condition found tbRes List
TQ, Thymoquinone: Click to Expand ⟱
Features: Anti-oxidant, anti-tumor
Thymoquinone is a bioactive compound found in the seeds of Nigella sativa, commonly known as black seed or black cumin.
Pathways:
-Cell cycle arrest, apoptosis induction, ROS generation in cancer cells
-inhibit the activation of NF-κB, Suppress the PI3K/Akt signaling cascade
-Inhibit angiogenic factors such as VEGF, MMPs
-Inhibit HDACs, UHRF1, and DNMTs

-Note half-life 3-6hrs.
BioAv low oral bioavailability due to its lipophilic nature. Note refridgeration of Black seed oil improves the stability of TQ.
DIY: ~1 part lecithin : 2–3 parts black seed oil : 4–5 parts warm water. (chat ai)
Pathways:
- usually induce ROS production in Cancer cells, and lowers ROS in normal cells
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- May Low AntiOxidant defense in Cancer Cells: NRF2↓(usually contrary), GSH↓ HO1↓(contrary), 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↓, VEGF↓, FAK↓, NF-κB↓, CXCR4↓, TGF-β↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PDKs↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, 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⟱
3570- TQ,    Thymoquinone alleviates the experimentally induced Alzheimer's disease inflammation by modulation of TLRs signaling
- in-vivo, AD, NA
*Inflam↓, (TQ), the main active constituent of Nigella sativa oil, has been reported by several previous studies for its potent anti-inflammatory effect.
*Aβ↓, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*TNF-α↓, TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-a compared to AD group reach- ing 39.85, 18.22, and 30.37 versus 65.30, r
*IL1β↓,
*TLR2↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses ( p < 0.05).
*IRF3↓,
*TLR4↓, TQ inhibits TLR-2 and TLR-4 and their downstream signaling molecule in a dose independent manner
*memory↑, TQ improves learning and memory ability in AD rat model
*NF-kB↓, TQ at all levels of doses for 14 consecutive days caused a significant decrease in NF-B expression
*MyD88↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4 by 84.35% and 63.30%, the expression of MyD88 by 79.65% and 68.36%, the expression of TRIF by 25.90% and 76.75%,
*TRIF↓,
*BBB↑, t crosses the blood brain barrier and exerts diverse therapeutic effects with respect to neuroinflammation.
*cognitive↑, Thus, we can hypothesize that TQ could improve cognition and the brain morphological changes by attenuating the detrimental inflammatory effect of the pro-inflammatory cytokines release

3565- TQ,    Thymoquinone as a potential therapeutic for Alzheimer’s disease in transgenic Drosophila melanogaster model
*cognitive↑, TQ at both concentrations resulted in a significant increase in behavioral activity, a significant reduction in the amount of reactive oxygen species (ROS), and restoration of depleted superoxide dismutase (SOD) and acetylcholine esterase (AChE) acti
*ROS↓,
*SOD↑,
*AChE↝, TQ was significantly evident in AChE activity since the enzyme activity was restored to 75.38% on day 15 and 92.23% on day 30
*Aβ↓,

3564- TQ,    The Potential Neuroprotective Effect of Thymoquinone on Scopolamine-Induced In Vivo Alzheimer's Disease-like Condition: Mechanistic Insights
- in-vivo, AD, NA
*Inflam↓, Thymoquinone (TQ) has demonstrated potential in exhibiting anti-inflammatory, anti-cancer, and antioxidant characteristics.
*AntiCan↑,
*antiOx↑,
*neuroP↑, TQ provided meaningful multilevel neuroprotection through its anti-inflammatory and its PPAR-γ agonist activity.
*cognitive↑, TQ has the potential to ameliorate cognitive deficits observed in SCOP-induced AD-like model, as evidenced by the improvement in behavioral outcomes,
*Aβ↓, significant decrease in the deposition of amyloid beta (Aβ).
*PPARγ↑, TQ showed a significant upregulation for PPAR-γ, synapsin-2, and miR-9
*NF-kB↓, pretreatment of the mice with TQ significantly (p < 0.001) lowered NF-κB by 62.68%
*p‑tau↓, TQ significantly (p < 0.001) decreased Ptau by 58.33% relatively to the disease control group
*MMP↑, Pretreatment with TQ restored the mitochondrial membrane potential (MMP)
*memory↑, Poorgholam et al. (2018), who elucidated that TQ ameliorated learning functioning and memory loss in a rat model of AD
*NF-kB↓, inhibitory effect of TQ on the activation of NF-κB
*ROS↓, TQ may possess neuroprotective properties hampering the mitochondrial membrane depolarization, ROS generation, and Aβ deposition in neurotoxicity model

