Thymoquinone Cancer Research Results

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">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">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

Rank	Pathway / Target Axis	Direction	Label	Primary Effect	Notes / Cancer Relevance	Ref
1	Reactive oxygen species (ROS)	↑ ROS	Driver	Upstream cytotoxic trigger	Primary studies show TQ rapidly increases ROS; antioxidant/ROS modulation attenuates downstream effects, supporting ROS as an initiating mechanism in multiple cancer contexts	(ref)
2	Glutathione (GSH) redox buffering	↓ GSH	Driver	Redox-collapse amplification	Same prostate cancer study reports early GSH depletion alongside ROS rise; together these form a redox “one-two punch” that helps explain selective stress in tumor cells	(ref)
3	Mitochondrial integrity (ΔΨm)	↓ ΔΨm	Driver	Mitochondrial dysfunction (MOMP axis)	Primary leukemia/cancer study reports disruption of mitochondrial membrane potential after TQ exposure (mitochondrial events central to TQ-mediated death)	(ref)
4	Intrinsic apoptosis (caspase-9 → caspase-3; PARP)	↑ caspases / ↑ apoptosis	Driver	Execution-phase cell death	Same primary paper reports activation of caspases (8/9/3) with mitochondrial involvement—core evidence for apoptosis as the major outcome pathway	(ref)
5	NF-κB signaling	↓ NF-κB activity	Secondary	Reduced pro-survival / inflammatory transcription	Colon cancer work: TQ induces cell death and chemosensitizes cells by inhibiting NF-κB signaling (explicit pathway-direction support)	(ref)
6	STAT3 signaling	↓ p-STAT3 / ↓ STAT3 activation	Secondary	Reduced survival/proliferation signaling	Gastric cancer study explicitly reports TQ suppresses constitutive STAT3 activation and related signaling readouts	(ref)
7	NRF2 antioxidant-response axis (NRF2/HO-1 program)	↑ NRF2 pathway (often as stress-response)	Adaptive	Cellular antioxidant counter-response	In TNBC context, a primary study reports TQ upregulates NRF2 (and evaluates downstream immune/checkpoint consequences), consistent with NRF2 acting as an adaptive response to redox stress	(ref)
8	HIF-1α hypoxia signaling	↓ HIF-1α protein / ↓ HIF-1α program	Adaptive	Loss of hypoxia survival signaling	Renal cancer hypoxia paper identifies TQ as suppressing HIF-1α and links this to selective killing under hypoxia	(ref)
9	Glycolysis / Warburg output (hypoxia-linked)	↓ glycolysis (↓ HIF-1α–mediated glycolytic genes; ↓ glycolytic metabolism)	Phenotypic	Metabolic suppression	In hypoxic renal cancer, TQ suppresses HIF-1α–mediated glycolysis; in CRC, TQ inhibits glycolytic metabolism alongside tumor growth limitation	(ref) \| (ref)

Scientific Papers found: Click to Expand⟱

4774-

5-FU,

TQ,

CoQ10,

Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation

in-vitro,

CRC,

AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas- pase-3).
p27↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.

2207-

AgNPs,

TQ,

Protective effects of Nigella sativa L. seeds aqueous extract-based silver nanoparticles on sepsis-induced damages in rats

in-vivo,

Nor,

Rats

*eff↑, Treatment with AgNPs led to a notable reduction in damages of liver, kidney, lung, stomach and duodenum.
*RenoP↑,
*hepatoP↑,
*MDA↓, AgNPs treated groups reduced the levels of tissues MDA and increased the levels of tissues SOD and GSH.
*SOD↑,
*GSH↑,
*TNF-α↓, The expression levels of TNF-α mRNA and IL-1β mRNA were reduced in the rats treated by silver nanoparticles.
*IL1β↓,

1920-

JG,

TQ,

PLB,

Natural quinones induce ROS-mediated apoptosis and inhibit cell migration in PANC-1 human pancreatic cancer cell line

in-vitro,

PC,

PANC1

ROS↑, thymoquinone, plumbagin and juglone were evaluated for their influence on reactive oxygen species (ROS) generation through 2,7-dichlorofluorescein diacetate (DCFDA) staining and they dramatically increased the intracellular ROS level in treated PANC-
TumCMig↓, inhibited PANC-1 cell migration
MMP9↓, reduced expression of matrix metalloproteinase-9 (MMP-9) in juglone-treated cells

4670-

RES,

CUR,

EGCG,

TQ,

Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrol

Review,

Nor,

*antiOx↑, Curcumin, epigallocatechin gallate (EGCG), thymoquinone, and resveratrol exhibit antioxidant, anti-inflammatory, and autophagy-enhancing effects that target core pathways involved in cellular senescence and tissue degeneration.
*Inflam↓,
*AntiAge↑, phytochemicals regulate key molecular players such as sirtuins, AMPK, NF-κB, and mTOR, offering promise in delaying age-associated pathologies and promoting longevity.
*SIRT1↑, Resveratrol (20 µM) ‘s contributions to mitochondrial function improvement are evident through its activation of the Sirt1/Sirt3-FoxO pathway
*SIRT3↑,
*FOXO↑,
*ROS↓, reduced intracellular ROS levels,

3417-

TQ,

Antiproliferative Effects of Thymoquinone in MCF-7 Breast and HepG2 Liver Cancer Cells: Possible Role of Ceramide and ER Stress

in-vitro,

BC,

MCF-7

in-vitro,

Liver,

HepG2

TumCP↓, Antiproliferative effect was exerted in cancer cells via TQ incubation at different doses and durations
NF-kB↓, TQ significantly decreased cell viability, S1P, C1P, NF-κB1 mRNA and NF-κB p65 protein levels in cancer cells compared to controls.
cl‑Casp3↑, cleaved caspase-3 levels in cancer cells treated with TQ. GRP78 mRNA and protein levels also increased in cancer cells treated with TQ
GRP78/BiP↑,
ER Stress↑, TQ-induced ceramide accumulation and ER stress in conjunction with decreased S1P, C1P and NF-κB mediated cell survival may promote cancer cell death by triggering apoptosis.
Apoptosis↑,

3407-

TQ,

Thymoquinone and its pharmacological perspective: A review

Review,

NA,

*antiOx↑, TQ has been reported for its antioxidant properties to combat oxidative stress in several literatures
*ROS↓, scavenges the highly reactive oxygen
*GSTs↑, induction of glutathione transferase and quinone reductase
*GSR↑,
*GSH↑, TQ induces the Glutathione production with simultaneous inhibition of superoxide radical production
*RenoP↑, Improved renal function against mercuric chloride, doxorubicin and cisplatin damage have been reported through TQ based induction of Glutathione
*IL1β↓, Decreased the levels of IL-1β, TNFα, MMP-13, cox-2 and PGE(2)
*TNF-α↓,
*MMP13↓,
*COX2↓, reducing COX-2 gene expression, it also inhibited colon cancer cell migration.
*PGE2↓,
*radioP↑, Normal cell protection from ionizing radiation in cancer cell treatment.
Twist↓, TQ treatment have evidenced the inhibition of TWIST1 promoter activity and reduces it expression in cancer cell line leading inhibition of epithelial-mesenchymal transition mediated metastasis
EMT↓,
NF-kB↓, inhibiting the NF-κB expression in breast cancer model of mice
p‑PI3K↓, TQ (20 M) decreased the activation of prostaglandin receptors EP2 and EP4 in LoVo colon cancer cells by reducing p-PI3K, p-Akt, p-GSK3, and -catenin.
p‑Akt↓,
p‑GSK‐3β↓,
DNMT1↓, TQ's anticancer effects are mediated by DNMT1-dependent (dependent DNA methylation mediates) DNA methylation,
HDAC↓, inhibiting histone deacetylase (HDAC)

