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↓, 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


HO-1, HMOX1: Click to Expand ⟱
Source:
Type:
(Also known as Hsp32 and HMOX1)
HO-1 is the common abbreviation for the protein (heme oxygenase‑1) produced by the HMOX1 gene.
HO-1 is an enzyme that plays a crucial role in various cellular processes, including the breakdown of heme, a toxic molecule. Research has shown that HO-1 is involved in the development and progression of cancer.
-widely regarded as having antioxidant and cytoprotective effects
-The overall activity of HO‑1 helps to reduce the pro‐oxidant load (by degrading free heme, a pro‑oxidant) and to generate molecules (like bilirubin) that can protect cells from oxidative damage

Studies have found that HO-1 is overexpressed in various types of cancer, including lung, breast, colon, and prostate cancer. The overexpression of HO-1 in cancer cells can contribute to their survival and proliferation by:
  Reducing oxidative stress and inflammation
  Promoting angiogenesis (the formation of new blood vessels)
  Inhibiting apoptosis (programmed cell death)
  Enhancing cell migration and invasion
When HO-1 is at a normal level, it mainly exerts an antioxidant effect, and when it is excessively elevated, it causes an accumulation of iron ions.

A proper cellular level of HMOX1 plays an antioxidative function to protect cells from ROS toxicity. However, its overexpression has pro-oxidant effects to induce ferroptosis of cells, which is dependent on intracellular iron accumulation and increased ROS content upon excessive activation of HMOX1.

-Curcumin   Activates the Nrf2 pathway leading to HO‑1 induction; known for its anti‑inflammatory and antioxidant effects.
-Resveratrol  Induces HO‑1 via activation of SIRT1/Nrf2 signaling; exhibits antioxidant and cardioprotective properties.
-Quercetin   Activates Nrf2 and related antioxidant pathways; contributes to anti‑oxidative and anti‑inflammatory responses.
-EGCG     Promotes HO‑1 expression through activation of the Nrf2/ARE pathway; also exhibits anti‑inflammatory and anticancer properties.
-Sulforaphane One of the most potent natural HO‑1 inducers; triggers Nrf2 nuclear translocation and upregulates a battery of phase II detoxifying enzymes.
-Luteolin    Induces HO‑1 via Nrf2 activation; may also exert anti‑inflammatory and neuroprotective effects in various cell models.
-Apigenin   Has been reported to induce HO‑1 expression partly via the MAPK and Nrf2 pathways; also known for anti‑inflammatory and anticancer activities.
Scientific Papers found: Click to Expand⟱
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

3254- PBG,    Brazilian green propolis water extract up-regulates the early expression level of HO-1 and accelerates Nrf2 after UVA irradiation
- in-vitro, Nor, NA
*HO-1↑, WEP acts as an early inducer of HO-1 and rapid activator of Nrf2 to protect against UVA-induced oxidative stress.
*NRF2↑,

1680- PBG,    Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N-(4-bromophenethyl) Caffeamide, a Propolis Derivative
- in-vitro, Nor, HS68
*ROS↓, K36H reduced UVA-induced intracellular reactive oxygen species generation
*NRF2↑, increased nuclear factor erythroid 2–related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme.
*HO-1↑,
*cJun↓, K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases,
*MMP1↓, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2
*MMP2↓,
*p‑cJun↓, K36H inhibited the phosphorylation of c-Jun and downregulated c-Fos expression
*cFos↓,
*BAX↓, K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression.
*Casp3↓,
*DNAdam↓, K36H reduced UVA-induced DNA damage.
*iNOS↓, K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E2 and nitric oxide.
*COX2↓,
*IL6↓,
*PGE2↓,
*NO↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Results for Effect on Cancer/Diseased Cells:

Total Targets: 0

Results for Effect on Normal Cells:
antiOx↑,2,   AP-1↓,1,   BAX↓,1,   BioAv↓,1,   BioAv↑,1,   Ca+2↓,1,   cardioP↑,1,   Casp3↓,1,   Catalase↑,2,   cFos↓,1,   cJun↓,1,   p‑cJun↓,1,   COX1↓,1,   COX2↓,2,   DNAdam↓,1,   ERK↓,1,   Glycolysis↑,1,   GPx↑,1,   GSH↑,2,   hepatoP↑,1,   HO-1↑,5,   IL10↑,1,   IL1β↓,2,   IL4↑,1,   IL6↓,1,   IL8↓,1,   Inflam↓,3,   iNOS↓,1,   LOX1↓,1,   MAPK↓,1,   MDA↓,2,   MMP1↓,1,   MMP2↓,1,   MMP9↓,1,   mtDam↓,1,   neuroP↑,1,   NF-kB↓,3,   NO↓,2,   NOS2↓,1,   NRF2↓,1,   NRF2↑,6,   p65↓,1,   PGE2↓,1,   Prx↑,1,   ROS↓,3,   ROS⇅,1,   SOD↑,2,   TGF-β↓,1,   TLR4↓,1,   TNF-α↓,3,   α-SMA↓,1,  
Total Targets: 51

Scientific Paper Hit Count for: HO-1, HMOX1
5 Propolis -bee glue
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:137  Target#:597  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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