3563- TQ,    Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ(1–42)-infused rat model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, TQ treatment ameliorated both impaired memory performance and IFN-γ levels
*IFN-γ↑,
*neuroP↑, TQ might be a strong candidate for preventing or delaying the symptoms of AD by reducing neurotoxicity via its anti-inflammatory activity
*Inflam↓,
*cognitive↑, recovery role of TQ in cognitive functions was also demonstrated in distinct models of neurodegeneration

3560- TQ,    Protective effects of thymoquinone on D-galactose and aluminum chloride induced neurotoxicity in rats: biochemical, histological and behavioral changes
- in-vivo, AD, NA
*cognitive↑, TQ significantly improved cognition
*SOD↑, TQ significantly increased SOD and TAC and decreased AChE activities.
*TAC↑,
*AChE↓,
*MDA↓, It also decreased MDA and NO levels as well as TNF-α immunoreactivity and increased BDNF and Bcl-2 levels as well as ACh immunoreactivity.
*NO↓,
*TNF-α↓,
*Bcl-2↑,
*Ach↑,
*neuroP↑, These results indicate that TQ holds potential for neuroprotection and may be a promising approach for the treatment of neurodegenerative disorders.

3559- TQ,    Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease
- Review, AD, NA - Review, Var, NA
*antiOx↑, promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory,
*Inflam↑, anti-inflammatory activity of TQ is mediated through the Toll-like receptors (TLRs)
*AChE↓, In addition, it shows anticholinesterase activity and prevents α-synuclein induced synaptic damage.
AntiCan↑, NS plant, has been proven to have a wide range of pharmacological interventions, including antidiabetic, anticancer, cardioprotective, retinoprotective, renoprotective, neuroprotective, hepatoprotective and antihypertensive effects
*cardioP↑,
*RenoP↑,
*neuroP↑,
*hepatoP↑,
TumCG↓, potential ability to inhibit tumor growth by stimulating apoptosis as well as by suppression of the P13K/Akt pathways, cell cycle arrest and by inhibition of angiogenesis
Apoptosis↑,
PI3K↓,
Akt↑,
TumCCA↑,
angioG↓,
*NF-kB↓, TQ inhibits nuclear translocation of NF-kB which subsequently blocks the production of NF-kB mediated neuroinflammatory cytokines
*TLR2↓, TQ administration at different doses (10, 20, 40 mg/kg) significantly down-regulated the mRNA expression of TLR-2, TLR-4, MyD88, TRIF and their downstream effectors Interferon regulatory factor 3 (IRF-3)
*TLR4↓,
*MyD88↓,
*TRIF↓,
*IRF3↓,
*IL1β↓, TQ also inhibits LPS induced pro-inflammatory cytokine release like IL-1B, IL-6 and IL-12 p40/70 via its interaction with NF-kB
*IL6↓,
*IL12↓,
*NRF2↑, Nuclear erythroid-2 related factor/antioxidant response element (Nrf 2/ARE) being an upstream signaling pathway of NF-kB signaling pathway, its activation by TQ
*COX2↓, TQ also inhibits the expression of all genes regulated by NF-kB, i.e., COX-2, VEGF, MMP-9, c-Myc, and cyclin D1 which distinctively lowers NF-kB activation making it a potentially effective inhibitor of inflammation, proliferation and invasion
*VEGF↓,
*MMP9↓,
*cMyc↓,
*cycD1↓,
*TumCP↓,
*TumCI↓,
*MDA↓, it prevents the rise of malondialdehyde (MDA), transforming growth factor beta (TGF-β), c-reactive protein, IL1-β, caspase-3 and concomitantly upregulates glutathione (GSH), cytochrome c oxidase, and IL-10 levels [92].
*TGF-β↓,
*CRP↓,
*Casp3↓,
*GSH↑,
*IL10↑,
*iNOS↑, decline of inducible nitric oxide synthase (iNOS) protein expression
*lipid-P↓, TQ prominently mitigated hippocampal lipid peroxidation and improved SOD activity
*SOD↑,
*H2O2↓, TQ is a strong hydrogen peroxide, hydroxyl scavenger and lipid peroxidation inhibitor
*ROS↓, TQ (0.1 and 1 μM) ensured the inhibition of free radical generation, lowering of the release of lactate dehydrogenase (LDH)
*LDH↓,
*Catalase↑, upsurge the levels of GSH, SOD, catalase (CAT) and glutathione peroxidase (GPX)
*GPx↑,
*AChE↓, TQ exhibited the highest AChEI activity of 53.7 g/mL in which NS extract overall exhibited 84.7 g/mL, which suggests a significant AChE inhibition.
*cognitive↑, Most prominently, TQ has been found to regulate neurite maintenance for cognitive benefits by phosphorylating and thereby activating the MAPK protein, particularly the JNK proteins for embryogenesis and also lower the expression levels of BAX
*MAPK↑,
*JNK↑,
*BAX↓,
*memory↑, TQ portrays its potential of spatial memory enhancement by reversing the conditions as observed by MWM task
*Aβ↓, TQ thus, has been shown to ameliorate the Aβ accumulation
*MMP↑, improving the cellular activity, inhibiting mitochondrial membrane depolarization and suppressing ROS

