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


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⟱
3408- TQ,    Thymoquinone: A small molecule from nature with high therapeutic potential
- Review, AD, NA - Review, Park, NA
*neuroP↑, The neuroprotective effect of TQ has been seen in various neurological disorders, including epilepsy, Parkinsonism, anxiety, depression, encephalomyelitis and Alzheimer’s disease
*hepatoP↑, Hepatoprotective activity
*cardioP↑, Cardioprotective activity
*Inflam↓, Anti-inflammatory activity
*antiOx↑, TQ is well known for its antioxidant activity
ChemoSen↑, combination of TQ with chemotherapeutic drugs shows very promising effects in different types of cancers and against different diseases in preclinical studies
eff↑, Along with curcumin and fluoxetine, TQ shows good activity as compared to alone
eff↑, Vascular endothelial growth factor (VEGF) activation lead to angiogenesis, which inhibited by a combination of resveratrol and TQ.
TumCP↓, TQ can inhibit tumor cell proliferation, inhibit carcinogen activation, arrest the cell cycle in different phases, induce apoptosis, inhibit proteasomes and inhibit angiogenesis.
TumCCA↑,
angioG↓,
cycA1↓, downregulation of cyclin A, cyclin D1, cyclin D2, cyclin E and cyclin-dependent kinases,
cycD1↓,
cycE↓,
CDK2↓,

3401- TQ,    Molecular mechanisms and signaling pathways of black cumin (Nigella sativa) and its active constituent, thymoquinone: a review
- Review, Var, NA
TumCP↓, thymoquinone can inhibit cancer cell proliferation through disruption of the PI3K/AKT pathway by upregulating phosphatase and tensin homolog
*antiOx↑, thymoquinone improve antioxidant enzyme activities, effectively scavenges free radicals, and thus protect cells from oxidative stress.
*ROS↓, modulate reactive oxygen species levels in tumor cells,
NRF2↑, regulate responses to oxidative stress and inflammation via Nrf2 and NF-κB pathways
NF-kB↓, Inhibits inflammatory response
TumCCA↑, arrest the cell cycle in the G2/M phase
*GABA↑, N. sativa and thymoquinone can elevate brain GABA content, and thus it may ameliorate epilepsy
P53↑,
P21↑,
AMPK↑,
neuroP↑, thymoquinone, exhibit various pharmacological activities, including neuroprotective, nephroprotective, cardioprotective, gastroprotective, hepatoprotective, and anti-cancer effects.
cardioP↑,
hepatoP↑,

3404- TQ,    The Neuroprotective Effects of Thymoquinone: A Review
- Review, Var, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, anti-inflammatory, antioxidant, antimicrobial, antiparasitic, anticancer, hypoglycemic, antihypertensive, and antiasthmatic effects.
AntiCan↑,
*TNF-α↓, TQ treatment (2.5, 5, and 10 μM) inhibited the release of TNF-α, IL-6, and IL-1β.
*IL6↓,
*IL1β↓,
*NF-kB↓, TQ treatment (2.5, 5 and 10 μM) inhibited NF-κB-dependent neuroinflammation in BV2 microglia via decreasing iNOS protein levels, κB inhibitor phosphorylation, and binding of NF-κB to the DNA
*iNOS↓,
*NRF2↑, activation of the Nrf2/ARE signaling pathway by TQ resulted in the inhibition of NF-κB-mediated neuroinflammation.
*neuroP↑, TQ has neuroprotection potential against Aβ1-42 in rat hippocampal by ameliorating oxidative stress.
*MMP↑, Thymoquinone ameliorated Aβ1-42-induced neurotoxicity and prevented the mitochondrial membrane potential depolarization and finally reduced the oxidative stress.
*ROS↓,
*MDA↓, Thymoquinone decreased the neuronal cell death in the hippocampal CA1 region and MDA level and increased glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities after forebrain ischemia.
*GSH↑,
*Catalase↑,
*SOD↑,
*IL12↓, Thymoquinone exhibited anti-inflammatory effects by decreasing several cytokines, including TNF-α, NF-κB, IL-6, IL-1β, IL-12p40/70, (CCL12)/MCP-5, (CCL2)/MCP-1, GCSF, and Cxcl 10/IP-10 of, NO, PGE2, and iNOS.
*MCP1↓,
*IP-10/CXCL-10↓,
*PGE2↓,

