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⟱

6462-

1,8-Cin,

Modes of Action of 1,8-Cineol in Infections and Inflammation

Review,

Var,

Review,

AD,

*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation

7953-

BuckWS,

RT,

Review of the protective effects of rutin on the metabolic function as an important dietary flavonoid

Review,

Nor,

*GastroP↑, The cytoprotective effects of rutin, including gastroprotective, hepatoprotective, and anti-diabetic effects, have been shown in several studies.
*hepatoP↑,
*AntiDiabetic↑,
*Inflam↓, rutin has several pharmacological effects such as anti-inflammatory and anti-glycation activities.
*BioAv↓, Rutin is absorbed more slowly than quercetin because rutin is hydrolyzed by some bacterial populations with rhamnosidase activity and its hydrophilic moiety is removed, whereas quercetin is absorbed from the small intestine in rats
*LDL↓, Rutin inhibited low-density lipoprotein (LDL) peroxidation and the Fenton reaction
*Fenton↓,
*AGEs↓, rutin and circulating metabolites of rutin can inhibit early glycation product formation, including both fluorescent and non-fluorescent AGEs induced by glucose glycation of collagen in vitro
*GSH↑, In addition, it prevented glutathione depletion in animals
*Dose↝, Rutin (10 mg/kg/daily/5 days) promoted colonic healing in TNBS rats.

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/DDIT3↑, ↑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/PTGS2↓, ↓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/PTGS2↓,
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

6873-

FA,

Ferulic acid: extraction, estimation, bioactivity and applications for human health and food

Review,

Nor,

*Inflam↓, This abundant phenolic compound exhibits significant antioxidant capacity and a broad spectrum of therapeutic effects, including anti‐inflammatory, antimicrobial, anticancer, antidiabetic, cardiovascular and neuroprotective activities.
*AntiBio↑,
AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*neuroP↑,
*ROS↓, FA is also a sports supplement that helps to remove oxidative stress from muscle tissue during fatigue.
*antiOx↑, FA has been shown to have powerful antioxidant effects.
*AGEs↓, The production of advanced glycation end‐products (AGEs) and xanthine oxidase activity was reduced by the use of FA
*Catalase↑, reduce ROS levels, boost (CAT) and SOD levels, and improve HEK293 cell viability.
*SOD↑,

7917-

IVT,

A review on the pharmacological effects of vitexin and isovitexin

Review,

Nor,

Review,

AD,

*antiOx↑, anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects.
*AntiCan↑,
*Inflam↓,
*neuroP↑,
*AChE↓, Anti-Alzheimer's disease Vitexin/isovitexin In vitro ChE enzyme assay Vitexin: IC 50 = 12.16 ± 3.58 (AChE) IC 50 = 6.73 ± 0.08 (BChE) IC 50 = 51.07 ± 3.31(BACE1) Isovitexin: IC 50 = 6.24 ± 1.15 (AChE) IC 50 = 6.48 ± 0.43 (BChE) IC 50 ≥ 100 (BA
*BChE↓,
*BACE/β-secretase↓,
*Stroke↓, Data showed that vitexin exhibits protective effect against cardiac ischemia/reperfusion (I/R) injury through inhibiting the I/R-induced decrease in coronary flow
*AntiAg↓, Vitexin-containing lime leaf significantly inhibited platelet aggregation in a concentration-dependent manner
*AntiDiabetic↑, Administered orally, vitexin and isovitexin significantly reduced postprandial blood glucose both in sucrose loaded normoglycemic mice and sucrose induced diabetic rat
*AGEs↓, vitexin and isovitexin, as AGE inhibitors,
*IL1β↓, inhibition in the pro-inflammatory cytokines such as IL-1β, IL6, IL-8, TNF-α,
*IL6↓,
*IL8↓,
*TNF-α↓,
*Obesity↓, Protective effects against obesity
*BioAv↝, Unusually, vitexin and isovitexin are poorly absorbed in the gastrointestinal tract [61]. They directly reached the colon where they were hydrolysed by the gut microflora through deglycosylation and ringopening of the heterocyclic C ring
*BioAv↓, oral bioavailability of vitexin was much low (approximately 5%

