Database Query Results : Resveratrol, , cognitive

RES, Resveratrol: Click to Expand ⟱
Features: polyphenol
Found in red grapes and products made with grapes.
Resveratrol is a polyphenol compound found in various plant species, including grapes, berries, and peanuts.
• Anti-inflammatory effects, Antioxidant effects:
- Antiplatelet aggregation for stroke prevention
- BioAvialability use piperine
- some sources may use Japanese knotweed roots (Reynoutria Japonica - root) as source which might contain Emodin (laxative)
-known as Nrf2 activator, both in cancer and normal cells. Which raises controversity of use in ROS↑ therapies. Interestingly there are reports of NRF2↑ and ROS↑ in cancer cells. This raises the question of if it is a chemosensitizer. However other reports indicate NRF2 droping with Res, indicating it maybe a chemosenstizer.
- RES is also considered to be them most effective natural SIRT1↑ -activating compound (STACs).

However, in the presence of certain metals, such as copper or iron, resveratrol can undergo a process called Fenton reaction, which can lead to the generation of reactive oxygen species (ROS). The pro-oxidant effects of resveratrol are often observed at high concentrations, typically above 50-100 μM, and in the presence of certain metals or other pro-oxidant agents. In contrast, the antioxidant effects of resveratrol are typically observed at lower concentrations, typically below 10-20 μM.

Clinical trials have used doses ranging from 150 mg to 5 grams per day. Lower doses (< 1 g/day) are often well-tolerated, but higher doses might be necessary for therapeutic effects and can be associated with side effects.

-Note half-life 1-3 hrs?.
BioAv poor: min 5uM/L required for chemopreventive effects, but 25mg Oral only yeilds 20nM. co-administration of piperine
Pathways:
- usually induce ROS production in cancer cells, while reducing ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓,
- Lowers AntiOxidant defense in Cancer Cells: NRF2(typically increased), TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓(wrong direction), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD133↓, CD24↓, β-catenin↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


cognitive, cognitive: Click to Expand ⟱
Source:
Type:
Cognitive


Scientific Papers found: Click to Expand⟱
3748- CUR,  RES,  Hup,  Riv,  Gala  Natural acetylcholinesterase inhibitors: A multi-targeted therapeutic potential in Alzheimer's disease
- Review, AD, NA
*AChE↓, natural phytocompounds such as Curcumin, Varenicline, Huperrtzine, Resveratrol, and Cycloastrageno have received FDA approval to treat Alzheimer's disease
*Inflam↓, Anti-amyloidogenic, anti-inflammatory, anti-ChE, anti – secretase
*Aβ↓, Prevent cognitive impairment and associated oxidative stress by reducing plaque formation
*cognitive↑,
*ROS↓,

3099- RES,    Resveratrol and cognitive decline: a clinician perspective
- Review, Nor, NA - NA, AD, NA
*antiOx↑, In preclinical models of cognitive decline, resveratrol displays potent antioxidant activity by scavenging free radicals, reducing quinone reductase 2 activity and upregulating endogenous enzymes.
*ROS↓,
*cognitive↑,
*neuroP↑,
*SIRT1↑, By inducing SIRT1, resveratrol may promote neurite outgrowth and enhance neural plasticity in the hippocampal region
*AMPK↑, Resveratrol also induces neurogenesis and mitochondrial biogenesis by enhancing AMP-activated protein kinase (AMPK), which is known to stimulate neuronal differentiation and mitochondrial biogenesis in neurons.
*GPx↑, figure 1
*HO-1↑,
*GSK‐3β↑,
*COX2↓,
*PGE2↓, Resveratrol also inhibits pro-inflammatory enzyme (i.e., COX-1 and -2) expression, reduces NF-κB activation as well as PGE2, NO, and TNF-α production, and cytokine release
*NF-kB↓,
*NO↓,
*Casp3↓,
*MMP3↓,
*MMP9↓,
*MMP↑, resveratrol attenuated ROS production and mitochondrial membrane-potential disruption; moreover, it restored the normal levels of glutathione (GSH) depleted by Aβ1-42
*GSH↑,
*other↑, resveratrol significantly increased cerebral blood flow (CBF) in the frontal cortex of young healthy humans.
*BioAv↑, receiving 200 mg/day of resveratrol in a formulation with quercetin 320 mg [53], in order to increase its bioavailability,
*memory↑, Resveratrol supplementation induced retention of memory and improved the functional connectivity between the hippocampus and frontal, parietal, and occipital areas, compared with placebo
*GlutMet↑, Also, glucose metabolism was improved and this may account for some of the beneficial effects of resveratrol on neuronal function.
*BioAv↓, The main problems related to the therapeutic or preventive use of resveratrol are linked to its low oral bioavailability and its short half-life in serum
*Half-Life↓,
*toxicity∅, On the other hand, the tolerability and safety profile of resveratrol is very high

4285- RES,    Resveratrol Rescues Tau-Induced Cognitive Deficits and Neuropathology in a Mouse Model of Tauopathy
- in-vivo, AD, NA
*tau↓, RSV significantly inhibited tau aggregation and tau oligomer-induced cytotoxicity, and blocked the uptake of extracellular tau oligomers by N2a cells
*cognitive↑, RSV treatment effectively rescued cognitive deficits, reducing the levels of phosphorylated tau, neuroinflammation and synapse loss in the brains of mice.
*Inflam↓,

