cAMP Cancer Research Results
cAMP, cyclic adenosine monophosphate: Click to Expand ⟱
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cAMP (cyclic adenosine monophosphate) is a secondary messenger molecule that plays a crucial role in various cellular processes, including cell signaling, metabolism, and gene expression. In the context of cancer, cAMP has been found to have both tumor-promoting and tumor-suppressing effects.
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Scientific Papers found: Click to Expand⟱
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner
*Inflam↓, LA and ALA attenuate neuroinflammation by modulating inflammatory signaling.
*other↝, ratio of LA to ALA in typical Western diets is reportedly 8–10:1 or higher, which is rather higher than the ideal ratio of LA to ALA (1–2:1) required to reach the maximal conversion of ALA to its longer chain PUFAs
*other↝, LA and ALA are essential PUFAs that must be obtained from dietary intake because they cannot be synthesized de novo
*neuroP↑, several studies have also suggested that lower dietary intake of LA influences AA metabolism in brain and subsequently causes progressive neurodegenerative disorders
*BioAv↝, LA cannot be synthesized in the human body
*adiP↑, study suggested that LA-rich oil consumption leads to the high levels of adiponectin in the blood [114], which could stimulate mitochondrial function in the liver and skeletal muscles for energy thermogenesis
*BBB↑, Although LA can penetrate the BBB, most of the LA that enters the brain cannot be changed into AA [48,49], and 59 % of the LA that enters the brain is broken down by fatty acid β-oxidation
*Casp6↓, In neurons, LA and ALA attenuate the activation of cleaved caspase-3/-9, p-NF-Kb and the production of TNF-a, IL-6, IL-1b, and ROS by binding GPR40 and GPR120.
*Casp9↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*ROS↓,
*NO↓, LA reduces NO production and inducible nitric oxide synthases (iNOS) protein expression in BV-2 microglia
*iNOS↓,
*COX2↓, ALA increases antioxidant enzyme activities in the brain [182] and inhibits the activation of COX-2 in AD models
*JNK↓, ALA has also been shown to suppress the activation of c-Jun N-terminal kinases (JNKs) and p-NF-kB p65 (Ser536), which is involved in inflammatory signaling
*p‑NF-kB↓,
*Aβ↓, and to inhibit Aβ aggregation and neuronal cell necrosis
*BP↓, LA also improves blood pressure, blood triglyceride and cholesterol levels, and vascular inflammation
*memory↑, One study suggested that long-term intake of ALA enhances memory function by increasing hippocampal neuronal function through activation of cAMP response element-binding protein (CREB) [192], extracellular signal-regulated kinase (ERK), and Akt signa
*cAMP↑,
*ERK↑,
*Akt↑,
cognitive?, Furthermore, ALA administration inhibits Aβ induced neuroinflammation in the cortex and hippocampus and enhances cognitive function
*cognitive↑, highlights β-caryophyllene's ability to mitigate key contributors to sleep loss-induced cognitive impairment, such as inflammation, oxidative stress, neuronal death, and reduced neuroplasticity
*Inflam↓,
*ROS↓,
*TLR4↓, by modulating various signaling pathways, including TLR4/NF-κB/NLRP3, MAPK, Nrf2/HO-1, PI3K/Akt, and cAMP/PKA/CREB.
*NF-kB↓,
*NLRP3↓,
*MAPK↓,
*NRF2↑,
*HO-1↑,
*PI3K↑,
*Akt↑,
*cAMP↑,
*PKA↑,
*CREB↑,
*ALAT↓, D-carvone significantly enhanced liver functions (ALT, AST), oxidant/antioxidant
status (MDA, SOD, GSH, total antioxidant capacity; TAC), as well as histopathological changes.
*AST↓, administration with D-carvone (50 mg/kg, bw) significantly reduced serum ALT and AST to 54.8% and 51% compared to the CCl4 model group, respectively
*MDA↓, decreased the MDA levels to 50.7%, while it restored the depleted GSH and SOD
levels to 233% and 221.5%, respectively
*SOD↑,
*GSH↑,
*TAC↑,
*eff↑, D-carvone effectively attenuated the progression of liver fibrosis, evident by the decreased collagen deposition and fibrosis score by Masson trichrome staining (MT) and α-SMA protein expression
*TGF-β1↓, significant downregulation of the pro-fibrogenic markers TGF-β1 and SMAD3 and upregulation of MMP9.