7903-

IVT,

Inhibition of advanced glycation end products by Isovitexin alleviates intestinal damage: Toward dietary strategies for gut health

in-vivo,

Nor,

n vivo Caenorhabditis elegans

*AGEs↓, Results demonstrated that ISV effectively inhibited AGEs formation in bovine serum albumin (BSA)-
*TAC↑, In C. elegans, ISV reduced AGEs accumulation, enhanced antioxidant capacity, and improved intestinal barrier function.
*IBI↑,
*TJ↑, upregulated tight junction proteins, and suppressed oxidative stress and apoptosis.
*ROS↓,
*Apoptosis↓,

7891-

IVT,

VT,

Effects of C-glycosylation on anti-diabetic, anti-Alzheimer's disease and anti-inflammatory potential of apigenin

NA,

AD,

*AntiDiabetic↑, Vitexin and isovitexin, naturally occurring C-glycosylated derivatives of apigenin, have been known to possess potent anti-diabetic, anti-Alzheimer's disease (anti-AD), and anti-inflammatory activities.
*Inflam↓,
*AGEs↓, isovitexin was found as the most potent inhibitor against RLAR, HRAR, AGE, AChE, and BChE while vitexin showed the most potent PTP1B inhibitory activity.
*AChE↓,
*BChE↓,
*PTP1B↓,

8105-

KAE,

Chemo-preventive and therapeutic effect of the dietary flavonoid kaempferol: A comprehensive review

Review,

Var,

Apoptosis↑, It induces apoptosis (HeLa cervical cancer cells), decreases cell viability (G2/M phase), downregulates phosphoinositide 3-kinase (PI3K)/AKT
tumCV↓,
TumCCA↑,
PI3K↓,
Akt↓,
EMT↓, suppresses protein expression of epithelial-mesenchymal transition (EMT)-related markers including N-cadherin, E-cadherin, Slug, and Snail, and metastasis-related markers such as matrix metallopeptidase 2 (MMP-2).
N-cadherin↓,
E-cadherin↓, nhibition of N‐cadherin, E‐cadherin, Slug, Snail, and MMP‐2, 9, and cathepsin B, D
Slug?,
Snail?,
MMP2↓,
MMP9↓,
CTSB↓,
CTSD↓,
Casp3↑, Activation of caspase signals such as caspase‐3, ‐8, and ‐9
Casp8↑,
Casp9↑,
TIMP2↓, Down‐regulation of phosphorylated TIMP2, AKT, and MMP2 levels
Akt↓,
TumCD↑, Induction of cell apoptotic cell death, intracellular free calcium elevation, and mitochondrial membrane potential disruption.
i-Ca+2↑,
MMP↓,
*ROS↓, Enhances the concentrations of superoxide dismutase, catalase, glutathione peroxidase, and glutathione‐S‐transferase.
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*AST↓, Lowers aspartate aminotransferase, alanine aminotransferase, malondialdehyde (MDA).
*ALAT↓,
*MDA↓,
*CYP2E1↓, Decreases activity of hepatic microsomal enzyme cytochrome 2E1 (CYP2E1) expression
*NRF2↑, Increases mRNA and protein expression of Nrf2‐regulated genes
*AGEs↓, Suppresses advanced glycation end products (AGEs)‐ receptor.
*IL6↓, Reduces levels of IL‐6, TNF‐α, and NF‐κB.
*TNF-α↓,
*NF-kB↓,
*Casp3↓, Lowers expressions of Caspase‐3 and Bax,
*BAX↓,
*antiAll↑, Antiallergic Inhibits COX2‐mediated production of prostaglandin D2 and prostaglandin F2α.
*COX2/PTGS2↓,
*PGE2↓,
*RUNX2↑, Increases expression of the osteoblast‐activated factors RUNX‐2, BMP‐2, osterix, collagen I, and SQSTM1/p62
*BMP2↑,
*COL1↑,
*p62↑,
*FASN↓, Reduces expressions of lipin1, FASN, LPAATθ (lysophosphatidic acid acyltransferase), SREBP‐1C (fatty acid synthetic proteins), and DGAT1 (triglyceride synthetic enzymes).
*DGAT1↓,
FOXP3↑, kaempferol significantly enhanced the inhibitory effect of proliferation, increased the FOXP3 expression level,
DNAdam↑, s induction of DNA damage, enhancement DNA condensation
ROS↑, anti‐cancer property is mainly defined by ROS accumulation due to catalase inhibition as depicted in Figure 2
Catalase↓,
*ROS↓, (A/R)‐induced injury of cardiomyocytes by increasing cell viability, lowering LDH release, reducing A/R‐induced ROS generation, loss of Δψm, and release of cytochrome c from mitochondria into cytosol.
*MMP↑,
*Cyt‑c↓,

