AGEs Cancer Research Results

AGEs, Advanced Glycation End Products: Click to Expand ⟱

Source:

Type:

Advanced Glycation End Products (AGEs) are highly reactive compounds formed when proteins or lipids become non-enzymatically glycated after exposure to sugars. AGEs accumulate with age and are implicated in various chronic diseases—including Alzheimer’s disease (AD).
-AGEs bind to Aβ peptides, increasing aggregation and plaque stability.
-AGEs activate kinases like GSK-3β and p38 MAPK, promoting tau phosphorylation.
-Human brains with AD show increased AGE-modified proteins and elevated RAGE expression.
-Blocking RAGE or reducing AGEs slows cognitive decline and pathology in mice.

Strategies to Reduce AGE Burden
-Low-AGE cooking (steaming, boiling), Mediterranean diet
- reduce processed meats, sugary baked goods, and fried foods.

Scientific Papers found: Click to Expand⟱

6010-

CGA,

The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review

Review,

Nor,

*antiOx↑, mainly shown as anti-oxidant, liver and kidney protection, anti-bacterial, anti-tumor, regulation of glucose metabolism and lipid metabolism, anti-inflammatory, protection of the nervous system,
*hepatoP↑,
*RenoP↑,
AntiTum↑,
*glucose↝,
*Inflam↓,
*neuroP↑,
*ROS↓, ↓Active oxygen (ROS) , ↓Keap1,↑Nrf2, ↑SOD, ↑CAT, ↑Glutathione Peroxidase (GSH-Px), ↑Glutathione (GSH), ↓MDA
*Keap1↓,
*NRF2↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*MDA↓,
*p‑ERK↑, ↑ERK1/2 phosphorylation
*GRP78/BiP↑, ↑Glucose regulatory protein 78 (GRP78)
*CHOP↑, ↑C/EBP homologous protein (CHOP)
*GRP94↑, ↑Glucose Regulatory Protein 94 (GRP94)
*Casp3↓, ↓Caspase-9/Caspase-3
*Casp9↓,
*HGF/c-Met↑, ↑Hepatocyte Growth Factor (HGF)
*TNF-α↓, ↓Tumor Necrosis Factor-α (TNF-α)/Interferonγ (IFN-γ)
*TLR4↓, ↓TLR4
*MAPK↓, ↓MAPK signal pathway
*IL1β↓, ↓Interleukin 1β (IL-1β)/Interleukin 6 (IL-6)
*iNOS↓, ↓Inducible Nitric Oxide Synthase (iNOS)
TCA↓, ↓Tricarboxylic acid cycle (TCA) ↓Glycolysis
Glycolysis↓,
Bcl-2↓, ↓Anti-apoptotic gene Bcl-2/Bcl-XL
BAX↑, ↑Pro-apoptotic gene Bax/Bcl-XS/Bad
MAPK↑, ↑p38 mitogen-activated protein kinase (p38 MAPK)
JNK↑, ↑c-Jun N-terminal Kinase (JNK)
CSCs↓, ↓Stem cell marker genes Nanog, POU5F1, Sox2, CD44, Oct4
Nanog↓,
SOX2↓,
CD44↓,
OCT4↓,
P53↑, ↑P53
P21↑, ↑p21
*SOD1↑, ↑CuZnSOD (SOD1)/MnSOD (SOD2)
*AGEs↓, ↓Glycosylation end products (AGEs)
*GLUT2↑, ↑Glucose Transporter 2 (GLUT2)
*HDL↑, ↑High-density lipoprotein (HDL)
*Fas↓, ↓Fatty acid synthase (FAS)
*HMG-CoA↓, ↓β-hydroxy-β-methylglutamyl-CoA (HMG-CoA) reductase
*NF-kB↓, ↑NF-κB signaling pathway
*HO-1↓, ↑Nrf2/HO-1 signaling pathway
*COX2↓, ↓Cyclooxygenase-2 (COX-2)
*TLR4↓, ↓Toll-like receptor 4 (TLR4)
*BioAv↑, One route may be immediate absorption in the stomach or upper gastrointestinal tract, and the other route may be slowly absorbed throughout the small intestine.
*BioAv↝, It indicates that the bioavailability of CGA is closely related to the metabolic capacity of the organism's gut flora
TumCP↓, CGA also inhibits the proliferation, migration, and invasion of cancer cells.
TumCMig↓,
TumCI↓,

5998-

Chit,

Trial: Chitosan can help reduce AGE levels in patients with prostate cancer.