3558- TQ,    Behavioral and histological study on the neuroprotective effect of thymoquinone on the cerebellum in AlCl3-induced neurotoxicity in rats through modulation of oxidative stress, apoptosis, and autophagy
- in-vivo, AD, NA
*MDA↓, TQ showed a significant decrease (P < 0.05) in levels of malondialdehyde (MDA) and nitric oxide (NO), associated with a significant increase (P < 0.05) in reduced glutathione (GSH) level.
*NO↓,
*GSH↑,
*neuroP↑, AD & TQ group exhibited substantial preservation of the cerebellum's histological structure, the Purkinje cells number and transverse diameter showed a high significant increase (P < 0.001) and a significant increase (P < 0.05), respectively in compa
*cognitive↑, TQ showed improvement in behavioral tests, biochemical and histological findings.

3557- TQ,    Thymoquinone protects against lipopolysaccharides-induced neurodegeneration and Alzheimer-like model in mice.
- in-vivo, AD, NA
*Inflam↓, Thymoquinone is a known anti-inflammatory agent with a strong antioxidant activity.
*antiOx↑,
*cognitive↑, LPS significantly impaired performance in the Y-maze and NORT and induced behavioural abnormalities, compared to control. These were all ameliorated by treatment with TQ (15-30mg/kg).
*TNF-α↓, TQ also significantly (P<0.05) reduced the concentration of LPS-induced TNF-α, IL-1β, AChE and expressions of amyloid-beta, microglia and β-secretase/mRNA in hippocampus and prefrontal cortex.
*IL1β↓,
*AChE↓,
*IL10↑, TQ increased IL-10/mRNA, ChaT, synaptophysin in hippocampus and PFC
*ChAT↑,
*Aβ↓, depleted synaptic protein and Aβ accumulation.

3556- TQ,    Thymoquinone alleviates the experimentally induced Alzheimer’s disease inflammation by modulation of TLRs signaling
- in-vivo, AD, NA
*Inflam↓, reported by several previous studies for its potent anti-inflammatory effec
*memory↑, TQ in improving learning and memory, using a rat model of AD induced by a combination of aluminum chloride (AlCl3) and d-galactose (d-Gal).
*cognitive↑, TQ improved AD rat cognitive decline, decreased Aβ formation and accumulation, significantly decreased TNF-α and IL-1β at all levels of doses
*Aβ↑,
*TNF-α↓, Fourteen consecutive days of TQ treatment at all levels of doses caused a significant decrease in the rats brain content of TNF-α compared to AD group reaching 39.85, 18.22, and 30.37 versus 65.30, respectively
*IL1β↓, TQ at all levels of doses significantly reduced the brain content of IL-1β compared to AD group reaching 36.55, 14.32, and 27.27 versus 53.65
*TLR2↓, TQ middle dose (20 mg/kg) significantly downregulated the expression of TLR-2 by 82.74% and 77.94% and the expression of TLR-4 by 84.35% and 63.30%,
*NF-kB↓, and significantly downregulated the expression of TLRs pathway components as well as their downstream effectors NF-κB and IRF-3 mRNAs at all levels of doses
*IRF3↓, expression of IRF-3 by 18.19% and 77.96%,
TLR4↓,
MyD88↓, expression of MyD88 by 79.65% and 68.36%
TRIF↓, expression of TRIF by 25.90% and 76.75%