3408-

TQ,

Thymoquinone: A small molecule from nature with high therapeutic potential

Review,

AD,

Review,

Park,

*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/CCNA1↓, downregulation of cyclin A, cyclin D1, cyclin D2, cyclin E and cyclin-dependent kinases,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,

3409-

TQ,

Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives

in-vivo,

Nor,

50 mg/kg

Forty adult male rats

*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,

*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

3411-

TQ,

Anticancer and Anti-Metastatic Role of Thymoquinone: Regulation of Oncogenic Signaling Cascades by Thymoquinone

Review,

Var,

p‑STAT3↓, Thymoquinone inhibited the JAK2-mediated phosphorylation of STAT3 on the 727th serine residue in SK-MEL-28 cells
cycD1/CCND1↓, levels of cyclin D1, D2, and D3 were reported to be reduced in STAT3-depleted SK-MEL-28 cells
JAK2↓, The JAK2/STAT3 pathway is inactivated by thymoquinone in B16-F10 melanoma cells
β-catenin/ZEB1↓, Levels of β-catenin and Wnt/β-catenin target genes, such as c-Myc, matrix metalloproteinase-7, and Met, were found to be reduced in thymoquinone-treated bladder cancer cells.
cMyc↓,
MMP7↓,
MET↓,
p‑Akt↓, Thymoquinone dose-dependently reduced the levels of p-AKT (threonine-308), p-AKT (serine-473), p-mTOR1, and p-mTOR2 in gastric cancer cells.
p‑mTOR↓,
CXCR4↓, Thymoquinone decreased the surface expression of CXCR4 on multiple myeloma cells
Bcl-2↓, Thymoquinone time-dependently decreased BCL-2 levels and simultaneously enhanced BAX levels
BAX↑,
ROS↑, Thymoquinone-mediated ROS accumulation triggered conformational changes in BAX that sequentially resulted in the activation of the mitochondrial apoptotic pathway
Cyt‑c↑, Thymoquinone effectively increased the release of cytochrome c into the cytosol
Twist↓, Thymoquinone downregulated TWIST1 and ZEB1 and simultaneously upregulated E-cadherin in SiHa and CaSki cell lines [82].
Zeb1↓,
E-cadherin↑,
p‑p38↑, Thymoquinone-induced ROS enhanced the phosphorylation of p38-MAPK in MCF-7 cells.
p‑MAPK↑,
ERK↑, The thymoquinone-induced activation of ERK1/2
eff↑, FR180204 (ERK inhibitor) significantly reduced the viability of thymoquinone and docetaxel-treated cancer cells [
ERK↓, Thymoquinone inhibited the proliferation, migration, and invasion of A549 cells by inactivating the ERK1/2 signaling cascade
TumCP↓,
TumCMig↓,
TumCI↓,

3412-

TQ,

Thymoquinone induces oxidative stress-mediated apoptosis through downregulation of Jak2/STAT3 signaling pathway in human melanoma cells

in-vitro,

Melanoma,

SK-MEL-28

in-vivo,

NA,

SK-MEL-28 tumor xenografts

Apoptosis↑, Q treatment induced apoptosis in SK-MEL-28 cells
JAK2↓, Interestingly, constitutive phosphorylation of Janus kinase 2 (Jak2) and signal transducer and activator of transcription 3 (STAT3) was markedly decreased following TQ treatment
STAT3↓,
cycD1/CCND1↓, TQ treatment downregulated STAT3-dependent genes including cyclin D1, D2, and D3 and survivin
survivin↓,
ROS↑, TQ increased the levels of reactive oxygen species (ROS)
eff↓, , whereas pretreatment with N-acetyl cysteine (NAC), a ROS scavenger, prevented the suppressive effect of TQ on Jak2/STAT3 activation and protected SK-MEL-28 cells from TQ-induced apoptosis.

3413-

TQ,

Thymoquinone induces apoptosis in human colon cancer HCT116 cells through inactivation of STAT3 by blocking JAK2- and Src‑mediated phosphorylation of EGF receptor tyrosine kinase

in-vitro,

CRC,

HCT116

tumCV↓, TQ significantly reduced the viability of human colon cancer HCT116 cells in a concentration- and time-dependent manner
Apoptosis↓, TQ induced apoptosis, which was associated with the upregulation of Bax and inhibition of Bcl-2 and Bcl-xl expression
BAX↑,
Bcl-2↓,
Casp9↑, TQ also activated caspase-9,-7, and -3, and induced the cleavage of poly-(ADP-ribose) polymerase (PARP).
Casp7↑,
Casp3↑,
cl‑PARP↑,
STAT3↓, TQ attenuated the expression of STAT3 target gene products, such as survivin, c-Myc, and cyclin-D1, -D2, and enhanced the expression of cell cycle inhibitory proteins p27 and p21.
survivin↓,
cMyc↓,
cycD1/CCND1↓,
p27↑,
P21↑,
EGFR↓, TQ attenuated the phosphorylation of upstream kinases, such as Janus-activated kinase-2 (JAK2), Src kinase and epidermal growth factor receptor (EGFR) tyrosine kinase
ROS↑, According to this study, TQ-induced cytotoxicity in DLD-1 colon cancer cells was associated with the generation of reactive oxygen species, activation of extracellular signal-regulated kinase and c-Jun-N-terminal kinase, and the cleavage of caspase-7

3414-

TQ,

Thymoquinone induces apoptosis through inhibition of JAK2/STAT3 signaling via production of ROS in human renal cancer Caki cells

in-vitro,

RCC,

Caki-1

tumCV↓, TQ significantly reduced the cell viability and induced apoptosis in Caki cells as evidenced by the induction of p53 and Bax, release of cytochrome c, cleavage of caspase-9, and -3 and PARP and the inhibition of Bcl-2 and Bcl-xl expression.
Apoptosis↑,
P53↑,
BAX↑,
Cyt‑c↑,
cl‑Casp9↑,
cl‑Casp3↑,
cl‑PARP↑,
Bcl-2↓,
Bcl-xL↓,
p‑STAT3↓, TQ inhibited the constitutive phosphorylation of signal transducer and activator of transcription-3 (STAT3) in Caki cells by blocking the phosphorylation of upstream Janus-activated kinase-2 (JAK2) kinases.
p‑JAK2↓,
STAT3↓, TQ attenuated the expression of STAT3 target gene products, such as survivin, cyclin D1, and D2.
survivin↓,
cycD1/CCND1↓,
ROS↑, Treatment with TQ generated ROS in these renal cancer cells.
eff↓, Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the inhibitory effect of TQ on the JAK2/STAT3 signaling and rescued cells from TQ-induced apoptosis

