casp3↑,1,   Casp8↑,1,   cl‑Casp8↑,2,   CDK1↓,1,   p‑CDK1↓,1,   CDK2↓,1,   CDK4↓,1,   CDK4↑,1,   CDK6↓,1,   CDK6↑,1,   ChemoSen↓,1,   ChemoSen↑,6,   ChemoSideEff↓,2,   CLDN2↓,1,   cMyc↓,1,   cognitive↑,1,   COX2↓,4,   CSCs↓,2,   cycA1↓,1,   CycB↓,2,   cycD1↓,2,   Cyt‑c↑,3,   DNAdam↑,2,   Dose?,3,   Dose↑,1,   Dose⇅,1,   Dose∅,4,   E-cadherin↓,1,   E-cadherin↑,2,   eff↓,2,   eff↑,22,   eff↝,2,   eff∅,1,   EGF↓,1,   eIF2α↑,1,   EMT↓,4,   eNOS↑,1,   ER Stress↑,4,   ERK↓,3,   ERK↑,1,   p‑ERK↑,1,   FAK↓,1,   p‑FAK↓,1,   p‑FAK↑,1,   Fas↓,1,   Fas↑,1,   FASN↓,1,   FOXO3↓,2,   GLUT1↓,2,   GLUT3↓,1,   Glycolysis↓,3,   GRP78/BiP↑,1,   GSK‐3β↓,3,   H3↓,1,   Half-Life↓,1,   HDAC↓,1,   HDAC8↓,1,   Hif1a↓,3,   HK2↓,4,   hTERT↓,1,   IL10↓,2,   IL10↑,2,   IL12↓,1,   IL1β↓,4,   IL1β↑,1,   IL2↑,2,   IL4↓,1,   IL6↓,4,   Inflam↓,2,   iNOS↓,2,   iNOS↑,1,   IRAK4↓,1,   JNK↓,1,   Ki-67↓,1,   LC3II↑,3,   LDH↓,4,   i-LDH↓,1,   LDHA↓,3,   lipid-P↑,2,   MALAT1↓,1,   MAPK↓,2,   MAPK↑,1,   MMP↓,12,   MMP↝,1,   MMP2↓,2,   MMP9↓,3,   MMP9↑,1,   MMPs↓,2,   mtDam↑,4,   mTOR↓,1,   NDRG1↑,1,   NF-kB↓,16,   NF-kB↑,1,   NOTCH1↑,1,   NRF2↓,1,   OCR↓,1,   OS↑,2,   P21↓,1,   P21↑,4,   p27↑,2,   P53↑,5,   P53↝,1,   p62↓,3,   p65↓,1,   p65↑,1,   P70S6K↓,1,   PAK1↓,1,   PARP↓,1,   cl‑PARP↑,1,   PCNA↓,1,   PD-L1↓,1,   PDK1↓,1,   PDK3↑,1,   PERK↑,1,   PFK↓,4,   PI3K↓,3,   PKM2↓,4,   pRB↓,1,   PTEN↑,1,   p‑PTEN↓,1,   PUMA↑,1,   RadioS↑,5,   RB1↑,1,   RenoP↑,1,   Rho↓,1,   ROCK1↓,1,   ROS↓,3,   ROS↑,19,   ROS⇅,1,   selectivity↑,4,   STAT↓,1,   STAT3↓,3,   Telomerase↓,1,   TIMP1↓,1,   TLR4↓,5,   TNF-α↓,5,   TOP1↓,1,   TP53↓,1,   TRAIL↑,2,   TRAILR↑,1,   TSP-1↑,1,   TumAuto↑,2,   TumCCA↓,1,   TumCCA↑,6,   TumCI↓,1,   TumCMig↓,4,   TumCP↓,6,   TumMeta↓,3,   uPA↓,1,   UPR↑,1,   VEGF↓,7,   Vim↓,3,   α-tubulin↓,1,   β-catenin/ZEB1↓,3,  
Total Targets: 184

Results for Effect on Normal Cells:
AChE↓,1,   ALAT↓,1,   AntiCan↑,1,   antiOx↑,3,   AP-1↓,1,   AST↓,1,   BG↓,1,   BioAv↓,2,   BioAv↑,1,   Ca+2↓,1,   cardioP↑,1,   Catalase↑,5,   COX1↓,1,   COX2↓,3,   ERK↓,1,   Glycolysis↑,1,   GPx↓,1,   GPx↑,3,   GSH↑,5,   GSR↓,1,   HbA1c↓,1,   hepatoP↑,2,   HO-1↑,3,   HSP70/HSPA5↑,1,   hyperG↓,1,   IFN-γ↑,1,   IL10↓,1,   IL10↑,1,   IL1β↓,4,   IL4↑,1,   IL5↓,1,   IL6↓,3,   IL8↓,2,   Inflam↓,7,   iNOS↓,1,   JNK↓,1,   LOX1↓,1,   MAPK↓,2,   MCP1↓,1,   MDA↓,6,   MMP2↓,1,   MMP9↓,3,   motorD↑,1,   MPO↓,1,   mtDam↓,1,   neuroP↑,3,   NF-kB↓,7,   NO↓,3,   NOS2↓,1,   NRF2↓,1,   NRF2↑,5,   p65↓,1,   Pain↓,1,   PGE2↓,1,   Prx↑,1,   ROS↓,6,   ROS⇅,1,   selectivity↑,1,   Sepsis↓,1,   SOD↑,6,   TGF-β↓,2,   TGF-β↑,1,   TLR4↓,2,   TNF-α↓,5,   toxicity∅,2,   VCAM-1↓,1,   α-SMA↓,2,  
Total Targets: 67

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
23 Propolis -bee glue
1 Caffeic acid
1 Chrysin
1 Hydroxycinnamic-acid
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:137  Target#:214  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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