3409- TQ,    Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives
- in-vivo, Nor, NA
*MDA↓, increased levels of malondialdehyde, TGF-β, CRP, NF-κB, TNF-α, IL-1β and caspase-3 associated with reduced levels of GSH, cyt-c oxidase, Nrf2 and IL-10. However, exposure of rats’ brain tissues to thymoquinone resulted ameliorated all these ef
*TGF-β↓,
*CRP↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*GSH↑,
*NRF2↑,
*IL10↑,
*neuroP↑, thymoquinone remediates sodium nitrite-induced brain impairment through several mechanisms including attenuation of oxidative stress
*ROS↓,
*Apoptosis↓,
*Inflam↓, TQ activates the Nrf2/ARE antioxidant mechanisms in its anti-inflammatory activity

3410- TQ,    Anti-inflammatory effects of thymoquinone and its protective effects against several diseases
- Review, Arthritis, NA
*Inflam↓, anti-inflammatory, anti-oxidant, and anti-apoptotic properties in several disorders such as asthma, hypertension, diabetes, inflammation, bronchitis, headache, eczema, fever, dizziness and influenza
*antiOx↑, anti-inflammatory and anti-oxidant effects via several molecular pathways
*COX2↓, TQ has been shown to suppress COX2 expression and the ensuing generation of prostaglandins
*NRF2↑, TQ also attenuates inflammation via the Nrf2 pathway [28]. Heme-oxygenase 1 (HO-1) has been shown to be stimulated by TQ
*HO-1↑,
*IL1β↓, oral TQ treatment caused a decrease in several pro-inflammatory regulators, such as interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor (TNFα), interferon γ (IFNγ) and prostaglandin E2 PGE(2)
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
*PGE2↓,
*cardioP↑, Cardioprotective activity of TQ through anti-inflammation
*Catalase↑, LPS diminished anti-oxidant enzymes including catalase (CAT) and superoxide dismutase (SOD) and the total thiol group. TQ treatment reduced these effects, restoring many of the LPS effects to basal levels
*SOD↑,
*Thiols↑,
*neuroP↑, Neuroprotective activity of TQ through anti-inflammation
*IL12↓, TQ diminished the levels of several cytokines such as IL-6, IL-1β, IL-12p40/70, chemokine C-C motif ligand 12 (CCL12)/monocyte chemotactic protein 5 (MCP-5), CCL2/MCP-1, granulocyte colony-stimulating factor (GCSF), and C-X-C motif chemokine 10 (Cxcl
*MCP1↓,
*CXCc↓,
*ROS↓, consistent with TQ’s efficacy in reducing ROS generation and the ensuing inflammation

3553- TQ,    Study Effectiveness and Stability Formulation Nanoemulsion of Black Cumin Seed (Nigella sativa L.) Essential Oil: A Review
- Review, Nor, NA
*AntiCan↑, antimicrobial, antifungal, antiviral, anticancer, anti-inflammatory, immunomodulatory, anthelmintic, antidiabetic, antidepressant, antifertility, antioxidant, anti-agiing, analgesic, hepatoprotector, cardioprotector, neuroprotector and others.
*Inflam↓,
*antiOx↑,
*AntiAge↑,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*eff↑, Nano-delivery system in the formulation of the black cumin seed (Nigella sativa L.) essential oil nanoemulsion as a whole shows that there is an increase in the stability of the preparation and the effectiveness of the active substance

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.

3554- TQ,    Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons
- in-vitro, AD, NA
*GSH↑, TQ restored the decrease in the intracellular antioxidant enzyme glutathione levels and inhibited the generation of reactive oxygen species induced by Aβ1–42.
*ROS↓,
*neuroP↑, Thus, the findings of our study suggest that TQ holds a neuroprotective potential and could be a promising therapeutic agent to reduce the risk of developing AD and other disorders of the central nervous system.
*Casp3↓, Aβ1–42 (5 μM) induced about 90% increase in the caspase 3/7 activities (**P < 0.01). However, TQ (100 nM) co-treatment restored caspase 3/7 activities to control sample level
*Casp7↓,
*antiOx↓, strong antioxidant capabilities, TQ has been demonstrated to protect the brain and the spinal cord from oxidative damage generated by different pathologies induced by a variety of free radicals
*H2O2↓, Intriguingly, the co-treatment with TQ restored the content of GSH and significantly inhibited the apparent increase in H2O2.