3415-

TQ,

The anti-neoplastic impact of thymoquinone from Nigella sativa on small cell lung cancer: In vitro and in vivo investigations

in-vitro,

Lung,

H446

1-100uM

tumCV↓, TQ reduced cell viability, induced apoptosis and cell cycle arrest, depleted ROS, and altered protein expression in associated signaling pathways.
TumCCA↑,
ROS↓, With regards to ROS in the current study, TQ dose-dependently decreased intracellular ROS levels in all SCLC cells except H446 cells upon 24-hour treatment with TQ.
CycB/CCNB1↑, TQ induced upregulation of cyclin B1 and cyclin D3 in H69-adherent and H446 cells, respectively. Cyclins A2, E1, and cdc2 were downregulated, while cyclin D3 was upregulated in H841-adherent cells
CycD3↑,
cycA1/CCNA1↓,
cycE/CCNE↓,
cDC2↓,
antiOx↑, TQ acted as an antioxidant.
PARP↓, TQ downregulated intratumoral PARP
NRF2↓, TQ exerts its antioxidative effect by upregulating nuclear protein nuclear factor-erythroid 2 related factor 2 (Nrf2), hence amplifying antioxidant response element (ARE) expression.
ARE/EpRE↑,
eff↑, To confirm that the antioxidative action of TQ is anti-survival for cells, H841 cells were employed as a model and treated with NAC. NAC confirmed that ROS depletion led to a decrease in the cell viability of SCLC cells.

3416-

TQ,

Thymoquinone induces apoptosis in bladder cancer cell via endoplasmic reticulum stress-dependent mitochondrial pathway

in-vitro,

Bladder,

T24/HTB-9

 TQ (20–100 μM) for 24 h

in-vitro,

Bladder,

253J

in-vitro,

Nor,

SV-HUC-1

TumCP↓, TQ has a significant cytotoxicity on bladder cancer cells and can inhibit their proliferation and induce apoptosis.
Apoptosis↑,
ER Stress↑, The protein changes of Bcl-2, Bax, cytochrome c and endoplasmic reticulum stress-related proteins (GRP78, CHOP, and caspase-12) revealed that the anticancer effect of TQ was associated with mitochondrial dysfunction and the endoplasmic reticulum stre
cl‑Casp3↑, TQ increased the cleaved subunits of caspase-3, caspase-8, caspase-7 and PARP (Fig. 2B) and increased caspase-3 activity (Fig. 2C) in a dose-dependent manner.
cl‑Casp8↑,
cl‑Casp7↑,
cl‑PARP↑,
Cyt‑c↑, can increase the release of cytochrome c
PERK↑, TQ increased the expression of PERK, IRE1 and ATF6 and the expression of downstream molecules such as p-eIF2a and ATF4 in a dose-dependent manner
IRE1↑,
ATF6↑,
p‑eIF2α↑,
ATF4↑,
GRP78/BiP↑, GRP78, IRE1, ATF6, ATF4 and CHOP was significantly increased after TQ treatment
CHOP↑,

3404-

TQ,

The Neuroprotective Effects of Thymoquinone: A Review

Review,

Var,

Review,

AD,

Review,

Park,

Review,

Stroke,

*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↓,

3418-

TQ,

Thymoquinone suppresses metastasis of melanoma cells by inhibition of NLRP3 inflammasome

in-vitro,

Melanoma,

A375

in-vivo,

NA,

B16F10) melanoma cell line

TumMeta↓, Thymoquinone causes inhibition of metastasis in vivo
TumCMig↓, Thymoquinone causes inhibition of migration by activation of NLRP3 inflammasome.
NLRP3↓,
Casp1↓, Inactivation of caspase-1 by thymoquinone resulted in inhibition of IL-1β and IL-18.
IL1β↓,
IL18↓,
ROS↓, Furthermore, inhibition of reactive oxygen species (ROS) by thymoquinone resulted in partial inactivation of NLRP3 inflammasome.
NF-kB↓, as well as inhibition of NF-κB, and hence suppressing growth and migration of melanoma cells.

3419-

TQ,

Thymoquinone, a Novel Multi-Strike Inhibitor of Pro-Tumorigenic Breast Cancer (BC) Markers: CALR, NLRP3 Pathway and sPD-L1 in PBMCs of HR+ and TNBC Patients

in-vitro,

BC,

PBMCs isolated from HR+ BC patients were treated with increasing concentrations of TQ (20, 50, and 100 µM) for 24, 48, and 72 h.

 peripheral blood mononuclear cells (PBMCs)

*NLRP3↓, TQ caused a non-significant impact on NLRP3 expression at 20 µM; then, a significant increase was noticed at 50 µM (**** p < 0.0001), followed by a complete abolishment in its expression at 100 µM
*IL1β↓, TQ significantly downregulated the expression of CALR, NLRP3 components and IL-1β together with the protein levels of secreted IL-1β and sPD-L1.
*Casp1?, TQ Significantly Inhibited Caspase-1 after 24, 48, and 72 h of Treatment in PBMCs of HR+ BC Patients

3420-

TQ,

Thymoquinone alleviates the accumulation of ROS and pyroptosis and promotes perforator skin flap survival through SIRT1/NF-κB pathway

in-vitro,

Nor,

HUVECs

in-vitro,

NA,

rat

*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,

3421-

TQ,

Insights into the molecular interactions of thymoquinone with histone deacetylase: evaluation of the therapeutic intervention potential against breast cancer

Analysis,

Nor,

in-vivo,

Nor,

in-vitro,

BC,

MCF-7

in-vitro,

Nor,

HaCaT

HDAC↓, The in silico findings were corroborated with an in vitro analysis, demonstrating the efficient role of TQ in the attenuation of global HDAC activity.
P21↑, reactivation of HDAC target genes (p21 and Maspin), induction of the pro-apoptotic gene Bax, down regulation of the anti-apoptotic gene Bcl-2 and arrest of the cell cycle at the G2/M phase.
Maspin↑,
BAX↑,
B2M↓,
TumCCA↑,
selectivity↑, higher cytotoxicity of TQ towards MCF-7 breast cancer cells in comparison to normal cells indicates the potential of TQ to be an anticancer drug.
*toxicity↓, Fortunately, in the case of normal cells, TQ elicits no lethal effect as that of TSA and almost all cells remained viable even at 100 μM TQ. above findings it is evident that TQ is non-toxic to normal cells
TumCMig↓, TQ inhibits migration and proliferation of breast cancer cells.
TumCP↓,

