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, NA
*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, NA
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.

4529- MAG,    Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A Review
- Review, Diabetic, NA
*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, NA - Review, Park, NA - Review, Diabetic, NA
*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, NA
*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, 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 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   TCA↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   JNK↑, 1,   MAPK↑, 1,   p27↓, 1,  

Transcription & Epigenetics ⓘ

pRB↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   mTOR↓, 1,   Nanog↓, 1,   OCT4↓, 1,   SOX2↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,  

Protein Aggregation ⓘ

AGEs↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   Obesity↓, 1,   Risk↓, 1,   Wound Healing↑, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

Mitochondria & Bioenergetics ⓘ

Insulin↓, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   CRM↑, 1,   glucose↓, 2,   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,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,   GSK‐3β↓, 1,  

Immune & Inflammatory Signaling ⓘ

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

Synaptic & Neurotransmission ⓘ

p‑tau↓, 2,  

Protein Aggregation ⓘ

AGEs↓, 5,   Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 2,   cardioP↑, 1,   cognitive↑, 2,   hepatoP↑, 2,   memory↑, 1,   Mood↑, 1,   neuroP↑, 4,   OS↑, 1,   RenoP↑, 1,   toxicity↝, 1,  
Total Targets: 62

Scientific Paper Hit Count for: AGEs, Advanced Glycation End Products
2 Vitamin B1/Thiamine
1 Chlorogenic acid
1 chitosan
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

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