Luteolin / Catalase Cancer Research Results

LT, Luteolin: Click to Expand ⟱
Features:
Luteolin a Flavonoid found in celery, parsley, broccoli, onion leaves, carrots, peppers, cabbages, apple skins, and chrysanthemum flowers.
-MDR1 expression, MMP-9, IGF-1 and Epithelial to mesenchymal transition.

Luteolin — a naturally occurring polyhydroxylated flavone (3′,4′,5,7-tetrahydroxyflavone) found in celery, parsley, peppers, broccoli and numerous medicinal plants. It is a dietary phytochemical and experimental small-molecule anticancer/anti-inflammatory agent rather than an approved anticancer drug. Standard abbreviation: LUT or Lut. Luteolin occurs as the free aglycone and as plant glycosides; after oral administration, circulating luteolin is dominated by glucuronide and sulfate conjugates rather than free aglycone. Its cancer pharmacology is pleiotropic and strongly model-dependent, with particularly recurrent effects on PI3K/AKT/mTOR, NF-κB, STAT3, redox regulation, mitochondrial apoptosis, EMT/invasion and cell-cycle control.

Primary mechanisms (ranked):

  1. PI3K/AKT/mTOR survival signaling suppression, reducing proliferation and facilitating apoptosis, autophagy or other programmed cell-death responses.
  2. Redox-selective stress modulation: commonly ↑ ROS in susceptible cancer cells together with ↓ NRF2/HO-1/GSH-associated antioxidant defenses, while frequently reducing oxidative stress and activating protective antioxidant systems in normal tissues.
  3. NF-κB and inflammatory survival signaling inhibition, with context-dependent suppression of TNF-α, IL-6, COX-2 and related inflammatory mediators.
  4. Mitochondrial/intrinsic apoptosis activation through ↓ mitochondrial membrane potential, ↑ BAX:BCL-2 ratio, cytochrome-c release and caspase activation.
  5. STAT3/JAK signaling suppression, reducing survival, stemness, inflammatory signaling and immune-evasion phenotypes in several tumor models.
  6. EMT, migration and invasion suppression through modulation of E-cadherin, N-cadherin, vimentin, MMP2/MMP9, FAK, YAP/TAZ and related pathways.
  7. Cell-cycle arrest through suppression of cyclins/CDKs and context-dependent induction of p21/p27 and p53 signaling.
  8. Metabolic and hypoxic adaptation inhibition, including HIF-1α, PKM2, HK2 and glycolytic signaling in selected models.
  9. Epigenetic modulation, including reported inhibition of DNMTs, HDAC-associated signaling and EZH2 in selected cancer models.
  10. Additional context-dependent cell-death mechanisms including ER stress, autophagy, ferroptosis and pyroptosis.

Bioavailability / PK relevance: Oral luteolin has poor aqueous solubility and unfavorable systemic availability of unconjugated aglycone. It is absorbed from the intestine but undergoes extensive intestinal and hepatic glucuronidation and sulfation. Animal studies report low absolute bioavailability of free luteolin, commonly in the low-single-digit to low-tens percentage range depending on formulation and analytical definition. Nanoemulsions, lipid/phospholipid systems, cyclodextrins, nanoparticles and other delivery systems can substantially improve exposure experimentally. Luteolin and particularly some circulating conjugates can interact with OATP1B1/OATP2B1 transporters; in-vitro CYP inhibition has also been reported, making pharmacokinetic drug interactions plausible at sufficiently high exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM luteolin, often 20–50 µM or higher. These concentrations generally exceed sustained concentrations of free luteolin expected after conventional oral dietary or supplemental dosing because extensive conjugation limits circulating aglycone. Consequently, direct translation of many cell-culture IC50 values to standard oral supplementation is weak. Local gastrointestinal exposure, metabolites, tissue deconjugation and optimized formulations may partly alter this limitation.

