HNE Cancer Research Results

HNE, 4-hydroxynonenal (HNE): Click to Expand ⟱
Source:
Type:
HNE is a lipid peroxidation product formed during oxidative stress and is considered both a signaling molecule and a cytotoxic agent depending on its cellular concentration and context.
– HNE is generated as a byproduct of the peroxidation of ω-6 polyunsaturated fatty acids.
– It serves as a marker of oxidative stress and can modify proteins, lipids, and DNA through covalent adduct formation.

• Dual Biological Effects
– At low to moderate concentrations, HNE can act as a signaling molecule, modulating pathways involved in cell proliferation, differentiation, and apoptosis.
– At higher concentrations, HNE is cytotoxic, causing cellular damage and contributing to cell death through protein dysfunction and DNA damage.
– This concentration-dependent activity means that HNE can have both pro-tumorigenic and anti-tumorigenic effects.

– Elevated levels of HNE in tissues or biological fluids are frequently used as indicators of oxidative stress within the tumor microenvironment.
Scientific Papers found: Click to Expand⟱
3869- Carno,    Carnosine, Small but Mighty—Prospect of Use as Functional Ingredient for Functional Food Formulation
- Review, AD, NA - Review, Stroke, NA
*ROS↓, carnosine scavenges reactive oxygen species (ROS)
*IronCh↑, it can chelate divalent metal ions: heavy metal chelating activity
*AntiAge↑, can slow down aging.
*antiOx↑, natural antioxidant [4] and has anti-inflammatory and neuroprotective properties
*Inflam↓,
*neuroP↑,
*lipid-P↓, Carnosine reduces lipid peroxidation, but also inhibits oxidative modification of protein exposed to hydroxyl radicals
*toxicity↓, carnosine can be recommended as a natural cure that has no side effects but is highly efficient
*NOX4↓, human kidney tubular epithelial (HK2) cells indicated that carnosine decreased NADPH oxidase (Nox) 4 expression and increased total superoxide dismutase (T-SOD) activity, thus reducing the production of intracellular ROS,
*SOD↑,
*HNE↓, Rising data indicate that carnosine acts as a scavenger of reactive and cytotoxic carbonyl species including 4-hydroxynonenal (HNE)
*IL6↓, anserine and/or carnosine supplementation significantly decreased IL-6, TNF-α, and IL-1β in pre-treated mice with MPTP-induced PD,
*TNF-α↓,
*IL1β↓,
*Sepsis↓, carnosine has a beneficial effect on reducing acute kidney injury due to septic shock
*eff↑, carnosine on ischemic stroke, there was a 29.4% average reduction in infarct volume with a clear dose-dependent effect (38.1% reduction on 1000 mg/kg dose compared with 13.2% for doses less than 500 mg/kg)
*GABA↝, In addition to the carnosine-histidine-histamine pathway, carnosine can also have a direct impact on CA1 pyramidal neurons [212] or act as a precursor for the neurotransmitter GABA
*Aβ↓, Several studies have reported that carnosine supplementation reduced β-amyloid cumulation in the hippocampus of a transgenic mouse model of AD
Glycolysis↓, carnosine has the ability to inhibit glycolysis and thus achieve an antitumor effect
AntiTum↑,
p‑Akt↓, significant reduction of Akt phosphorylation in the U87 glioblastoma cell line
TumCCA↑, Carnosine has an effect in bladder cancer by stopping the G1 phase cell cycle by increasing p21WAF1 expression and decreasing cyclin/CDK complexes
angioG↓, inhibits angiogenesis by suppressing VEGFR-2
VEGFR2↓,
NF-kB↓, suppressing nuclear factor kB (NF-κB) signaling pathway activation in human colon cancer cells