3422-

TQ,

Thymoquinone, as a Novel Therapeutic Candidate of Cancers

Review,

Var,

selectivity↑, TQ selectively inhibits the cancer cells’ proliferation in leukemia [9], breast [10], lungs [11], larynx [12], colon [13,14], and osteosarcoma [15]. However, there is no effect against healthy cells
P53↑, It also re-expressed tumor suppressor genes (TSG), such as p53 and Phosphatase and tensin homolog (PTEN) in lung cancer
PTEN↑,
NF-kB↓, antitumor properties by regulating different targets, such as nuclear factor kappa B (NF-Kb), peroxisome proliferator-activated receptor-γ (PPARγ), and c-Myc [1], which resulted in caspases protein activation
PPARγ↓,
cMyc↓,
Casp↑,
*BioAv↓, Due to hydrophobicity, there are limitations in the bioavailability and drug formation of TQ.
BioAv↝, TQ is sensitive to light; a short period of exposure results in severe degradation, regardless of the solution’s acidity and solvent type [27]. It is also unstable in alkaline solutions because TQ’s stability decreases with rising pH
eff↑, Encapsulating TQ with CS improves the uptake and bioavailability of TQ but has low encapsulation efficiency (35%)
survivin↓, TQ showed antiproliferative and pro-apoptotic potency on breast cancer through the suppression of anti-apoptotic proteins, such as survivin, Bcl-xL, and Bcl-2
Bcl-xL↓,
Bcl-2↓,
Akt↓, treating doxorubicin-resistant MCF-7/DOX cells with TQ inhibited Akt and Bcl2 phosphorylation and increased the expression of PTEN and apoptotic regulators such as Bax, cleaved PARP, cleaved caspases, p53, and p21 [
BAX↑,
cl‑PARP↑,
CXCR4↓, inhibited metastasis with significant inhibition of chemokine receptor Type 4 (CXCR4), which is considered a poor prognosis indicator, matrix metallopeptidase 9 (MMP9), vascular endothelial growth factor Receptor 2 (VEGFR2), Ki67, and COX2
MMP9↓,
VEGFR2↓,
Ki-67↓,
COX2↓,
JAK2↓, TQ at 25, 50 and 75 µM inhibited JAK2 and c-Src activity and induced apoptosis by inhibiting the phosphorylation of STAT3 and STAT3 downstream genes, such as Bcl-2, cyclin D, survivin, and VEGF, and upregulating caspases-3, caspases-7, and caspases-9
cSrc↓,
Apoptosis↑,
p‑STAT3↓,
cycD1/CCND1↓,
Casp3↑,
Casp7↑,
Casp9↑,
N-cadherin↓, downregulated the mesenchymal genes expression N-cadherin, vimentin, and TWIST, while upregulating epithelial genes like E-cadherin and cytokeratin-19.
Vim↓,
Twist↓,
E-cadherin↑,
ChemoSen↑, The combined treatment of 5 μM TQ and 2 μg/mL cisplatin was more effective in cancer growth and progression than either agent alone in a xenograft tumor mouse model.
eff↑, TQ–artemisinin hybrid therapy (2.6 μM) showed an enhanced ROS generation level and concomitant DNA damage induction in human colon cancer cells, while not affecting nonmalignant colon epithelial at 100 μM
EMT↓, TQ inhibits the survival signaling pathways to reduce carcinogenesis progress rate, and decreases cancer metastasis through regulation of epithelial to mesenchymal transition (EMT).
ROS↑, Apoptosis is induced by TQ in cancer cells through producing ROS, demethylating and re-expressing the TSG
DNMT1↓, inhibits DNMT1, figure 2
eff↑, TQ–vitamin D3 combination significantly reduced pro-cancerous molecules (Wnt, β-catenin, NF-κB, COX-2, iNOS, VEGF and HSP-90) a
EZH2↓, reduced angiogenesis by downregulating significant angiogenic genes such as versican (VCAN), the growth factor receptor-binding protein 2 (Grb2), and enhancer of zeste homolog 2 (EZH2), which participates in histone methylatio
hepatoP↑, Moreover, TQ improved liver function as well as reduced hepatocellular carcinoma progression
Zeb1↓, TQ decreases the Twist1 and Zeb1 promoter activities,
RadioS↑, TQ combined with radiation inhibited proliferation and induced apoptosis more than a TQ–cisplatin combination against SCC25 and CAL27 cell lines
HDAC↓, TQ has inhibited the histone deacetylase (HDAC) enzyme and reduced its total activity.
HDAC1↓, as well as decreasing the expression of HDAC1, HDAC2, and HDAC3 by 40–60%
HDAC2↓,
HDAC3↓,
*NAD↑, In non-cancer cells, TQ can increase cellular NAD+
*SIRT1↑, An increase in the levels of intracellular NAD+ led to the activation of the SIRT1-dependent metabolic pathways
SIRT1↓, On the other hand, TQ induced apoptosis by downregulating SIRT1 and upregulating p73 in the T cell leukemia Jurkat cell line
*Inflam↓, TQ treatment of male Sprague–Dawley rats has reduced the inflammatory markers (CRP, TNF-α, IL-6, and IL-1β) and anti-inflammatory cytokines (IL-10 and IL-4) triggered by sodium nitrite
*CRP↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*eff↑, The TQ–piperin combination has also decreased the oxidative damage triggered by microcystin in liver tissue and reduced malondialdehyde (MDA) and NO, while inducing glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathi
*MDA↓,
*NO↓,
*GSH↑,
*SOD↑,
*Catalase↑,
*GPx↑,
PI3K↓, repressing the activation of vital pathways, such as JAK/STAT and PI3K/AKT/mTOR.
mTOR↓,

3406-

TQ,

SeNPs,

A study to determine the effect of nano-selenium and thymoquinone on the Nrf2 gene expression in Alzheimer’s disease

in-vivo,

AD,

nano-selenium (5 mg/kg); thymoquinone (2 mg/kg);

50 albino male rats

*NRF2↑, Nrf2 mean expression levels in the nano-selenium-treated rats, the thymoquinone-treated rats, and the rats that were given both treatments all increased significantly compared to AD rats with no treatment.
*GSH↑, TQ and SeNPs demonstrated improvement in the levels of different biomarkers (Nrf2, Aβ-42, TNF-α, GSH & MDA) reversing them toward the normal levels.
*MDA↓, the mean brain tissue MDA levels in groups 3, 4, and 5 (27.37 ± 9.42, 29.23 ± 12.18, and 23.28 ± 4.89 nmol/mg protein, respectively) were significantly lower than those in group 2
*TNF-α↓, mean serum levels of TNF-α in groups 3, 4, and 5 (63.03 ± 11.07, 66.05 ± 9.96, and 36.41 ± 10.53 pg/ml) were found to be considerably lower than those in group 2

3405-

TQ,

doxoR,

Protective effect of thymoquinone against doxorubicin-induced cardiotoxicity and the underlying mechanism

vitro+vivo,

NA,

mice

*cardioP↑, thymoquinone can alleviate doxorubicin-induced cardiac toxicity in mice.
*NRF2↑, alleviate iron death in mouse cardiomyocytes by activating the Nrf2/HO-1 signaling pathway
*HO-1↑,
*ROS↓, Thymoquinone can also alleviate oxidative stress in mouse cardiomyocytes
*NQO1↑, similar effects on the expression levels of NQO1, COX-2, and NOX4
*COX2↓, implied
*NOX4↓, implied
*GPx4↑,
*FTH1↑, Reduces free iron, limiting ferroptosis
*p‑mTOR↓,
*TGF-β↓,

3424-

TQ,

Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein Complex

Review,

Var,

DNMT1↓, In this review, we highlight TQ as a potential multitarget single epidrug that functions by targeting the UHRF1/DNMT1/HDAC1/G9a complex
HDAC1↓,
TumCCA↑, inhibition of cell division, promotion of cell cycle arrest, activation of ROS production, induction of apoptosis and inhibition of tumor angiogenesis and metastasis
ROS↑,
Apoptosis↑,
angioG↓,
TumMeta↓,
selectivity↑, When compared to its effects on cancer cells, TQ has no or only mild cytotoxic effects on matched normal cells, such as normal human fibroblast cells [
BioAv↓, poor pharmacokinetics and chemical stability of TQ
BioAv↓, TQ is heat and light-sensitive, and it has poor solubility in aqueous media, which affects its biodistribution
HDAC1↓, T-ALL TQ decreased in the expression of HDAC1, 4 and 9
HDAC4↓,
UHRF1↓, TQ induces auto-ubiquitination of UHRF1 and subsequent degradation in cancer cells [23] by targeting its RING domain, which is the only domain of the UHRF1 structure that exhibits enzymatic activity
selectivity↑, via a specific inhibition of UHRF1 expression levels in cancer cells without affecting its expression in normal human cells.
G9a↓, TQ could quite possibly inhibit G9a and/or delocalize it from chromatin through its effects on UHRF1.