Clinical evidence status: Predominantly preclinical, but no longer exclusively preclinical. A 2025 single-arm phase I study administered luteolin 50 mg/day for six months to five men with localized prostate cancer undergoing active surveillance; no treatment-related adverse events were reported, but the study was far too small and uncontrolled to establish anticancer efficacy. A larger phase II single-arm multicenter Japanese study of 50 mg/day for one year is currently recruiting with a planned enrollment of 40 patients. Luteolin is therefore best categorized as early-human/phase I–II investigational evidence, not established cancer therapy. Preclinical evidence for chemotherapy and radiotherapy sensitization is substantial but remains cancer-, drug- and genotype-dependent.


-Note half-life 2–3 hours
BioAv low, but could be improved with Res, or blend of castor oil, kolliphor and polyethylene glycol
Pathways:
- induce ROS production in cancer cell but a few reports of reduction. Always seems to reduce ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑">Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, LDHA↓, HK2↓, GRP78↑,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, TrxR**, - Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

-"Additionally, when reacted with concentrated sulfuric acid, a zinc salt is produced, resulting in a dark red and yellow solution. These color changes serve as a strong basis for the identification of luteolin"

Common Dietary and Plant Sources of Luteolin

Source Luteolin Content Approximate Equivalent Relative Source Level Notes
Bird chili 1035 mg/kg 103.5 mg/100 g Very high Highest source in the cited quantitative food table; concentration may vary substantially by cultivar, maturity and analytical method.
Belimbi leaves 464.5 mg/kg 46.45 mg/100 g Very high Leaf material; not a common Western dietary source.
Onion leaves 391 mg/kg 39.1 mg/100 g Very high Green onion/scallion-type leaf tissue can contain substantially more luteolin than onion bulbs.
Belimbi fruit 202 mg/kg 20.2 mg/100 g High Tropical fruit source.
Dried asam gelugur 107.5 mg/kg 10.75 mg/100 g High Dried plant material; dry-weight concentration is not directly comparable with fresh vegetables.
Celery 80.5 mg/kg 8.05 mg/100 g High One of the most commonly cited dietary sources of luteolin; content differs among celery varieties and plant parts.
Broccoli 74.5 mg/kg 7.45 mg/100 g High Common dietary source. Other compositional surveys report a broad range, indicating strong cultivar and methodology effects.
Carrot 37.5 mg/kg 3.75 mg/100 g Moderate Common dietary source; luteolin may occur predominantly in glycosylated forms.
Green chili 33 mg/kg 3.3 mg/100 g Moderate Content varies substantially among Capsicum species and cultivars.
Limau purut leaves 30.5 mg/kg 3.05 mg/100 g Moderate Kaffir lime leaves; primarily used as a culinary herb rather than consumed in large quantities.
French bean 11 mg/kg 1.1 mg/100 g Low to moderate Common food source but substantially lower than celery, broccoli or onion leaves in the cited dataset.
White radish 9 mg/kg 0.9 mg/100 g Low Lower-luteolin dietary source in the cited dataset.
Parsley Approximately 19.75 mg/100 g dried Approximately 197.5 mg/kg dried High Frequently cited as a rich luteolin-containing herb. Dry-weight values should not be compared directly with fresh-weight vegetables.
Thyme Approximately 51 mg/100 g Approximately 510 mg/kg Very high Herb source reported in reviews; intake per serving is usually small despite the high concentration.
Peppermint Approximately 11.33 mg/100 g fresh Approximately 113.3 mg/kg High Fresh peppermint is a relatively concentrated herbal source.
Spinach Approximately 1.11 mg/100 g Approximately 11.1 mg/kg Low to moderate Common dietary source but lower than many herbs and celery-family plants.
Cabbage Approximately 0.4–0.6 mg/100 g Approximately 4–6 mg/kg Low Widely consumed but generally a relatively dilute luteolin source.
Black olives Approximately 3.2–17.5 mg/100 g Approximately 32–175 mg/kg Moderate to high Luteolin concentration depends strongly on olive cultivar and processing.
Green olives Approximately 0.2–1.2 mg/100 g Approximately 2–12 mg/kg Low to moderate Generally reported at lower concentrations than black olives.
Apple peel Variable Not consistently quantified Low to moderate Luteolin is reported principally in the peel rather than the flesh; concentration is cultivar-dependent.
Chrysanthemum flowers Variable Not consistently quantified Potentially high Traditional medicinal/tea source containing luteolin and luteolin glycosides.