3432- TQ,    Thymoquinone: Review of Its Potential in the Treatment of Neurological Diseases
- Review, AD, NA - Review, Park, NA
*memory↑, It could be utilized to treat drug misuse or dependence, and those with memory and cognitive impairment
*cognitive↑,
*ROS↓, TQ protects brain cells from oxidative stress, which is especially pronounced in memory-related regions.
*Inflam↓, TQ’s antioxidant and anti-inflammatory properties protect brain cells from damage and inflammation.
*antiOx↑,
*TLR1↓, TQ’s role in inhibiting Toll-like receptors (TLRs) and some inflammatory mediators, leading to reduced inflammation and neurotoxicity.
*AChE↓, TQ has been shown in clinical studies to block acetylcholinesterase (AChE) activity, which increases acetylcholine (ACh).
*MMP↑, TQ ameliorates and prevents Aβ-induced neurotoxicity and mitochondrial membrane depolarization by inhibiting ROS formation and reducing oxidative stress by antioxidant properties.
*neuroP↑, TQ has an essential role in the neuroprotective impact on hippocampal cells after cerebral ischemia through the inhibition of lipid peroxidation
*lipid-P↓,
*SOD↑, This effect is due to the antioxidant activity of TQ on the levels of the superoxide dismutase (SOD) and GSH activities.
*GSH↑,
*Ach↑, TQ has been shown in clinical studies to block acetylcholinesterase (AChE) activity, which increases acetylcholine (ACh).


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Results for Effect on Cancer/Diseased Cells:
Akt↑,1,   angioG↓,1,   AntiCan↑,1,   Apoptosis↑,1,   MyD88↓,1,   PI3K↓,1,   TLR4↓,1,   TRIF↓,1,   TumCCA↑,1,   TumCG↓,1,  
Total Targets: 10

Results for Effect on Normal Cells:
Ach↑,2,   AChE↓,5,   AChE↝,1,   AntiCan↑,1,   antiOx↑,4,   Aβ↓,5,   Aβ↑,1,   BAX↓,1,   BBB↑,1,   Bcl-2↑,1,   cardioP↑,1,   Casp3↓,1,   Catalase↑,1,   ChAT↑,1,   cMyc↓,1,   cognitive↑,10,   COX2↓,1,   CRP↓,1,   cycD1↓,1,   GPx↑,1,   GSH↑,3,   H2O2↓,1,   hepatoP↑,1,   IFN-γ↑,1,   IL10↑,2,   IL12↓,1,   IL1β↓,4,   IL6↓,1,   Inflam↓,6,   Inflam↑,1,   iNOS↑,1,   IRF3↓,3,   JNK↑,1,   LDH↓,1,   lipid-P↓,2,   MAPK↑,1,   MDA↓,3,   memory↑,6,   MMP↑,3,   MMP9↓,1,   MyD88↓,2,   neuroP↑,6,   NF-kB↓,5,   NO↓,2,   NRF2↑,1,   PPARγ↑,1,   RenoP↑,1,   ROS↓,4,   SOD↑,4,   TAC↑,1,   p‑tau↓,1,   TGF-β↓,1,   TLR1↓,1,   TLR2↓,3,   TLR4↓,2,   TNF-α↓,4,   TRIF↓,2,   TumCI↓,1,   TumCP↓,1,   VEGF↓,1,  
Total Targets: 60

Scientific Paper Hit Count for: cognitive, cognitive
10 Thymoquinone
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:162  Target#:557  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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