3403-

TQ,

A multiple endpoint approach reveals potential in vitro anticancer properties of thymoquinone in human renal carcinoma cells

in-vitro,

RCC,

786-O

TQ (1-100 μM) for 24 and 48 h

8.4 uM for 48 h

tumCV↓, TQ treatment clearly decreased cell viability in a concentration- and time-dependent manner.
ROS↑, TQ concentrations from 1 to 20 uM moderately increased ROS levels in approximately 20-30% comparing to control cells
TumCCA↑, an increase in the sub-G1 population was observed, especially at 30 μM,
eff↓, The co-treatment with GSH increases the cell viability of TQ-exposed cells
TumCI↓, As depicted in Fig. 8 (A-B), the % of invasion of 786-O cells treated with TQ (1 uM, 10 h) significantly decreased to 75.2% of controls

3402-

TQ,

Enhanced Apoptosis in Pancreatic Cancer Cells through Thymoquinone-rich Nigella sativa L. Methanol Extract: Targeting NRF2/HO-1 and TNF-α Pathways

in-vitro,

PC,

PANC1

in-vitro,

PC,

MIA PaCa-2

tumCV↓, TQ significantly decreased viability at 20 μM
NRF2↑, TQ enhances the expression of NRF2 and its downstream target HO-1, promoting antioxidant responses and cellular protection.
HO-1↑,
TNF-α↓,

3401-

TQ,

Molecular mechanisms and signaling pathways of black cumin (Nigella sativa) and its active constituent, thymoquinone: a review

Review,

Var,

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↑,

3400-

TQ,

Chemo,

Thymoquinone Ameliorates Carfilzomib-Induced Renal Impairment by Modulating Oxidative Stress Markers, Inflammatory/Apoptotic Mediators, and Augmenting Nrf2 in Rats

in-vitro,

Nor,

10 and 20 mg/kg b.w.)

TQ against CFZ-induced renal toxicity in rats

*GSH↑, 10 and 20 mg/kg TQ significantly decreased serum markers and increased antioxidant enzymes.
*SOD↑, TQ treatment (10 mg/kg) resulted in a significant rise in GSH (p < 0.001), CAT (p < 0.0001), and SOD
*lipid-P↓, highest doses of TQ (20 mg/kg) resulted in a significant reduction in lipid peroxidation compared to the CFZ group
*IL1β↓, TQ treatment considerably reduced IL-1β, IL-6, TNF-α, and caspase-3 concentrations.
*IL6↓,
*TNF-α↓,
*Casp3↓,
*Catalase↑,
*NRF2↑, TQ enhanced Nrf2 expression (p < 0.001), and this effect was only seen with 20 mg/kg
*RenoP↑, Degenerative kidney alterations caused by CFZ were reduced with TQ treatment (10 and 20 mg/kg

3399-

TQ,

Anticancer Effects of Thymoquinone through the Antioxidant Activity, Upregulation of Nrf2, and Downregulation of PD-L1 in Triple-Negative Breast Cancer Cells

in-vitro,

BC,

MDA-MB-231

NA,

BC,

MDA-MB-468

ROS↓, The results show that TQ exhibits considerable antioxidant activity and decreases the generation of H2O2,
H2O2↓,
Catalase↑, at the same time increasing catalase (CAT) activity, superoxide dismutase (SOD) enzyme, and glutathione (GSH
SOD↑,
GSH↑,
NQO1↑, TQ treatment increased the levels of the different genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM in both cell lines
GCLM↑,
NRF2↑, Nrf2 mRNA and protein expression were also significantly increased in TQ-treated TNBC cells
PD-L1↓, increased mRNA levels while decreasing PD-L1 protein expression in both cell lines
GSSG↑, Interestingly, a significant increase in GSSG was only found at 5 µM (p < 0.01), followed by a 50% significant reduction (p > 0.001) in GSSG at 15 µM of TQ.
GPx1⇅, TQ boosted GPX1 in MDA-MB-468 cells while decreasing GPX1 in MDA-MB-231 TNBC cells
GPx4↓, mda-mb-231

3398-

TQ,

5-FU,

Impact of thymoquinone on the Nrf2/HO-1 and MAPK/NF-κB axis in mitigating 5-fluorouracil-induced acute kidney injury in vivo

in-vivo,

Nor,

50-100mg/kg bw

Male albino Wistar rats

*RenoP↑, Pre-, post-, and cotreatment with TQ alleviated kidney injury
*TAC↑, by replenishing antioxidant reserves, reducing serum toxicity, decreasing ROS generation and lipid peroxidation, downregulating p38 MAPK/NF-κB axis/pathway proteins, and upregulating Nrf2 and HO-1,
*ROS↓, high-dose TQ alleviated ROS and H2O2 levels in groups III and IV
*lipid-P↓,
*p38↓,
*MAPK↓,
*NF-kB↓,
*NRF2↑,
*HO-1↑,
*MDA↓, TQ diminishes MDA levels
*GPx↑, GPx, GR, and CAT : restoration of GSH reserves and the abovementioned antioxidant enzymes
*GSR↑,
*Catalase↑,
*BUN↓, noticeable inhibition was observed in BUN, Cr, LDH, and KIM-1 at both doses
*LDH↓,
*IL1β↓, downregulation of IL-1β, diminishing inflammation

3397-

TQ,

Thymoquinone: A Promising Therapeutic Agent for the Treatment of Colorectal Cancer

Review,

CRC,

6-112uM (table 1)