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/CDKN1B↓,
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↓,

7826-

QC,

MBS,

Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review

Review,

AD,

Review,

Stroke,

Review,

Park,

*Stroke↓, quercetin improved AD, ischemic stroke, and Parkinson’s disease, as well as aging, neuroinflammation, and daily intakes of advanced glycation end products (AGEs) or alumimum-induced cognitive impairments.62
*Inflam↓,
*AGEs↓,
*cognitive↑, quercetin (100 mg/kg, intragastrically, i.g.) to 6 month old 3xTg-AD mice for one year significantly prevented cognitive impairments, β-amyloidosis, and tauopathy.
*memory↑, clinical trial indicated that the memory recall improved in the early stage AD patients who consume quercetin-enriched onion powder
*Dose↝, (containing 80 mg quercetin aglycone) daily for 4 weeks compare to those who take white onion powder (containing less than 5 mg quercetin aglycone),
*neuroP↑, implying its great neuroprotective potentials in AD.65
*p‑tau↓, quercetin inhibited tau hyperphosphorylation in a cell model induced by okadaic acid
*GSK‐3β↓, through suppressing tau phosphorylationrelated kinases, such as GSK-3β and CDK5
*CDK5↓,

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/PTGS2↓, 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 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

antiAll↑, 1, AntiArt↑, 1, AntiBio↑, 1, Stroke↓, 2,

Redox & Oxidative Stress(tgid=1) ⓘ

4-HNE↓, 1, antiOx↑, 5, Catalase↑, 4, CYP2E1↓, 2, Fenton↓, 1, GPx↑, 4, GSH↑, 3, GSTs↑, 1, HDL↑, 1, HO-1↓, 1, Keap1↓, 1, lipid-P↓, 2, MDA↓, 3, NQO1↑, 1, NRF2↑, 3, ROS↓, 10, SOD↑, 5, SOD1↑, 1, TAC↑, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

Insulin↓, 1, MMP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1, AMPK↑, 1, CRM↑, 1, DGAT1↓, 1, FASN↓, 1, glucose↓, 3, glucose↝, 1, GlucoseCon↑, 1, GLUT2↑, 1, glyC↓, 1, HMG-CoA↓, 1, LDL↓, 1,

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1, BAX↓, 1, BMP2↑, 1, Casp3↓, 2, Casp9↓, 1, Cyt‑c↓, 1, Fas↓, 1, HGF/c-Met↑, 1, iNOS↓, 1, MAPK↓, 2,

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1, GRP78/BiP↑, 1, GRP94↑, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↓, 1, p‑ERK↑, 1, GSK‐3β↓, 3, RUNX2↑, 1,

Migration(tgid=13) ⓘ

AntiAg↓, 1, CDK5↓, 1, COL1↑, 1, PTP1B↓, 1, TJ↑, 1, VCAM-1↓, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2, GastroP↑, 2, IBI↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 3, ICAM-1↓, 1, IL10↑, 1, IL1β↓, 4, IL4↓, 1, IL6↓, 4, IL8↓, 1, Inflam↓, 9, MUC2↓, 1, NF-kB↓, 4, PGE2↓, 2, TLR4↓, 2, TNF-α↓, 4,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 3, BChE↓, 2, BDNF↑, 1, GABA↑, 1, p‑tau↓, 3,

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 15, Aβ↓, 4, BACE/β-secretase↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2, BioAv↑, 5, BioAv↝, 2, Dose↝, 3, eff↑, 2, Half-Life↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, AST↓, 1, GutMicro↑, 1, IL6↓, 4, MUC19↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1, AntiDiabetic↑, 8, cardioP↑, 3, cognitive↑, 3, hepatoP↑, 5, memory↑, 3, Mood↑, 1, neuroP↑, 10, Obesity↓, 2, OS↑, 1, RenoP↑, 2, toxicity↓, 1, toxicity↝, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 115

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

3 Isovitexin
2 Vitamin B1/Thiamine
1 1,8-Cineole
1 buckwheat sprouts
1 Rutin
1 Chlorogenic acid
1 chitosan
1 Chrysin
1 D-limonene
1 Ferulic acid
1 Vitexin
1 Kaempferol
1 Magnolol
1 Metformin
1 Quercetin
1 Mung Bean Sprouts

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(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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