*SMAD3↓,
*MMP9↑,
*NRF2↑, D-carvone promotes the Nrf2 signaling pathway which might contribute to the antioxidative activity of D-carvone
*antiOx↑,
*hepatoP↑,
*Inflam↓, D-carvone administration appreciably reduced the inflammatory cells’ infiltration and pro-inflammatory modulators release provoked by liver injury
*NF-kB↓, D-carvone include downregulation of NF-κB
*NO↓, D-carvone has been reported to diminish the excessively produced NO by macrophages and Kupffer cells in the injured liver
*cAMP↑, carvone has been found to activate the cyclic adenosine monophosphate (cAMP) signaling pathway
*ROS↓, by Inhibiting Oxidative Stress
*Aβ↓, emodin (especially 80 mg/kg/d) reduced the levels of β-amyloid and tau phosphorylation, decreased the levels of β-site amyloid precursor protein-cleaving enzyme 1, and improved the activity of protein phosphatase 2A.
*p‑tau↓,
*PP2A↑,
*cAMP↑, hippocampi of HCY-E40 and HCY-E80 rats, the neuron numbers, levels of synaptic proteins, and phosphorylation of the cAMP responsive element-binding protein at Ser133 were increased
*5LO↓, In addition, depressed microglial activation and reduced levels of 5-lipoxygenase, interleukin-6, and tumor necrosis factor α were also observed.
*IL6↓,
*TNF-α↓,
*ROS↓, Lastly, hyperhomocysteinemia-induced microangiopathic alterations, oxidative stress, and elevated DNA methyltransferases 1 and 3β were rescued by emodin.
*DNMT1↓,
*ROS↓, PEMF treatment significantly counteracted H2O2- and Aβ-induced cytotoxicity by restoring cell viability, reducing reactive oxygen species production, and improving catalase activity.
*Catalase↑,
*MMP↑, PEMFs preserved the mitochondrial membrane potential and decreased caspase-3 activation and chromatin condensation
*Casp3↓,
*p‑ERK↓, Mechanistically, PEMFs inhibited ERK phosphorylation and enhanced cAMP levels, CREB phosphorylation, and BDNF expression
*cAMP↑,
*p‑CREB↑,
*BDNF↑,
*neuroP↑, PEMFs modulate multiple stress response systems, promoting neuroprotection under oxidative and amyloidogenic conditions.
*Inflam↓, PEMF-induced CM was capable of enhancing the migration of chondrocytes and MSCs as well as mitigating cellular inflammation and apoptosis.
*Apoptosis↓,
*other↑, modulating the paracrine function of MSCs for the enhancement and re-establishment of cartilage regeneration in states of cellular stress.
*PGE2↓, studies showing PEMF inhibition of the PGE2 and cycloxigenase-2 (COX-2) pathways, reducing the expression of pro-inflammatory cytokines (IL-6, IL-8) while augmenting anti-inflammatory factors (cAMP, IL-10) in synovial fibroblasts from bovine and ost
*COX2↓,
*IL6↓,
*IL8↓,
*cAMP↑,
*IL10↑,
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Functional Outcomes(tgid=23) ⓘ
cognitive?, 1,
Total Targets: 1
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↑, 1, HO-1↑, 1, MDA↓, 2, NRF2↑, 3, ROS↓, 6, SOD↑, 2, TAC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
adiP↑, 1, ALAT↓, 1, cAMP↑, 7, CREB↑, 1, p‑CREB↑, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 2, Apoptosis↓, 1, Casp3↓, 2, Casp6↓, 1, Casp9↓, 2, iNOS↓, 2, JNK↓, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, other↑, 1, other↝, 2,
DNA Damage & Repair(tgid=10) ⓘ
DNMT1↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↑, 1, p‑ERK↓, 1, PI3K↑, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, MMP9↑, 1, PKA↑, 1, SMAD3↓, 1, TGF-β1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 3, IL10↑, 1, IL1β↓, 2, IL2↓, 1, IL6↓, 4, IL8↓, 1, INF-γ↓, 1, Inflam↓, 5, NF-kB↓, 2, p‑NF-kB↓, 1, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 1, ChAT↑, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, NLRP3↓, 1, PP2A↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, eff↑, 2, Half-Life↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 1, IL6↓, 4,
Functional Outcomes(tgid=23) ⓘ
cognitive↑, 3, hepatoP↑, 1, memory↑, 1, neuroP↑, 3,
Total Targets: 71
Scientific Paper Hit Count for: cAMP, cyclic adenosine monophosphate
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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