ChemoSen↑, TQ can be used synergistically with chemotherapeutic agents to enhance their anticancer effects and to influence the expression of signaling pathways and other genes important in cancer development.
*Half-Life↝, These parameters remained associated with an elimination half-life (t1/2) of 63.43 ± 10.69 and 274.61 ± 8.48 min for intravenous and oral administration, respectively
*BioAv↝, TQ is characterized by slow absorption, rapid metabolism, rapid elimination and low physicochemical stability, which limits its pharmaceutical applications
*antiOx↑, Biologically active compounds from Nigella sativa have been shown to have antioxidant, antimicrobial, anti-inflammatory, antidiabetic, hepatoprotective, antiproliferative, proapoptotic, antiepileptic and immunomodulatory activities,
*Inflam↓,
*hepatoP↑,
TumCP↓, TQ exerts tumorigenic effects in a variety of ways, including modulation of the epigenetic machinery and effects on proliferation, the cell cycle, apoptosis, angiogenesis, carcinogenesis and metastasis
TumCCA↑,
Apoptosis↑,
angioG↑,
selectivity↑, TQ has low toxicity to normal cells, as confirmed by several studies, including studies on normal mouse kidney cells, normal human lung fibroblasts and normal human intestinal cells.
JNK↑, activation of c-Jun N-terminal kinases (JNK) and p38, as well as the phosphorylation of nuclear factor-?B (NF-?B) and the reduction of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K) activi
p38↑,
p‑NF-kB↑,
ERK↓,
PI3K↓,
PTEN↑, showing higher expression of p21/p27/PTEN/BAX/Cyto-C/Casp-3
Akt↓, TQ has also been shown to downregulate the PI3K/PTEN/Akt/mTOR and WNT/?-catenin pathways, which are critical for tumorigenesis
mTOR↓,
EMT↓, downregulating the epithelial to mesenchymal transition (EMT) transcription factors twist-related protein 1 (TWIST1) and E-cadherin
Twist↓,
E-cadherin↓,
ROS⇅, TQ has been shown to act as an antioxidant at low concentrations. Higher concentrations, however, induce apoptosis of cancer cells through the induction of oxidative stress
*Catalase↑, Thymoquinone upregulates the expression of genes encoding specific enzymes, such as catalase, superoxide dismutase, glutathione reductase, glutathione S-transferase and glutathione peroxidase, whose role is to protect against reactive oxygen species
*SOD↑,
*GSTA1↑,
*GPx↑,
*PGE2↓, TQ has the ability to downregulate NF-?B, interleukin-1?, tumor necrosis factor alpha, cyclooxygenase-2 (COX-2,) matrix metalloproteinase 13 (MMP-13), prostaglandin E2 (PGE2), the interferon regulatory factor, which are associated with inflammation a
*IL1β↓,
*COX2↓,
*MMP13↓,
MMPs↓, Figure 2
TumMeta↓,
VEGF↓,
STAT3↓, TQ affects the induction of apoptosis in cancer cells by blocking the signal transducer and activator of transcription 3 (STAT3) signaling
BAX↑, upregulation of Bax and inhibition of Bcl-2 and B-cell lymphoma-extra large (Bcl-xl) expression, as well as activated caspase-9, -7 and -3, and induced cleavage of poly (ADP-ribose) polymerase (PARP).
Bcl-2↑,
Casp9↑,
Casp7↑,
Casp3↑,
cl‑PARP↑,
survivin↓, TQ also attenuated the expression of STAT3 target gene products, such as survivin, c-Myc and cyclin-D1, -D2, and enhanced the expression of cell cycle inhibitory proteins p27 and p21
cMyc↓,
cycD1/CCND1↓,
p27↑,
P21↑,
GSK‐3β↓, TQ reduces the levels of p-PI3K, p-Akt, p-glycogen synthase kinase 3 (p-GSK3?) and ?-catenin, thereby inhibiting downstream COX-2 expression, which in turn leads to a reduction in PGE2
β-catenin/ZEB1↓,
chemoP↑, results support the potential use of thymoquinone in colorectal cancer chemoprevention, as TQ is effective in protecting and treating the DMH-initiated early phase of colorectal cancer.

2353-

TQ,

The effects of thymoquinone on pancreatic cancer: Evidence from preclinical studies

Review,

PC,

BioAv↝, Along with its high lipophilicity, TQ has slow absorption, rapid metabolism, rapid elimination, low bioavailability, and low physicochemical stability.
BioAv↑, TQ encapsulation passively directs the drug to the liver and releases the drug in a controlled and effective manner, improving the oral bioavailability of this hydrophobic molecule.
MUC4↓, TQ can decrease the expression of mucin 4 glycoprotein (MUC4), expressed in an exacerbated way in pancreatic cancer cells,
PKM2↓, The pyruvate kinase M2 isoform (PKM2), involved in the metabolism of cancer cells, showed a negative regulation in the presence of a TQ + GEM CI of 36 ± 0.66 and 25 ± 5.25 on the MIA PaCa-2 and PANC-1 cells, respectively.
eff↑, TQ can exert a synergistic effect with juglone, another cytotoxic dietary molecule for pancreatic cancer cells
TumVol↓, TQ significantly reduced by 67 % of the tumour size of the animals
HDAC↓, TQ modifies the H4 acetylation by decreased histone deacetylases (HDACs) expression inducing the pro-apoptotic signalling pathway
NF-kB↓, 10 µM MiaPaCa-2, BxPC-3, AsPC-1, HPAC ↓cell growth, ↑apoptosis, ↑NF-κB, ↓Bcl-2, ↓Bcl-xL, ↓survivin, ↓XIAP, ↓COX-2, ↓PGE
Bcl-2↓,
Bcl-xL↓,
survivin↓,
XIAP↓,
COX2↓,
PGE1↓,

2139-

TQ,

Thymoquinone regulates microglial M1/M2 polarization after cerebral ischemia-reperfusion injury via the TLR4 signaling pathway

in-vivo,

Nor,

acute ischemic stroke using a mouse middle cerebral artery ischemia-reperfusion (I/R) model.

*TLR4↓, TQ inhibits the TLR4 / NF-κB pathway to regulate microglia polarization.
*NF-kB↓,
*Inflam↓, TQ attenuates inflammation in brain I/R by affecting microglia polarization.
*Hif1a↑, TQ can activate Hif-1α to counter-regulate the TLR4 / NF-κB pathway.
*motorD↑, TQ could improve the motor deficits caused by I/R.

2138-

TQ,

Thymoquinone has a synergistic effect with PHD inhibitors to ameliorate ischemic brain damage in mice

in-vivo,

Nor,

TQ (5 mg/kg

Male C57 mice were used to establish an ischemic stroke model by using endothelin-1

*Hif1a↑, TQ can activate the HIF-1α pathway and its downstream genes such as VEGF, TrkB, and PI3K, which in turn enhance angiogenesis and neurogenesis.
*VEGF↑,
*TrkB↑,
*PI3K↑,
*angioG↑, which in turn enhance angiogenesis and neurogenesis.
*neuroG↑,
*motorD↑, TQ has the same effect as DMOG to activate HIF-1 α and can improve motor dysfunction after ischemic stroke

2137-

TQ,

Gastroprotective activity of Nigella sativa L oil and its constituent, thymoquinone against acute alcohol-induced gastric mucosal injury in rats

in-vivo,

Nor,

Male Wistar albino rats

*GSH↑, NS also increased gastric glutathione content (GSH), enzymatic activities of gastric superoxide dismutase (SOD) and glutathione-S-transferase (GST)
*SOD↑,
*GSTA1↑,

2136-

TQ,

Nigella sativa and thymoquinone suppress cyclooxygenase-2 and oxidative stress in pancreatic tissue of streptozotocin-induced diabetic rats

in-vivo,

Nor,

streptozotocin (STZ)-induced diabetic rats

*COX2↓, TQ significantly suppressed the expression of COX-2 enzyme in the pancreatic tissue.
*lipid-P↓, TQ treatment also suppressed pancreatic tissue lipid peroxidation malondialdehyde levels and increased the level of superoxide dismutase antioxidant enzyme
*SOD↑, Treatment with TQ (GE) restored SOD levels to normal after 30 days, with significant increases in SOD levels compared with the STZ-induced diabetic group
*ROS↓, TQ suppressed the induced expression of the inflammatory enzyme COX-2 in pancreatic tissues of STZ diabetic rats, which in turn will lead to a decrease in the production of ROS and thus providing protection against the destruction of A cells.
*Inflam↓, results may be attributed to the anti-inflammatory properties of N. sativa and TQ.
*NF-kB↓, TQ dose- and time-dependently significantly reduced COX-2 expression in pancreatic ductal adenocarcinoma cells paralleled with inhibition of NF-kB