Luteolin — Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K / AKT / mTOR survival signaling ↓ PI3K; ↓ p-AKT; ↓ mTOR ↔ / adaptive modulation R–G ↓ survival and proliferation; ↑ cell death One of the most recurrent anticancer signaling effects; confirmed in multiple tumor systems and newer NSCLC studies.
2 ROS and antioxidant defense ↑ ROS; ↓ SOD/GSH/NRF2/HO-1 (context-dependent) ↓ ROS; ↑ antioxidant defenses (context-dependent) P–R Selective oxidative stress in susceptible tumors Biphasic and highly context-dependent. ROS generation can be mechanistically upstream of NF-κB inhibition, JNK activation, apoptosis and radiosensitization.
3 NRF2 / HO-1 antioxidant survival axis ↓ NRF2; ↓ HO-1 (model-dependent) ↑ NRF2; ↑ HO-1 (model-dependent) R–G ↓ tumor antioxidant capacity and drug resistance Especially relevant in NRF2-high cancer cells. Luteolin has sensitized tumor cells to chemotherapy through NRF2 suppression, whereas NRF2 activation contributes to normal-tissue protection.
4 NF-κB inflammatory survival signaling ↓ NF-κB; ↓ inflammatory survival signaling ↓ pathological NF-κB activation R–G ↑ apoptosis; ↓ inflammation and survival ROS accumulation can participate upstream in some tumor models; not all NF-κB inhibition requires ROS.
5 Mitochondria and intrinsic apoptosis ↓ MMP; ↑ BAX; ↓ BCL-2; ↑ Cyt-c; ↑ caspase-9/3 ↔ / ↓ mitochondrial injury under oxidative-stress conditions R–G ↑ mitochondrial apoptosis A common downstream execution mechanism following AKT inhibition, ROS elevation or ER stress.
6 JAK / STAT3 signaling ↓ STAT3; ↓ p-STAT3 ↔ / ↓ inflammatory STAT3 R–G ↓ proliferation, stemness and immune escape Recent work also links PRDX2 inhibition to JAK2/STAT3 suppression and ↓ PD-L1 in lung adenocarcinoma.
7 EMT and metastatic signaling ↓ EMT; ↑ E-cadherin; ↓ N-cadherin; ↓ vimentin; ↓ MMP2/9 ↔ G ↓ migration, invasion and metastasis PI3K/AKT, TGF-β/Smad, YAP/TAZ, FAK and related axes contribute depending on tumor type.
8 Cell-cycle control ↑ G1 or G2/M arrest; ↓ cyclins/CDKs; ↑ p21/p27 ↔ (model-dependent) G ↓ proliferation Cell-cycle phase varies with tumor lineage and concentration.
9 p53 / JNK apoptotic signaling ↑ JNK; ↑ p53 stability/activity (context-dependent) ↔ R–G ↑ apoptosis and chemotherapy response Cisplatin sensitization can depend strongly on functional p53.
10 Glycolysis and metabolic adaptation ↓ glycolysis; ↓ PKM2; ↓ HK2; ↓ ATP (model-dependent) ↔ G ↓ metabolic support for proliferation Not universal across cancers; strongest evidence comes from selected hepatocellular and other metabolically dependent models.
11 HIF-1α and hypoxic adaptation ↓ HIF-1α; ↓ hypoxic adaptation ↔ G ↓ angiogenesis and hypoxia tolerance Reported in breast, colon and other cancer models; linked to reduced VEGF signaling.
12 VEGF and angiogenesis ↓ VEGF; ↓ VEGFR signaling ↔ / anti-inflammatory vascular effects G ↓ tumor angiogenesis Predominantly preclinical evidence.
13 ER stress and unfolded protein response ↑ PERK/eIF2α/ATF4/CHOP; ↑ ER stress (model-dependent) ↓ pathological ER stress in several injury models R–G ↑ tumor cell death Illustrates luteolin's frequently opposite stress response in malignant versus nonmalignant models.
14 Autophagy ↑ Beclin-1; ↑ LC3-II; ↓ p62 (context-dependent) ↔ / protective modulation G Autophagic stress or contribution to cell death Can be cytotoxic or cytoprotective depending on cancer model and treatment context.
15 GPX4-dependent ferroptosis ↓ GPX4; ↓ GSH; ↑ lipid oxidation; ↑ ferroptosis ↔ / ↓ ferroptotic injury in some normal-tissue models R–G ↑ ferroptotic cancer-cell death Recent colon-cancer work supports GPX4-linked ferroptosis plus enhanced antitumor immune activation.
16 Epigenetic regulation ↓ DNMT activity; ↓ HDAC-associated signaling; ↓ EZH2 (model-dependent) ↔ / context-dependent G Re-expression of growth-suppressive programs Mechanistically interesting but less broadly established than AKT, redox and inflammatory pathways.
17 YAP / Wnt and tumor immunity ↓ YAP; ↓ Wnt-associated signaling; ↓ immune escape ↑ CTL functional activity indirectly G ↑ antitumor T-cell effectiveness 2025 animal work suggests luteolin can enhance tumor-specific CTL therapy; clinical relevance remains unproven.
18 Chemosensitization ↑ response to cisplatin and several other agents (drug-dependent) Variable; possible tissue protection in other contexts G ↓ treatment resistance Mechanisms include ↓ NRF2, ↓ AKT, ↑ p53/JNK, mitochondrial apoptosis and suppression of resistance pathways. Evidence remains predominantly preclinical.
19 Radiosensitization ↑ radiation-induced ROS and apoptosis Potential radioprotection reported in nonmalignant models R–G ↑ radiation response In NSCLC models, p38/ROS/caspase signaling increased radiosensitivity; tumor versus normal-tissue effects require careful context separation.
20 Clinical Translation Constraint High in-vitro concentrations often required Systemic exposure dominated by conjugated metabolites G Limits translation of cell-culture potency Poor aqueous solubility, extensive phase-II metabolism, formulation dependence, possible transporter/drug interactions and extremely limited controlled human oncology evidence remain major constraints.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr



