condition found tbRes List
CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown

Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments caused marked increase in ChAT positive cells.

3579- CUR,  SNP,    Metal–Curcumin Complexes in Therapeutics: An Approach to Enhance Pharmacological Effects of Curcumin
- Review, NA, NA
*IronCh↑, It is well established that curcumin strongly chelates several metal ions, including boron, cobalt, copper, gallium, gadolinium, gold, lanthanum, manganese, nickel, iron, palladium, platinum, ruthenium, silver, vanadium, and zinc.
*BioAv↑, Metal–curcumin complexes increase the solubility, cellular uptake, and bioavailability and improve the antioxidant, anti-inflammatory, antimicrobial, and antiviral effects of curcumin.
*antiOx↑,
*Inflam↓,
*BioAv↑, complexes of curcumin with transition metals may provide another approach to overcome the issues associated with curcumin.
ROS↑, curcumin–metal complexes with liposomes present enhanced cellular uptake and ROS generation in cancer cells and thus cause increased cytotoxicity
*neuroP↑, Since curcumin has the ability to cross the blood–brain barrier due to its hydrophobic nature, it can strongly chelate the metal ions in the brain and prevent metal-induced neurotoxicity.
*eff↑, Curcumin with silver nanoparticle formates also increases the solubility and stability of curcumin in complexes. Curcumin reduces and caps the silver nanoparticles, which increases its stability and solubility in water

3580- CUR,    Curcumin Acts as Post-protective Effects on Rat Hippocampal Synaptosomes in a Neuronal Model of Aluminum-Induced Toxicity
- in-vivo, AD, NA
*ROS↓, curcumin post-treatment significantly improved oxidative damage and morphological alterations, and suppressed cytochrome c and caspase 3 activities
*Cyt‑c↓,
*Casp3↓,
*neuroP↑, curcumin had more therapeutic effects than protective effects in AlCI3-induced neurotoxicity.

2817- CUR,    Neuroprotection by curcumin: A review on brain delivery strategies
- Review, Nor, NA
*BioAv↝, blood–brain barrier (BBB) is the major obstacle for the delivery of curcumin into the brain, limiting its therapeutic potential.
neuroP↑, Although it appears to possess important neuroprotective properties, the utility of curcumin is limited because of its poor brain bioavailability owing to poor absorption and stability at physiological pH, high rate of metabolism, rapid systemic elim

2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, Curcumin has an outstanding safety profile and a number of pleiotropic actions with potential for neuroprotective efficacy, including anti-inflammatory, antioxidant, and anti-protein-aggregate activities.
*Inflam↓,
*antiOx↑,
*BioAv↓, despite concerns about poor oral bioavailability, curcumin has at least 10 known neuroprotective action
*AP-1↓, Curcumin inhibition of AP-1 and NF-κB-mediated transcription occurs at relatively low (<100 nM) doses and might be due to inhibition of histone acetylase (HAT) or activation of histone deacetylase (HDAC) activity
*NF-kB↓,
*HATs↓,
*HDAC↑,
Dose↑, At high doses (>3 µM) that are relevant to colon cancer but unlikely achievable with oral delivery in plasma and tissues outside of the gut, curcumin can act as an alkylating agent,10 a phase II enzyme inducer,11 and stimulate antioxidant response el
*ROS↓, We also found that curcmin reduced oxidative damage, inflammation, and cognitive deficits in rats receiving CNS infusions of toxic Aβ
*cognitive↑,
*Aβ↓, dose-dependently blocked Aβ aggregation at submicromolar concentrations

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Results for Effect on Cancer/Diseased Cells:
Dose↑,1,   neuroP↑,1,   NF-kB↓,1,   other↑,1,   ROS↑,1,  
Total Targets: 5

Results for Effect on Normal Cells:
Ach↑,1,   AChE↓,2,   AIF↓,1,   Akt↑,1,   antiOx↑,3,   AP-1↓,1,   Apoptosis↓,1,   ATP↑,1,   Aβ↓,2,   BBB↑,1,   Bcl-2↑,1,   BioAv↓,1,   BioAv↑,2,   BioAv↝,2,   cardioP↑,1,   Casp3↓,2,   Casp9↓,1,   Catalase↑,1,   ChAT↑,1,   cognitive↑,3,   COX2↓,1,   Cyt‑c↓,1,   DNAdam↓,1,   eff↑,1,   Ferritin↑,1,   GPx↑,1,   GSH↑,2,   GSK‐3β↓,1,   GSR↓,1,   H2O2↓,1,   HATs↓,1,   HDAC↑,1,   HO-1↑,1,   HO-2↓,1,   IL1β↓,2,   IL2↓,1,   IL4↓,1,   IL6↓,1,   INF-γ↓,1,   Inflam↓,4,   iNOS↓,1,   IronCh↑,2,   LDH↓,1,   LDL↓,1,   lipid-P↓,1,   MDA↓,2,   memory↑,1,   neuroP↑,6,   NF-kB↓,1,   NO↓,2,   NRF2↑,2,   PGE2↓,1,   PI3K↑,1,   ROS↓,5,   SOD↑,1,   STAT↓,1,   tau↓,1,   TNF-α↓,1,  
Total Targets: 58

Scientific Paper Hit Count for: neuroP, neuroprotective
7 Curcumin
1 Boron
1 Silver-NanoParticles
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:1105  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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