Trial,

Pca,

AGEs↓, Chitosan that can help reduce AGE (advanced glycation endproducts) levels in patients with prostate cancer.
Wound Healing↑, Chitosan is approved by the FDA for use in wound dressings
Obesity↓, been used in published clinical trials for weight loss but is not approved for the purposes of this study.

6135-

CHr,

Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review

Review,

Var,

Review,

AD,

Inflam↓, various cancers has been demonstrated and it modulates cell signaling pathways, including inflammation, angiogenesis, apoptosis, autophagy, and the cell cycle.
angioG↓,
Apoptosis↑,
TumAuto↑,
TumCCA↑,
BioAv↓, Despite its promising pharmacological activities, the clinical utility of chrysin remains limited due to its poor bioavailability, low solubility, limited permeability, and rapid metabolism.
Half-Life↓,
BioAv↓, The oral bioavailability of chrysin has been reported to range from 0.003% to 0.02%, with a maximum plasma concentration between 12 and 64 nM
*ROS↓, The study reported that chrysin administration protected the kidneys and liver of rats from oxidative damage induced by chronic ethanol consumption
*hepatoP↑, Hepatoprotective Potential
*RenoP↑, The renal protective effect of chrysin was related to increasing the antioxidant enzyme activities and decreasing the regulation of serum renal toxicity markers.
TET1↑, chrysin meaningfully induced the expression of TET1 in GC cells.
MMP9↓, hrysin might contribute to its anticancer effects by regulating MMP-9 expression.
cMyc↓, Both c-Myc and Ki-67 expressions were found to be suppressed in the tumor tissues treated with chrysin and G1-treated tumor tissues
Ki-67↓,
CBR1↓, chrysin directly interacts with CBR1, inhibiting its enzymatic activity at both the molecular and cellular levels.
ROS↑, This inhibition led to elevated intracellular ROS levels, triggering ROS-dependent autophagy
ChemoSen↑, chrysin enhances pancreatic cancer cell sensitivity to gemcitabine by inducing ferroptosis death, both in vitro and in vivo
Bax:Bcl2↑, chrysin increased the Bax/Bcl-2 expression ratio in ATC cells following treatment
PUMA↑, PUMA and Notch-1 were activated, and Slug was inactivated by chrysin treatment
NOTCH1↑,
*AntiDiabetic↑, Anti-Diabetic Potential
*neuroP↑, Neuroprotective Effects
*GABA↑, treatment of chrysin improves levels of GABA, monoamines, glutamic acid, and their metabolites in three brain regions, while also inhibiting DNA fragmentation markers like 8-HdG as well as BDNF.
*DNAdam↓,
*BDNF↑,
*memory↑, protective effects of chrysin against memory impairments associated with hippocampal neurogenesis
*AGEs↓, figure 6
*Aβ↓,
*cardioP↑, Cardioprotective Effects
*AntiArt↑, Anti-Arthritis Potential
eff↑, combination potential was higher than apigenin or chrysin alone.
eff↑, combination of quercetin enhanced the toxic effects of chrysin on the cell lines
*eff↑, neuroprotective synergistic effects of chrysin and kaempferol revealed therapeutic potential in mitigating cerebral ischemi
RadioS↑, study reported that treatment of MDA-MB-231 cells with chrysin in combination with radiation therapy (RT) caused synergistic antitumor properties.
eff↑, the combination of metformin and chrysin demonstrated pronounced synergistic cytotoxic effects on cancer cells
ChemoSen↑, chrysin was combined with a low dose of cisplatin, the resulting growth inhibition was significantly enhanced.
eff↑, demonstrating greater potency than chrysin or silver nanoparticles alone [198].

