AChE Cancer Research Results

AChE, acetylcholinesterase: Click to Expand ⟱
Source:
Type:
AChE is an enzyme that rapidly hydrolyzes the neurotransmitter acetylcholine into choline and acetate, terminating cholinergic signals.
- In some cancers, studies have reported reduced AChE activity, which may contribute to an accumulation of acetylcholine.
- Lower levels or loss of AChE expression/activity have been associated with more aggressive tumor behavior and poor prognosis, possibly due to unchecked cholinergic signaling.

For AD (Alzheimer's), AChE inhibitors are used, to allow ACh, and ChAT to increase along with acetyl-CoA
-Natural AChE inhibitors: Ferulic Acid, Caffeic Acid, Rosmarinic Acid, Sage
-AChE inhibitors only temporarily relieve some of the disease’s cognitive symptoms and do not stop the patient’s cognitive loss
-adverse effects such as disorientation, falls, dizziness, and fatigue may occur with these medications and should be used only as recommended

- Natural AChE inhibitors paper
Scientific Papers found: Click to Expand⟱
6400- ANE,  FEO,    A comprehensive review of the neurological effects of anethole
- Review, AD, NA
*neuroP↑, Preclinical studies have suggested several pharmacological effects for anethole including neuroprotective properties.
*antiOx↓, Anethole's principal anti-oxidant abilities are due to three mechanisms: increased antioxidant enzyme activity, free radical scavenging, and metal ion chelation
*ROS↓,
*Inflam↓, Anti-inflammatory properties of Anethole
*TNF-α↓, TA decreased inflammatory edema by reducing the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukine (IL)-1β, and IL-6
*IL1β↓,
*IL6↓,
*motorD↑, TA has been found to protect against cerebral ischemia, improve motor coordination, lower brain water content, and attenuate excitatory mediators.
*MAOA↓, potentially by inhibiting brain MAO-A activity and the reduction of oxidative stress
*memory↑, The effect of fennel has been studies on memory function in rodents. In this regards, various studies have determined that this plant, which is rich in anethole, improved memory
*AChE↑, investigation revealed that fennel extract strongly suppressed acetylcholinesterase.
*PI3K↑, anethole boosted the expression of phosphoinositide 3-kinases (PI3K), protein kinase B (PKB), also known as AKT, and the mammalian target of rapamycin (mTOR) genes in the hippocampus.
*Akt↑,
*mTOR↑,

5252- MAG,    Insights on the Multifunctional Activities of Magnolol
- Review, Var, NA
BioAv↓, However, the low water solubility, the low bioavailability, and the rapid metabolism of magnolol dramatically limit its clinical application.
*Inflam↓, biological activities of magnolol, including anti-inflammatory, antimicroorganism, antioxidative, anticancer, neuroprotective, cardiovascular protection, metabolism regulation, and ion-mediating activity.
*Bacteria↓,
*antiOx↑,
*neuroP↑,
*cardioP↑,
CYP1A1↓, Magnolol isreported to inhibit the activity of CYP1A with an IC50value of 1.62 𝜇M,
*PPARγ↑, greatly upregulate the expression of PPAR𝛾 and suppress the expression of NF-𝜅B signaling, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) and the production of ROS in bronchoalveolar lavage fluid
*NF-kB↓,
*COX2↓,
*iNOS↓,
*ROS↓,
Apoptosis↑, Pretreatment of combina-tion of magnolol with honokiol significantly decreases cellviability and proliferation and increases cell apoptosis
TumCCA↑, Magnolol at lower doses can cause cell cycle arrest atG0/G1 phase, decrease the expression of cyclin D1, cyclin A,and CDK2, and increase the expression of p21
cycD1/CCND1↓,
cycA1/CCNA1↓,
CDK2↓,
P21↑,
TumCG↓, magnolol significantly inhibits cell growth,migration, and invasion, accompanied by decreased expres-sion of Ki67, proliferating cell nuclear antigen (PCNA),matrix metalloproteinases 2 (MMP-2),
TumCMig↓,
TumCI↓,
Ki-67↓,
PCNA↓,
MMP2↓,
MMP9↓,
MMP7↓,
DNAdam↑, In nonsmall cell lung cancer A549, H441, and H520 celllines (NSCLC), magnolol selectively induces DNA fragmen-tation, decreases mitochondrial membrane potential (Δ𝜓m),and inhibits cell proliferation
MMP↓,
TumCP↓,
selectivity↑, However, there is no obvious cytotoxicity of magnololto normal human bronchial epithelial cells.
PI3K↓, magnolol activates the expression of p38 and JNK and attenuates the activity of PI3K/Akt and ERK1/2 in A549 cells [
Akt↓,
H2O2↓, magnolol decreases the production of H2O2 and the expression of HIF-1𝛼 and increases the degradationof HIF-1𝛼.
Hif1a↓,
*BDNF↑, neurotrophic factor (BDNF) and glial fibrillary acidic protein(GFAP) are downregulated ... effectively reverses the effects
*NRF2↑, Magnolol inhibits NF-𝜅B and MAPK signaling pathways and apoptosis and activates NRF2/KEAP1
*AChE↑, table 1