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).

2092- TQ,    Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease
- Review, AD, NA
*iNOS↓, PC12normal: downregulated the iNOS expression along with NO level; (5) had a protective role of intracellular oxidative stress, by restoring the ROS level
*ROS↓,
*GSH↑, SH-SY5Y(normal): increasing the GSH levels.
*neuroP↑, TQ was able to reduce the neurotoxicity induced by Aß in an in vitro model of undifferentiated pheochromocytoma rat cell line, PC-12,
*MMPs↓, reestablishment of the abnormal levels of Matrix metalloproteinases (MMPs) and ROS
*MMP↑, E18, through the inhibition of ROS formation, and mitochondrial membrane depolarization.
*TXNIP↓, TQ was able to downregulate ... Thioredoxin-interacting protein (Txnip) and to upregulate the expression of Peroxiredoxin 1 (Prdx 1)
*Prx↑,
*memory↑, Bargi et al. (2017), reported that TQ was able, yet at lower doses, to improve memory impairments induced by LPS in rats.
*MDA↓, decreased level of markers of oxidative damage in brain tissues such as NOS, malondialdehyde (MDA) as well as an increased activity of SOD and catalase in hippocampus and cortex
*SOD↑,
*Catalase↑,
*BioAv↑, nanoemulsion may enhance the oral bioavailability and brain delivery.

2089- TQ,    Modulation of Hydrogen Peroxide-Induced Oxidative Stress in Human Neuronal Cells by Thymoquinone-Rich Fraction and Thymoquinone via Transcriptomic Regulation of Antioxidant and Apoptotic Signaling Genes
- in-vitro, Nor, SH-SY5Y
*neuroP↑, neuroprotective properties of Thymoquinone-rich fraction (TQRF) and TQ against hydrogen peroxide- (H2O2-) induced neurotoxicity in differentiated human SH-SY5Y cells were investigated.
*ROS↓, reducing intracellular ROS levels
*SOD1↑, upregulated SOD1 and catalase gene
*Catalase↑,

2126- TQ,    Biological and therapeutic activities of thymoquinone: Focus on the Nrf2 signaling pathway
- Review, Nor, NA
*antiOx↑, several biological effects, including antioxidant, antibacterial, antineoplastic, nephroprotective, hepatoprotective, gastroprotective, neuroprotective, anti-nociceptive, and anti-inflammatory activities.
*Bacteria↓,
*RenoP↑,
*hepatoP↑,
*neuroP↑,
*Inflam↓,
*Keap1↓, beneficial effects are mostly related to modulation of the Nrf2 signaling pathway by blockage of Keap1, stimulating the expression of the Nrf2 gene, and inducing the nuclear translocation of Nrf2
*NRF2↑,
*other↝, lots of references for normal cell reactions