6281-

DL,

Applications of Limonene in Neoplasms and Non-Neoplastic Diseases

Review,

Var,

Review,

AD,

Review,

Diabetic,

*antiOx↑, spanning antioxidant, anti-inflammatory, antitumor, antidiabetic, neuroprotective, and gastroprotective domains.
AntiTum↑,
*AntiDiabetic↑,
*neuroP↑, The neuroprotective potential of limonene has been demonstrated in different neurodegenerative diseases (NDs), including multiple sclerosis, stroke, epilepsy, Alzheimer’s disease (AD), and anxiety
*GastroP↑,
*ROS↓, we explore its molecular mechanisms, ranging from reactive oxygen species mitigation
*toxicity↓, Its low toxicity and high bioavailability support its potential as a safe adjunct or alternative in phytotherapy.
*BioAv↑,
ChemoSen↑, combining limonene with tamoxifen increases the anticancer efficacy by inducing apoptosis in MCF 7 BC cells
BAX↑, MCF-7 cells, D-limonene treatment significantly increases the expression of Bcl-2-associated X protein (Bax) and p53 while downregulating Bcl-2, inducible nitric oxide synthase (iNOS), and COX-2
P53↓,
Bcl-2↓,
iNOS↓,
COX2↓,
eff↑, IC50 of free limonene was reported to be 985.00 μg/mL, whereas its encapsulation in chitosan nanoparticles (LimChiNPs) significantly reduced the IC50 to 650.70 μg/mL.
ROS↑, Furthermore, this dual therapy augmented intracellular reactive oxygen species production and promoted cell cycle arrest predominantly at the G1 phase via the modulation of cyclin D1 and B1 [20].
TumCCA↑,
cycD1/CCND1↓,
CycB/CCNB1↓,
TumCMig↓, migration capacity of MCF-7 cells was also markedly inhibited under the combined regimen, suggesting potential to curb metastatic progression
*lipid-P↓, Limonene therapy resulted in a decrease in lipid peroxidation levels and an increase in the level of glutathione, a major antioxidant that helps protect cells from damage
*GSH↑,
*SOD↑, Moreover, the activity of antioxidant enzymes (SOD and glutathione peroxidase (GPx)) was improved, indicating that the body’s natural defense system was functioning better again
*GPx↑,
*hepatoP↑, limonene treatment has been shown to mitigate liver damage caused by DEN/2-AAF exposure by reinforcing the antioxidant defenses in hepatic cells
*glucose↓, D-limonene consistently lowered fasting glucose and HbA1c, improved lipid profiles, and enhanced antioxidant defenses (e.g., increased SOD, CAT, and GSH levels)
*AGEs↓, D-limonene has been shown to inhibit the formation of advanced glycation end products (AGEs) through multiple mechanisms,
*Obesity↓, Notably, limonene also stimulates differentiation and glucose uptake in adipocytes, suggesting a role in counteracting insulin resistance and obesity-related metabolic dysfunction
*Aβ↓, The neuroprotective properties of limonene find expression in suppressing Aβ-induced cell death and decreasing ROS levels
*AChE↓, Further insights into the molecular mechanism of limonene’s inhibition of AChE have been provided by molecular dynamics simulations

4529-

MAG,

Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A Review

Review,

Diabetic,

*AntiDiabetic↑,
*glucose↓, magnolol administered to rats with type 2 diabetes reduced fasting blood glucose and plasma insulin levels, without affecting their body weight
*SOD↑, increase in SOD and CAT activity
*Catalase↑,
*ROS↓, Magnolol acts as a free radical scavenger which was proven in numerous in vitro and in vivo studies
*MDA↓, decrease in MDA level
*GPx↑, increase in SOD, CAT and GPx activities, decrease in MDA level and CYP2E1 activity in the liver
*CYP2E1↓,
*AGEs↓, decrease in AGEs level in kidney glomeruli
*IL10↑, increase in IL-10 level in the plasma
*neuroP↑, numerous reports on the protective effect of magnolol on the nervous system, it can be assumed that this lignan may also have neuroprotective effects in the course of diabetes
*GutMicro↑, In the case of the intestinal microflora, honokiol had a beneficial effect on obtaining microbiota homeostasis increasing the amount of Akkermansia bacteria and reducing the amount of Oscillospira bacteria

5795-

MET,

Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes

Review,

AD,

Review,

Park,

Review,

Diabetic,

*AntiDiabetic↑, Metformin has been designated as one of the most crucial first-line therapeutic agents in the management of type 2 diabetes mellitus.
*AMPK↑, acts majorly by activating AMPK (Adenosine Monophosphate-Activated Protein Kinase) in the cells and reducing glucose output from the liver.
*glyC↓, It also decreases advanced glycation end products and reactive oxygen species production in the endothelium apart from regulating the glucose and lipid metabolism
*ROS↓,
*cardioP↑, hence minimizing the cardiovascular risks.
*neuroP↑, Preclinical studies have also shown some evidence of metformin’s neuroprotective role in Parkinson’s disease, Alzheimer’s disease, multiple sclerosis and Huntington’s disease.
*Half-Life↝, The plasma half-life of metformin is 2–3 hours, and the active duration is about 6–10hrs.
*toxicity↝, Metformin use for an extended period is linked to a deficiency of vitamin B12.
*BioAv↑, Absolute bioavailability 50–60% in healthy individuals
*glucose↓, Conventionally, it is quite established that metformin lowers blood glucose primarily by its action on the liver
*AGEs↓, Metformin decreases the synthesis of AGE (“Advanced Glycation End”) product formation and hyperglycaemic-induced ROS (“Reactive Oxygen Species”) production
AntiCan↑, There is growing evidence that metformin has anti-cancer effects based on clinical and preclinical studies.
Risk↓, reported that metformin use might decrease the risk of lung cancer within T2D patients as compared to other conventional agents.
TumCP↓, Several studies on cancer cell lines have observed that metformin treatment leads to inhibition of development and proliferation and induces apoptosis of the cancer cells
Apoptosis↑,
TumCCA↑, Metformin was found to block the cell cycle in the “G(0)/G(1)” phase
cycD1/CCND1↓, and this was observed with a sharp drop in the cyclin D1 levels, pRb phosphorylation, and elevated p27(kip) expression.
pRB↓,
p27↓,
mTOR↓, as well as inhibits the mTOR pathway that is activated by insulin.
Casp↑, Metformin is also responsible for inducing caspase-dependent apoptosis along with c- JNK (“Jun N-Terminal Kinase”) activation, oxidative stress and mitochondrial depolarization.
ROS↑,
MMP↓,
ChemoSen↑, patients who received metformin along with the chemotherapy had better pathologic responses as compared to the group without metformin
*hepatoP↑, effects including cardioprotective, hepatoprotective, anti-malignant, and geroprotective effects
*CRM↑, mechanism behind the process of calorie restriction is a reduction in insulin
*Insulin↓,