3612- RES,    Resveratrol in Alzheimer's disease: a review of pathophysiology and therapeutic potential
- Review, AD, NA
*other↑, Resveratrol demonstrates beneficial and protective effects in AD models and seems to provide a promising therapeutic alternative.
*Aβ↓, Disaggregation of Aβ-peptides
*Inflam↓, Activated microglia seem to be an important target of the neuroprotective activity of resveratrol, resulting in the reduc- tion of pro-inflammatory factors 3
*NF-kB↓, its ability to inhibit the NF-κB signaling pathway in activated microglia
*neuroP↑, Neuroprotective effects were also observed with the injection of resveratrol in rats (100 μM/5 μL),
*HO-1↑, which reduced amyloid accumulation, protected animals against neuronal death, increased antioxidant enzyme heme oxygenase-1 (HO-1) expression, and suppressed lipid peroxidation in the hippocampus.
*lipid-P↓,
*COX2↓, inhibiting the generation of TNF, APP, cyclooxygenase (COX)-2 and NF-κB phosphorylation in the hippocampus
*AMPK↑, Resveratrol is a potent activator of AMPK, thereby implicating another pathway through that its neuroprotective effects may be exerted
*Catalase↑, Resveratrol (10 μM) attenuated lipid peroxidation and upregulated antioxidant enzyme levels, such as catalase, superoxide dismutase (SOD), and glutathione reductase (GR).
*SOD↑,
*GSR↑,
*ROS↓, administration of resveratrol (10 and 20 μM) reduced ROS production in cells treated with AGEs
*MMP9↓, attenuated neuroinflammation, reduced proinflammatory markers, and decreased MMP-9 in the CSF
*cognitive↑, Resveratrol also attenuated the patients’ cognitive and functional decline
*SIRT1↑, neuroprotection is through the activation of the sirtuin 1 (SIRT1) pathway, which in turn inhibits the activation of the NF-κB signaling pathway.
*IL1β↓, reducing Aβ-induced memory and learning impairment and decreasing the expression of proinflammatory cytokines (IL-1β and IL-6)
*IL6↓,

3100- RES,    Neuroprotective effects of resveratrol in Alzheimer disease pathology
- Review, AD, NA
*neuroP↑, several studies have reported interesting insights about the neuroprotective properties of the polyphenolic compound resveratrol
*BioAv↓, However, resveratrol’s low bioavailability originating from its poor water solubility and resulting from its short biological half-life
*Half-Life↓,
*BioAv↑, encapsulation in liposomal formulations
*BBB↑, Resveratrol being a lipophilic compound can readily cross the BBB via transmembrane diffusion
*NRF2↑, resveratrol into aged cells leading to the activation of cellular Nrf2-mediated antioxidant defense systems
*BioAv↓, An oral dose of 25 mg results in less than 5 μg/mL in the serum following absorption through the gastrointestinal tract, corresponding to approximately a 1000-fold decrease in bioavailability.
*BioAv↑, Treatment with pterostilbene also produced a sevenfold rise in its oral bioavailability than the parent resveratrol
*SIRT1↑, Amongst all the naturally occurring activators of SIRT 1, resveratrol is considered to be the most effective SIRT 1 activator.
*cognitive↑, Pterostilbene has shown to be a potent modulator of cognition and cellular oxidative stress associated with AD
*lipid-P↓, Figure 2
*HO-1↑,
*SOD↑,
*GSH↑,
*GPx↑,
*G6PD↑,
*PPARγ↑,
*AMPK↑,
*Aβ↓, Lowered Aβ levels by activating AMPK pathway

3921- VitD3,  RES,    Vitamin D Combined with Resveratrol Prevents Cognitive Decline in SAMP8 Mice
- in-vivo, AD, NA
*cognitive↑, The combination of VD and RSV significantly increased time spent in target quadrant and the number of crossing via MWM test
*Aβ↓, In hippocampus, the combined intervention significantly reduced soluble Aβ42 level and BACE1 protein expression
*BACE↓,
*p‑tau↓, combined treatment significantly reduced phosphorylation of tau at serine404 and p-p53, as well as enhanced p-CREB protein expression
*p‑CREB↑,
*p‑NF-kB↓, The combination also significantly reduced GFAP and p-NFκB p65 in both hippocampus and cortex
*neuroP↑, combined intervention might exert greater neuroprotective effects in SAMP8 mice,


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

Results for Effect on Cancer/Diseased Cells:

Total Targets: 0

Results for Effect on Normal Cells:
AChE↓,1,   AMPK↑,3,   antiOx↑,1,   Aβ↓,4,   BACE↓,1,   BBB↑,1,   BioAv↓,3,   BioAv↑,3,   Casp3↓,1,   Catalase↑,1,   cognitive↑,6,   COX2↓,2,   p‑CREB↑,1,   G6PD↑,1,   GlutMet↑,1,   GPx↑,2,   GSH↑,2,   GSK‐3β↑,1,   GSR↑,1,   Half-Life↓,2,   HO-1↑,3,   IL1β↓,1,   IL6↓,1,   Inflam↓,3,   lipid-P↓,2,   memory↑,1,   MMP↑,1,   MMP3↓,1,   MMP9↓,2,   neuroP↑,4,   NF-kB↓,2,   p‑NF-kB↓,1,   NO↓,1,   NRF2↑,1,   other↑,2,   PGE2↓,1,   PPARγ↑,1,   ROS↓,3,   SIRT1↑,3,   SOD↑,2,   tau↓,1,   p‑tau↓,1,   toxicity∅,1,  
Total Targets: 43

Scientific Paper Hit Count for: cognitive, cognitive
6 Resveratrol
1 Curcumin
1 Huperzine A/Huperzia serrata
1 Rivastigmine
1 Galantamine
1 Vitamin D3
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:141  Target#:557  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page