2122- TQ,    Review on Molecular and Therapeutic Potential of Thymoquinone in Cancer
- Review, Var, NA
ChemoSen↓, Chemosensitization by TQ is mostly limited to in vitro studies, and it has potential in therapeutic strategy for cancer
*ROS↓, its scavenging ability against freeradicals, including reactive oxygen species (ROS;
*GSH↑, TQ reduces the cellular oxidative stress by inducing glutathione (GSH)
RenoP↑, TQ protects the kidney against ifosfamide, mercuric chloride, cisplatin, and doxorubicin-induced damage by preventing renal GSH depletion and antilipid peroxidation
hepatoP↑, TQ ameliorated hepatotoxicity of carbon tetrachloride as seen by the significant reduction of the elevated levels of serum enzymes and significant increase of the hepatic GSH content
COX2↓, TQ induces inhibition of PGE2 and COX-2, in a COX-2 overexpressing HPAC cells (PC cells).
NF-kB↓, NF-κB is a molecular target of TQ in cance
chemoP↑, TQ is a chemopreventive agent for prostate cancer
neuroP↑, The beneficial effect of TQ as a neuroprotective agent in inhibiting viability of human neuroblastoma cell line SH-SY5Y
TumCCA↑, TQ, it reportedly induces G1 cell cycle arrest in osteosarcoma cancer cells (COS31) as well as in human colon cancer cells (HCT-116),
P21↑, TQ caused a dramatic increase in p21WAF1 , (Cip1), and p27 (Kip1) and blocked the progression of synchronized LNCaP cells from G1 to S phase,
p27↑,
ROS↑, TQ on p53 deficient lymphoblastic leukemia Jurkat cells and found TQ treatment produced intracellular ROS pro- moting a DNA damage-related cell cycle arrest and triggered apoptosis
DNAdam↑,
MUC4↓, in pancreatic cancer cells and it was found that TQ downregulates MUC-4 expression through the proteasomal pathway

2119- TQ,    Dual properties of Nigella Sativa: anti-oxidant and pro-oxidant
- Review, Var, NA
*ROS↓, NS has both anti-oxidant and pro-oxidant properties in different cell types hence should be used carefully because it acts as a cytoprotective or cytotoxic agent in inflammatory and malignant conditions respectively.
ROS↑, malignant conditions
chemoP↑, It is reported that nigella can reduce the toxic effects of anticancer drugs
RenoP↑, NS has been shown to improve multiple organ toxicity in models of oxidative stress
hepatoP↑,
NLRP3↓, NLRP3 inflammasome was inactivated partially by inhibition of ROS in melanoma cells by TQ administration.
neuroP↑, NS oil has been found to be neuroprotective against oxidative stress in epileptogenesis
NF-kB↓, TQ has been shown to exhibit down regulation of NF-κB expression in lung cancer cells and in osteosarcoma cells
P21↑, TQ up regulated the expression of p21 and down regulated the histone deacetylase (HDAC) activity and induced histone hyperacetylation causing induction of apoptosis and inhibition of proliferation in pancreatic cancer cell
HDAC↓,
Apoptosis↑,
TumCP↓,
GSH↓, TQ was found to decrease glutathione (GSH) levels in prostate cancer cells resulting in up-regulated expression of GADD45 alpha
GADD45A↑,
GSK‐3β↑, TQ caused the apoptosis of tumor cells by modulation of wnt signaling through activation of GSK-3β

2100- TQ,    Dual properties of Nigella Sative: Anti-oxidant and Pro-oxidant
- Review, NA, NA
ROS⇅, Pubmed data indicated that NS has both anti-oxidant and pro-oxidant properties in different cell types
*antiOx↑, NS acts as an anti-oxidant by scavenging ROS [4]. It can ameliorate ischemic reperfusion injury conditions and attenuated ROS in heart [5] intestine [6] and kidney [7]
*SOD↑, improved the activities of various enzymes like superoxide dismutase [SOD] and myeloperoxidase (MPO)
*MPO↑,
*neuroP↑, NS oil has been found to be neuroprotective against oxidative stress in epileptogenesis, pilocarpine-induced seizures [25] and opioid tolerance
*chemoP↑, Anticancer drugs leave toxic effect due to over-production of ROS. NS oil or TQ can potentially up-regulate anti-oxidant mechanisms caused by anticancer drug
*radioP↑, NS seed extracts can protect normal tissue from oxidative damage during radiotherapy of cancer patients [35,36]
NF-kB↓, TQ has been shown to exhibit down regulation of NF-κB expression in lung cancer cells
IAP1↓, Anti-apoptotic (IAP1, IAP2, XIAP Bcl-2, Bcl-xL, survivin), proliferative (cyclin D1, cyclooxygenase-2, and c-Myc) and angiogenic genes (matrix metalloproteinase-9 orMMP-9) and vascular endothelial growth factor (VEGF) were down-regulated
IAP2↓,
XIAP↓,
Bcl-xL↓,
survivin↓,
COX2↓,
MMP9↓,
VEGF↓,
ROS↑, TQ causes release of ROS in ABC cells which in turn inhibits NF-κB activity
P21↑, TQ up regulated the expression of p21 and down regulated the histone deacetylase (HDAC) activity and induced histone hyperacetylation causing induction of apoptosis and inhibition of proliferation in pancreatic cancer cell
HDAC↓,
GSH↓, TQ was found to decrease glutathione (GSH) levels in prostate cancer cells resulting in up-regulated expression of GADD45 alpha (growth arrest and DNA damage inducible gene) and AIF
GADD45A↑,
AIF↑,
STAT3↓, TQ suppressed the STAT 3; the signal transducer and activator of transcription which is involved in the abnormal transformation of a number of human malignancies [53].