2135-

TQ,

Thymoquinone induces heme oxygenase-1 expression in HaCaT cells via Nrf2/ARE activation: Akt and AMPKα as upstream targets

in-vitro,

Nor,

HaCaT

TQ (1, 5,
10, 20 lM) for 6 h

skin cells

*HO-1↑, TQ induced the expression of HO-1 in HaCaT/ Cells treated with TQ (1, 5, 10, 20 lM) for 6 h induced the expression of HO-1 protein. maximal induction observed until 12 h and then returned to basal level time thereafter
*NRF2↑, Treatment with TQ increased the localization of nuclear factor (NF)-erythroid2-(E2)-related factor-2 (Nrf2) in the nucleus and elevated the antioxidant response element (ARE)-reporter gene activity.
*e-ERK↑, TQ induced the phosphorylation of extracellular signal-regulated kinase (ERK), Akt and cyclic AMP-activated protein kinase-α (AMPKα).
*e-Akt↑,
*AMPKα↑,
*ROS⇅, Treatment of HaCaT cells with TQ resulted in a concentration-dependent increase in the intracellular accumulation of ROS (most occurs at 20uM concentration -see figure 5A) (later it drops the ROS)
*eff↓, pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKα activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells
*tumCV∅, does not change much 1-20uM of TQ (normal cells) see figure 1A

3573-

TQ,

Chronic diseases, inflammation, and spices: how are they linked?

Review,

Var,

NF-kB↓, Bladder cancer ↓NF-κB, ↓XIAP
XIAP↓,
PI3K↓, Cholangiocarcinoma ↓PI3K/Akt, ↓NF-κB
Akt↓,
STAT3↓, Gastric cancer ↓STAT3, ↓JAK2, ↓c-Src
JAK2↓,
cSrc↓,
PCNA↓, Lung cancer ↓PCNA, ↓CD1, ↓MMP-2, ↓ERK1/2
MMP2↓,
ERK↓,
Ki-67↓, Multiple myeloma ↓Ki-67, ↓VEGF, ↓Bcl-2, ↓p65
Bcl-2↓,
VEGF↓,
p65↓,
COX2↓, Myeloid leukemia ↓NF-κB, ↓CD1, ↓COX-2, ↓MMP-9
MMP9↓,

3561-

TQ,

Studi In Silico Potensi Piperine, Piperlongumine, dan Thymoquinone Sebagai Obat Alzheimer

NA,

AD,

*AChE↓, For interaction with AChe, piperine PIP is the best, followed by piperlongumine PL and TQ.
*BBB↑, TQ was able to penetrate the blood brain barrier (BBB) easily and has potentially active biological activity

3562-

TQ,

ACETYLCHOLINESTERASE AND GROWTH INHIBITORY EFFECTS–VARIOUS GRADES OF N. SATIVA OILS

Review,

AD,

Review,

Var,

*AChE↓, Black cumin oil containing 5% thymoquinone showed a dose-dependent increase in the acetylcholinesterase inhibition (64.47% inhibition at the dose of 20 μg/ml) which is similar to that of the standard acetylcholinesterase inhibitor donepezil
*other↓, Certain data suggest that cancer survivors have a decreased risk of Alzheimer’s disease.

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,

A rat model of AD was established in 6 month-old rats

*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

3564-

TQ,

The Potential Neuroprotective Effect of Thymoquinone on Scopolamine-Induced In Vivo Alzheimer's Disease-like Condition: Mechanistic Insights

in-vivo,

AD,

Thirty mice

*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

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↓,

3570-

TQ,

Thymoquinone alleviates the experimentally induced Alzheimer's disease inflammation by modulation of TLRs signaling

in-vivo,

AD,

 rat model of AD induced by a combination of aluminum chloride (AlCl3

*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

3571-

TQ,

The Role of Thymoquinone in Inflammatory Response in Chronic Diseases

Review,

Var,

Review,

Stroke,

*BioAv↓, TQ has poor bioavailability and is hydrophobic, prohibiting clinical trials with TQ alone.
*BioAv↑, TQ nanoparticle formulation shows better bioavailability than free TQ,
*Inflam↓, anti-inflammatory effects of TQ involve multiple complex signaling pathways as well as molecular mechanisms
*antiOx↑, antioxidant activity from the inhibition of oxidative stress
*ROS↓,
*GSH↑, GSH prevented ROS-mediated oxidative stress damage
*GSTs↑, TQ was found to exhibit antioxidant properties by increasing the levels of GSH and glutathione-S-transferase enzyme alpha-3 (GSTA3)
*MPO↓, TQ significantly reduced the disease activity index (DAI) and myeloperoxidase (MPO) activity, protecting the internal microenvironment of the colon.
*NF-kB↓, TQ reduced NF-κB signaling gene expression while alleviating the increase of COX-2 in skin cells induced by 12-O-tetradecanoylphorbol-13-acetate
*COX2↓,
*IL1β↓, reduced the expression of inflammatory factors such as IL-1β, TNF-α, IFN-γ, and IL-6
*TNF-α↓,
*IFN-γ↓,
*IL6↓,
*cardioP↑, TQ may exhibit substantial effects in the control of inflammation in CVD
*lipid-P↓, TQ reduces lipid accumulation and enhances antioxidant capacity and renal function.
*TAC↑,
*RenoP↑,
Apoptosis↑, Breast cancer TQ induces apoptosis and cell cycle arrest; reduces cancer cell proliferation, colony formation, and migration;
TumCCA↑,
TumCP↓,
TumCMig↓,
angioG↓, Colorectal Cancer (CRC) TQ inhibits the angiogenesis
TNF-α↓, Lung cancer TQ inhibits tumor cell proliferation by causing lung cancer cell apoptosis to significantly arrest the S phase cell cycle and significantly reduce the activity of TNF-a and NF-κB
NF-kB↓,
ROS↑, Pancreatic cancer TQ significantly increases the level of ROS production in human pancreatic cancer cells
EMT↓, TQ initiates the miR-877-5p and PD-L1 signaling pathways, inhibiting the migration and EMT of bladder cancer cells.
*Aβ↓, TQ significantly reduced the expression of Aβ, phosphorylated-tau, and BACE-1 proteins.
*p‑tau↓,
*BACE↓,
*TLR2↓, Parkinson’s disease (PD) TQ inhibits activation of the NF-κB pathway. TQ reduces the expression of TLR-2, TLR-4, MyD88, TNF-α, IL-1β, IFN-β, IRF-3, and NF-κB.
*TLR4↓,
*MyD88↓,
*IRF3↓,
*eff↑, TQ pretreatment produced a dose-dependent reduction in the MI area and significantly reduced the elevation of serum cardiac markers caused by ISO.
eff↑, Curcumin and TQ induced apoptosis and cell cycle arrest and reduced cancer cell proliferation, colony formation, and migration in breast cancer cells
DNAdam↑, nanomedicine with TQ that induced DNA damage and apoptosis, inhibited cell proliferation, and prevented cell cycle progression
*iNOS↓, TQ significantly reduced the expression of COX-2 and inducible nitric oxide synthase (iNOS)

3572-

TQ,

Enhanced oral bioavailability and hepatoprotective activity of thymoquinone in the form of phospholipidic nano-constructs

in-vivo,

Nor,

TQ, phospholipid nanoconstructs (PNCs)

*BioAv↑, After oral administration of a single dose of PNC, it showed a relative bioavailability of 386.03% vis-à-vis plain TQ suspension
*hepatoP↑, TQ-loaded PNC demonstrated significant enhanced hepato-protective effect vis-à-vis pure TQ suspension and silymarin, as evidenced by reduction in the ALP, ALT, AST, bilirubin, and albumin level and ratified by histopathological analysis.
*ALAT↓,
*ALP↓,
*AST↓,

3560-

TQ,

Protective effects of thymoquinone on D-galactose and aluminum chloride induced neurotoxicity in rats: biochemical, histological and behavioral changes

in-vivo,

AD,

orally TQ (20 mg/kg/dose) dissolved in corn oil
daily for 14 consecutive days

Forty Sprague Dawley male albino rats

*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.