3947- Shank,    Convolvulus pluricaulis (Shankhapushpi) ameliorates human microtubule-associated protein tau (hMAPτ) induced neurotoxicity in Alzheimer's disease Drosophila model
- in-vivo, AD, NA
*OS↑, C. pluricaulis significantly offsets hMAPτ induced early death and extends the lifespan and diminishes the level of τ protein in tauopathy Drosophila.
*antiOx↑, C. pluricaulis also enhances the antioxidant enzyme activities and ameliorates the τ-induced oxidative stress and restore the depleted AChE activity in the fly model.
*ROS↓,
*AChE↑,
*neuroP↑, also reveals that it is a potent neuroprotective agent
*memory↑, Treatment using C. pluricaulis is enhancing the memory and increased AChE activity in hippocampal regions associated with the learning and memory functions in the young and old mice was reported

6460- TUR,  CUR,    Neuroprotective Effect of Turmeric Extract in Combination with Its Essential Oil and Enhanced Brain Bioavailability in an Animal Model
- in-vivo, AD, NA
*memory↑, Aluminum impairs spatial learning and memory, which was significantly reversed with TE+EO by 28.6% (25 mg/kg) and 39.4% (50 mg/kg).
*lipid-P↓, A significant reduction in aluminum-induced lipid peroxidation was observed
*GSH↑, Also, the levels of glutathione, acetylcholinesterase, and catalase were improved with TE+EO.
*AChE↑, Our study results show that the levels of AChE decreased in response to Al, and TE+EO elevated it to the normal levels.
*Catalase↑,
*BioAv↑, The enhancement of brain and plasma bioavailability even at low dose (HED 142 mg in 70 kg adult) was due to the presence of turmerones in TE+EO, which acts as inhibitors of the p-glycoprotein pathway, the significant bottleneck in curcumin absorpti
*P-gp↓,
*BioAv↑, curcumin alone vs. curcuminoids with turmerones, which showed a sixfold increase in the bioavailability with the latter
*SOD↑, increase in the levels of GSH, CAT, SOD, and total proteins.
*BBB↑, The observed effect of TE+EO could be linked with its ability to cross the blood-brain barrier, bind to redox metal ions, and neutralize free radicals.
*ROS↓,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

CYP1A1↓, 1,   H2O2↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

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

PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,   MMP2↓, 1,   MMP7↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 2,   Catalase↑, 1,   GSH↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 4,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   iNOS↓, 1,  

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

mTOR↑, 1,   PI3K↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

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

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↑, 4,   BDNF↑, 1,   MAOA↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   memory↑, 3,   motorD↑, 1,   neuroP↑, 3,   OS↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 32

Scientific Paper Hit Count for: AChE, acetylcholinesterase
1 Anethole/trans-Anethole
1 Fennel Oil/Foeniculum vulgare
1 Magnolol
1 Shankhpushpi
1 Turmerones
1 Curcumin
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#:1329  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page