4312-

VitB1/Thiamine,

Pharmacological thiamine levels as a therapeutic approach in Alzheimer's disease

Review,

AD,

*eff↑, AD patients revealed that increasing blood thiamine to pharmacologically high levels using benfotiamine has potential efficacy in treating persons with early AD.
*cognitive↑, role of thiamine in memory/cognition
*memory↑,
*GlucoseCon↑, Thiamine deficiency in normal and transgenic rodent models of AD leads to multiple AD like changes including: decreased brain glucose utilization (8), increased inflammation (9) and neuron loss (10), diminished cholinergic function (11)
*Aβ↓, and exacerbated formation of plaques and tangles (12)
*Inflam↓,
*antiOx↑, Thiamine has many other actions including acting as an antioxidant
*p‑tau↓, Total tau and tau phosphorylation are sensitive to thiamine levels. Treatment with benfotiamine, diminishes phosphorylation of tau.
*AGEs↓, Even marginal thiamine deficiency increases AGE. Benfotiamine/thiamine diminishes AGE
*Dose↝, The trial showed that benfotiamine at a dose of 600 mg per day is safe and very well tolerated in patients with early AD.

4311-

VitB1/Thiamine,

Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy

in-vivo,

AD,

mouse model

*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 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

AntiArt↑, 1,

Redox & Oxidative Stress ⓘ

4-HNE↓, 1, antiOx↑, 3, Catalase↑, 2, CYP2E1↓, 1, GPx↑, 3, GSH↑, 2, HDL↑, 1, HO-1↓, 1, Keap1↓, 1, lipid-P↓, 1, MDA↓, 2, NQO1↑, 1, NRF2↑, 2, ROS↓, 6, SOD↑, 3, SOD1↑, 1,

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, CRM↑, 1, glucose↓, 3, glucose↝, 1, GlucoseCon↑, 1, GLUT2↑, 1, glyC↓, 1, HMG-CoA↓, 1,

Cell Death ⓘ

Casp3↓, 1, Casp9↓, 1, Fas↓, 1, HGF/c-Met↑, 1, iNOS↓, 1, MAPK↓, 1,

Protein Folding & ER Stress ⓘ

CHOP↑, 1, GRP78/BiP↑, 1, GRP94↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1,

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1, GSK‐3β↓, 1,

Barriers & Transport ⓘ

GastroP↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 2, IL10↑, 1, IL1β↓, 2, Inflam↓, 3, NF-kB↓, 2, TLR4↓, 2, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

AChE↓, 1, BDNF↑, 1, GABA↑, 1, p‑tau↓, 2,

Protein Aggregation ⓘ

AGEs↓, 7, Aβ↓, 4,

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

GutMicro↑, 1,

Functional Outcomes ⓘ

AntiDiabetic↑, 4, cardioP↑, 2, cognitive↑, 2, hepatoP↑, 4, memory↑, 2, Mood↑, 1, neuroP↑, 6, Obesity↓, 1, OS↑, 1, RenoP↑, 2, toxicity↓, 1, toxicity↝, 1,
Total Targets: 71

Scientific Paper Hit Count for: AGEs, Advanced Glycation End Products

2 Vitamin B1/Thiamine
1 Chlorogenic acid
1 chitosan
1 Chrysin
1 D-limonene
1 Magnolol
1 Metformin

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#:1375  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

AGEs Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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