4172-

TQ,

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

in-vivo,

AD,

rats

*cognitive↑, TQ-administered rats showed a profound beneficial effect on avoidance-related learning ability, associated with an increase in the hippocampal mRNA and protein levels of brain-derived neurotrophic factor (BDNF),
*BDNF↑,
*p‑CREB↑, TQ stimulates the phosphorylation of cAMP-response element-binding protein (CREB), the upstream signaling molecule in the BDNF pathway.
*ROS↓, chronic administration of TQ decreased lipid peroxide and reactive oxygen species levels in the hippocampus.
*memory↑, TQ plays a role in memory improvement in adult rats and that the CREB/BDNF signaling pathways are involved in mediating the actions of TQ in hippocampal neurogenesis.

4173-

TQ,

Thymoquinone Can Improve Neuronal Survival and Promote Neurogenesis in Rat Hippocampal Neurons

in-vivo,

NA,

 TQ (20 mg kg-1 d-1 )

 15 days to adult rats

*neuroP↑, TQ significantly increases the number of hippocampal neurons.
*Casp3↓, TQ significantly decreases the amount of Caspase-3 expression and the cleavage of poly ADP ribose polymerase, indicating a decrease in apoptosis.
*Apoptosis↓,
*ERK↑, ERK, GSK-3, JNK, CREB, and iNOS proteins are found to be positively regulated by TQ.
*JNK↑,
*CREB↑,
*iNOS↑,
*BDNF∅, gene expression of synapsin, synaptophysin, NGF, AKT, Bax, NFkB, and p53 and the protein expression of BDNF and nNOS are not affected by TQ.

4538-

TQ,

Thymoquinone Anticancer Effects Through the Upregulation of NRF2 and the Downregulation of PD‐L1 in MDA‐MB‐231 Triple‐Negative Breast Cancer Cells

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

MDA-MB-468

antiOx↑, TQ exhibits considerable antioxidant activity and decreases the generation of H2O2, at the same time increasing catalase (CAT) activity, superoxide dismutase (SOD) enzyme, and glutathione (GSH).
H2O2↓, Thymoquinone Decreases Hydrogen Peroxide Levels in TNBC
Catalase↑, Thymoquinone Increased Catalase Enzyme Activities in TNBC Cells
SOD↑, Increased Superoxide Dismutase (SOD) Enzyme Activities in Thymoquinone-TreatedTNBC Cells
GSH↑, significant induction of the total GSH and GSSG levels was measured in TQ-treated MDA-MB-231 cells
PRNP↑, TQ treatment increased the levels of the different genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM in both cell lines with significant large-fold change in MDA-MB-468
NQO1↑,
GCLM↑,
NRF2↑, Nrf2 mRNA and protein expression were also significantly increased in TQ-treated TNBC cells
PD-L1↓, , TQ administration increased mRNA levels while decreasing PD-L1 protein expression in both cell lines
chemoPv↑, TQ modifies the expression of multiple oxidative-stress-antioxidant system genes, ROS, antioxidant enzymes, Nrf2, and PD-L1 protein, pointing to the therapeutic potential and chemopreventive utilization of TQ in TNBC
ROS↓, Our study revealed that in the MDA-MB-231 TNBC cell line (Figure 2A), intracellular ROS generation was reduced by 10 (p = 0.0321), 15 (p = 0.0061), and 27% (p = 0.0004) at concentrations of 5, 10, and 15 μM, respectively,

Showing Research Papers: 1 to 50 of 138
Page 1 of 3 HSP&page=2&exSp=open">Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 138

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 8, Catalase↑, 6, GPx↑, 3, GPx4↑, 1, GSH↑, 9, GSR↑, 2, GSTA1↑, 2, GSTs↑, 2, HO-1↑, 5, lipid-P↓, 4, MDA↓, 7, MPO↓, 1, NOX4↓, 1, NQO1↑, 1, NRF2↑, 8, ROS↓, 14, ROS⇅, 1, SIRT3↑, 1, SOD↑, 10, SOD1↑, 1, TAC↑, 3, Thiols↑, 1,

Metal & Cofactor Biology ⓘ

FTH1↑, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, BUN↓, 1, CREB↑, 1, p‑CREB↑, 1, LDH↓, 1, NAD↑, 1, PPARγ↑, 1, SIRT1↑, 3,

Cell Death ⓘ

e-Akt↑, 1, Apoptosis↓, 3, Bcl-2↑, 1, Casp1?, 1, Casp1↓, 1, Casp3↓, 3, iNOS↓, 2, iNOS↑, 1, JNK↑, 1, MAPK↓, 1, p38↓, 1, Pyro?, 1,

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1, other↓, 1, tumCV∅, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1, e-ERK↑, 1, FOXO↑, 1, p‑mTOR↓, 1, neuroG↑, 1, PI3K↑, 1,

Migration ⓘ

MMP13↓, 2, MMP9↑, 1, TGF-β↓, 2,

Angiogenesis & Vasculature ⓘ

angioG↑, 2, eNOS↑, 1, Hif1a↑, 2, NO↓, 2, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

ASC?, 1, COX2↓, 6, CRP↓, 2, CXCc↓, 1, IFN-γ↓, 2, IFN-γ↑, 1, IL10↑, 1, IL12↓, 2, IL18↓, 1, IL1β↓, 13, IL6↓, 5, Inflam↓, 13, IP-10/CXCL-10↓, 1, MCP1↓, 2, MyD88↓, 2, NF-kB↓, 10, PGE2↓, 4, TLR2↓, 2, TLR4↓, 3, TNF-α↓, 11, TRIF↓, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 3, AChE↝, 1, BDNF↑, 1, BDNF∅, 1, GABA↑, 1, p‑tau↓, 2, TrkB↑, 1,

Protein Aggregation ⓘ

Aβ↓, 4, BACE↓, 1, NLRP3↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 2, BioAv↝, 1, eff↓, 1, eff↑, 3, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 1, CRP↓, 2, IL6↓, 5, LDH↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 1, cardioP↑, 4, cognitive↑, 6, hepatoP↑, 4, memory↑, 4, motorD↑, 2, neuroP↑, 8, OS↑, 1, radioP↑, 1, RenoP↑, 5, toxicity↓, 1,

Infection & Microbiome ⓘ

IRF3↓, 2,
Total Targets: 119

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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:162  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Thymoquinone Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Home Page