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Results for Effect on Cancer/Diseased Cells:
AIF↑,1,   Akt↑,1,   AMPK↑,1,   angioG↓,2,   AntiCan↑,2,   Apoptosis↑,2,   Bcl-xL↓,1,   cardioP↑,1,   CDK2↓,1,   chemoP↑,2,   ChemoSen↓,1,   ChemoSen↑,1,   COX2↓,2,   cycA1↓,1,   cycD1↓,1,   cycE↓,1,   DNAdam↑,1,   eff↑,2,   GADD45A↑,2,   GSH↓,2,   GSK‐3β↑,1,   HDAC↓,2,   hepatoP↑,3,   IAP1↓,1,   IAP2↓,1,   MMP9↓,1,   MUC4↓,1,   neuroP↑,3,   NF-kB↓,4,   NLRP3↓,1,   NRF2↑,1,   P21↑,4,   p27↑,1,   P53↑,1,   PI3K↓,1,   RenoP↑,2,   ROS↑,3,   ROS⇅,1,   STAT3↓,1,   survivin↓,1,   TumCCA↑,4,   TumCG↓,1,   TumCP↓,3,   VEGF↓,1,   XIAP↓,1,  
Total Targets: 45

Results for Effect on Normal Cells:
Ach↑,2,   AChE↓,4,   AntiAge↑,1,   AntiCan↑,2,   antiOx↓,1,   antiOx↑,9,   Apoptosis↓,1,   Aβ↓,2,   Bacteria↓,1,   BAX↓,1,   Bcl-2↑,1,   BioAv↑,1,   cardioP↑,4,   Casp3↓,3,   Casp7↓,1,   Catalase↑,5,   chemoP↑,1,   cMyc↓,1,   cognitive↑,6,   COX2↓,2,   CRP↓,2,   CXCc↓,1,   cycD1↓,1,   eff↑,1,   GABA↑,1,   GPx↑,1,   GSH↑,8,   H2O2↓,2,   hepatoP↑,4,   HO-1↑,1,   IFN-γ↓,1,   IFN-γ↑,1,   IL10↑,2,   IL12↓,3,   IL1β↓,4,   IL6↓,3,   Inflam↓,9,   Inflam↑,1,   iNOS↓,2,   iNOS↑,1,   IP-10/CXCL-10↓,1,   IRF3↓,1,   JNK↑,1,   Keap1↓,1,   LDH↓,1,   lipid-P↓,2,   MAPK↑,1,   MCP1↓,2,   MDA↓,6,   memory↑,5,   MMP↑,5,   MMP9↓,1,   MMPs↓,1,   MPO↑,1,   MyD88↓,1,   neuroP↑,16,   NF-kB↓,5,   NO↓,2,   NRF2↑,5,   other↝,1,   PGE2↓,2,   PPARγ↑,1,   Prx↑,1,   radioP↑,1,   RenoP↑,2,   ROS↓,12,   SOD↑,7,   SOD1↑,1,   TAC↑,1,   p‑tau↓,1,   TGF-β↓,2,   Thiols↑,1,   TLR1↓,1,   TLR2↓,1,   TLR4↓,1,   TNF-α↓,4,   TRIF↓,1,   TumCI↓,1,   TumCP↓,1,   TXNIP↓,1,   VEGF↓,1,  
Total Targets: 81

Scientific Paper Hit Count for: neuroP, neuroprotective
19 Thymoquinone
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:162  Target#:1105  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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