4-HNE Cancer Research Results

4-HNE, 4‑Hydroxynonenal: Click to Expand ⟱
Source:
Type:
4‑Hydroxynonenal (4‑HNE) is a key bioactive aldehyde generated during lipid peroxidation, and it can form adducts with proteins, DNA, and other biomolecules.

4‑HNE can act as a “double‐edged sword”. At moderate concentrations, it might activate signaling pathways that promote cell proliferation and survival, potentially contributing to tumor growth. At higher concentrations, the same molecule may induce cytotoxicity and apoptosis.

-A biomarker of ferroptosis(high levels)
-Elevated levels of 4‑HNE adducts are sometimes associated with chemoresistance and poor clinical outcomes, highlighting its potential role in prognostication.
Scientific Papers found: Click to Expand⟱
5901- CAR,    Neuroprotective role of carvacrol in ischemic brain injury: a systematic review of preclinical evidence and proposed TRPM7 involvement
- Review, Stroke, NA
*neuroP↑, improved neurological scores when carvacrol was given before or shortly after injury.
*ROS↓, studies showed reduced oxidative damage (MDA, 4-HNE), increased antioxidant enzymes (SOD, CAT, GPx), lower apoptosis (cleaved caspase-3), and variable changes in TRPM7 expression.
*MDA↓,
*4-HNE↓,
*SOD↑,
*Catalase↑,
*GPx↑,
*Apoptosis↓,
*cl‑Casp3↓,
*TRPM7⇅, variable changes in TRPM7 expression
*BBB↓, Natural products such as carvacrol can cross the blood-brain barrier and have been reported to inhibit TRPM7 in vitro
*TRPM7↓,

3761- H2,    Therapeutic Inhalation of Hydrogen Gas for Alzheimer's Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study
- Human, AD, NA
*cognitive↑, the mean individual ADAS-cog change showed significant improvement after 6 months of H2 treatment (−4.1) vs. untreated patients (+2.6).
*BBB↑, H2 has the ability to cross the blood-brain barrier (BBB) by gaseous diffusion without a specific drug delivery system
*ROS↓, An oxidized form of porphyrin catalyzes the reaction of H2 with hydroxyl radicals, the most oxidative free radicals, to reduce the oxidative stress.
*NRF2↑, secondary anti-oxidative function, H2 activates NF-E2-related factor 2 (Nrf2) [9], which reduces oxidative stress through the expression of a variety of anti-oxidant enzymes
*Inflam↓, H2 relieves inflammation by decreasing pro-inflammatory cytokines [38].
*NFAT↓, resulting in suppressing the nuclear factor of activated T cell (NFAT) transcription pathway to down-regulate pro-inflammatory cytokines
*FAO↓, H2 inhibits the free radical chain reaction, resulting in a decrease in fatty acid peroxidation and its end-products such as 4-hydroxyl-nonenal (4-HNE),
*4-HNE↓,
*PGC-1α↑, In turn, the decrease in 4-HNE promotes the expression of PGC-1α, followed by increasing FGF21,
*Ferroptosis↓, H2 has an anti-cell-death function by inhibiting ferroptosis through a decrease in peroxide [36], and by down- and up-regulating pro- and anti-death factors, respectively

4007- K+,    The increased potassium intake improves cognitive performance and attenuates histopathological markers in a model of Alzheimer's disease
- in-vivo, AD, NA
*p‑tau↓, We observed that an increase in K(+) intake leads to a change in the aggregation pattern of the Aβ peptide, a partial decrease in some epitopes of tau phosphorylation and improvement in the cognitive performance.
*cognitive↑,
*Inflam↓, We also observed a decrease in markers related to inflammation and oxidative stress such as glial fibrillary acidic protein (GFAP), interleukin 6 (IL-6) and 4-hydroxynonenal (4-HNE).
*ROS↓,
*IL6↓,
*4-HNE↓,
*other↝, Together, our data support the idea that changes in diet, such as an increase in K(+) intake, may be important in the prevention of AD onset as a non-pharmacological therapy.