6824- EMD,    Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review
- Review, AD, NA
*Inflam?, Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties.
*antiOx↑,
*tau↓, While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects.
*Aβ↓,
*neuroP↑, In recent years, several studies have advocated for a robust neuroprotective function of emodin
*ROS↓,
*memory↑, Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature
*cognitive↑,
*other↝, Well-known sources of emodin include Rheum palmatum,10Polygonum cuspidatum,11Aloe vera,12Polygonum multifarum,13 and Casia obtusofolia.
*AChE↓, potent in vitro inhibition of AChE (IC50 of 21.8 μM), in addition to amelioration of H2O2-induced oxidative damage in PC12 cells
*BACE↓, potent inhibition of the activities of BACE-1 (IC50 of 4.5 μM) and AChE (IC50 of 9.7 μM); and strong and mixed-type inhibition for BACE-1 (Ki of 20 μM) in kinetic studies
*LC3II↓, Inhibition of autophagic (LC3-II and beclin-1)
*Beclin-1↓,
*p‑tau↓, 80 mg/kg/day for 2 weeks (intragastric administration) repression of the levels of BACE-1, Aβ species and phosphorylated-tau, stimulation of CREB signaling
*CREB↑,
*HNE↓, downregulation of Aβ and phosphorylated-tau levels, reduced oxidative damage and 4-HNE levels
*BioAv↓, Bioavailability of exogenously administered emodin suffers from some issues, including its weak intestinal absorption, high rate of elimination, and first-pass metabolism
*BioAv↝, bioavailability of orally supplemented emodin may show appreciable dependence on gender, given that there are four times higher plasma levels of emodin in male rats, compared to females after a single oral dosing of emodin at 8 mg/kg body weight.
*BioAv↑, pretreatment with stilbene glucosides from Radix Polygoni Multiflori prevents glucuronidation of emodin, and increases its plasma concentration upon oral administration
*BioAv↑, cotreatment with piperine was also found to inhibit glucuronide formation of orally administered emodin, while increasing the bioavailability of its free form
*BioAv↑, Nanoemulsification may also decreses the clearance of orally administered emodin, while increasing its brain distribution and bioavailability.
*BioAv↑, Lastly, treatment of emodin with sodium hydroxide to form its sodium salt may represent another strategy for improving the solubility and bioavailability of emodin
BioAv↑, ultrasound-sensitive emodin-containing lecithin-based nanoformulations squamous cell carcinoma FaDu and CAL-27 cells neck squamous cell carcinoma sonodynamic therapy-based beneficial actions
*HO-1↑, figure 3, neuroproctive
*PKCδ↑,
*Akt↑,
*NLRP3↓,
*NF-kB↓,
*TLR3↓,

3924- PTS,    Effect of resveratrol and pterostilbene on aging and longevity
- Review, AD, NA - Review, Stroke, NA
*antiOx↓, Firstly, pterostilbene act as an antioxidant against various free radicals,
*ROS↑, reducing ROS production
*SOD↑, as well as increasing SOD and glutathione (GSH) activation via the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in neuronal cells [44].
*GSH↑,
*NRF2↑, by activating Nrf2
*MDA↓, pterostilbene reduced malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), aconitase-2 and 8-hydroxydeoxyguanosine (8-OHdG) level;
*HNE↓,
*Inflam↓, Pterostilbene has been reported as a potential anti- inflammatory agent
*MAPK↓, pterostilbene inhibited mitogen-activated protein kinase (MAPK) activation and the production of pro-inflammatory cytokine (interleukin-6 [IL-6] and TNF-a)
*IL6↓,
*TNF-α↓,
*HO-1↑, through upregulating heme oxygenase-1 (HO-1) to prevent hypoxic-ischemic brain injury in neonatal rats
*cardioP↑, beneficial health effects of resveratrol and pterostilbene on cardioprotection, neuroprotection
*neuroP↑,
*CRM↑, as a calorie restriction mimic
*NLRP3↓, nhibiting pro-inflammatory cytokine such as IL-1b and NLRP3 inflammasome activation,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiTum↑, 1,  
Total Targets: 8

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 2,   GSH↑, 1,   HNE↓, 3,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 1,   NOX4↓, 1,   NRF2↑, 1,   ROS↓, 2,   ROS↑, 1,   SOD↑, 2,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CREB↑, 1,   CRM↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   MAPK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   LC3II↓, 1,  

Migration(tgid=13) ⓘ

PKCδ↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 2,   Inflam?, 1,   Inflam↓, 2,   NF-kB↓, 1,   TLR3↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   GABA↝, 1,   tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioAv↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   cardioP↑, 1,   cognitive↑, 1,   memory↑, 1,   neuroP↑, 3,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 47

Scientific Paper Hit Count for: HNE, 4-hydroxynonenal (HNE)
1 Carnosine
1 Emodin
1 Pterostilbene
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

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