4296- QC,    A Flavonoid on the Brain: Quercetin as a Potential Therapeutic Agent in Central Nervous System Disorders
- Review, AD, NA
*Inflam↓, Commonly recognized as an anti-inflammatory agent, quercetin not only limits capillary vessel permeability by inhibiting hyaluronidase but also blocks cyclooxygenases and lipoxygenases.
*COX2↓,
*5LO↓,
*antiOx↑, well-known antioxidant (recognized as one of the most potent antioxidant flavonoids, considered to be stronger than vitamin C or tocopherols
*BioAv↝, Quercetin-Loaded Nanocarriers—New Delivery to Better Availability
*GPx↑, Que at two higher doses improved the antioxidant enzymes (glutathione peroxidase, superoxide dismutase (SOD), Na+/K+-ATPase) supplies and elevated the levels of ACh
*SOD↑,
*Ach↑,
*4-HNE↓, whereas the levels of peroxidation product, 4-HNE, were reduced in the striatum
*CREB↑, A recent study showed a positive influence on the expression of the hippocampal FoxG1/CREB/BDNF signaling pathway [93]
*BDNF↑,
*ROS↓, quercetin exerted antioxidant (reducing ROS, increasing SOD, GST, GSH activity) as well as anti-inflammatory activity (suppressing IL-1β, IL-6, TNF-α, COX-2, microglial activation) [
*GSH↑,
*IL1β↓,
*IL6↓,
*TNF-α↓,

4311- VitB1/Thiamine,    Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy
- in-vivo, AD, NA
*Aβ↓, Thiamine deficiency exacerbates amyloid beta (Aβ) deposition, tau hyperphosphorylation and oxidative stress.
*p‑tau↓, BFT activates the Nrf2/ARE pathway and is a promising therapeutic agent for the treatment of diseases with tau pathology, such as AD
*ROS↓,
*cognitive↑, Benfotiamine (BFT) rescued cognitive deficits and reduced Aβ burden in amyloid precursor protein (APP)/PS1 mice.
*OS↑, Chronic dietary treatment with BFT increased lifespan, improved behavior, reduced glycated tau, decreased NFTs and prevented death of motor neurons.
*Mood↑,
*neuroP↑,
*Inflam↓, BFT administration significantly ameliorated mitochondrial dysfunction and attenuated oxidative damage and inflammation.
*NRF2↑, BFT and its metabolites (but not thiamine) trigger the expression of Nrf2/antioxidant response element (ARE)-dependent genes in mouse brain
*PGC-1α↑, BFT administration resulted in an upregulation of PGC-1α mRNA levels in P301S TG mice
*AGEs↓, BFT treatment reduced advanced glycation end products
*4-HNE↓, BFT administration led to a significant reduction in the fluorescence signal for both 3-NT and 4-HNE
*NQO1↑, Exposure to BFT upregulated the mRNA levels of NQO1 in TG mice
*COX2↓, Our findings showed that BFT treatment induced a significant decrease in COX-2 (Fig. 7E, P < 0.05), TNF-α (Fig. 7F, P < 0.05), IL-1β (Fig. 7H, P < 0.05), and NF-κB p65
*TNF-α↓,
*IL1β↓,
*NF-kB↓,
*GSK‐3β↓, Exposure to BFT improves cognitive impairment and reduces the amyloid burden in APP/PS1 TG mice in a dose-dependent fashion and was reported to diminish tau phosphorylation, which was attributed to decreased GSK-3β activity (26).


Showing Research Papers: 1 to 5 of 5

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

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

4-HNE↓, 5,   antiOx↑, 1,   Catalase↑, 1,   Ferroptosis↓, 1,   GPx↑, 2,   GSH↑, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 5,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

CREB↑, 1,   FAO↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   cl‑Casp3↓, 1,   Ferroptosis↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   TRPM7↓, 1,   TRPM7⇅, 1,  

Migration ⓘ

5LO↓, 1,   NFAT↓, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 2,   IL6↓, 2,   Inflam↓, 4,   NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,  

Functional Outcomes ⓘ

cognitive↑, 3,   Mood↑, 1,   neuroP↑, 2,   OS↑, 1,  
Total Targets: 42

Scientific Paper Hit Count for: 4-HNE, 4‑Hydroxynonenal
1 Carvacrol
1 Hydrogen Gas
1 Potassium
1 Quercetin
1 Vitamin B1/Thiamine
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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