Luteolin — Alzheimer’s disease relevance: Luteolin has substantial preclinical neuroprotective evidence and is sufficiently relevant to Alzheimer’s disease to warrant a separate database section. Reported effects include ↓ amyloid-β production/accumulation, ↓ BACE1-associated amyloidogenic processing, ↓ tau hyperphosphorylation, ↓ neuroinflammation, ↓ oxidative stress, ↓ NLRP3/NF-κB signaling and ↑ BDNF/TrkB-associated neuroplasticity. Acetylcholinesterase inhibition has also been reported. However, evidence remains predominantly cellular and animal; convincing disease-modifying clinical evidence in Alzheimer’s disease is absent. Oral bioavailability and blood-brain exposure of free luteolin remain important translational constraints.

Clinical evidence status: Preclinical. Contemporary reviews identify Alzheimer’s disease as the neurodegenerative disorder in which luteolin has been studied most extensively, but explicitly note that clinical therapeutic evidence remains deficient.

Luteolin — Alzheimer’s Disease Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Neuroinflammation / NF-κB ↓ NF-κB; ↓ IL-1β; ↓ IL-6; ↓ TNF-α ↓ chronic neuroinflammation Among the most consistently proposed neuroprotective actions.
2 Amyloid-β pathology ↓ Aβ; ↓ Aβ42 ↓ amyloid burden Supported predominantly by cellular and animal studies.
3 BACE1 / amyloidogenic processing ↓ BACE1 ↓ amyloidogenic APP processing Potential upstream mechanism contributing to reduced Aβ generation.
4 Tau phosphorylation ↓ p-tau ↓ tau pathology Multiple preclinical models report reduced abnormal tau phosphorylation.
5 Oxidative stress / NRF2 ↓ ROS; ↑ NRF2; ↑ antioxidant defenses ↓ neuronal oxidative injury Direction differs from the pro-oxidant effect frequently exploited in cancer cells.
6 NLRP3 inflammasome ↓ NLRP3 ↓ inflammasome-driven neuronal inflammation Potential bridge between redox stress and neuroinflammation.
7 BDNF / TrkB neuroplasticity ↑ BDNF; ↑ TrkB ↑ synaptic and neuronal support Observed in several neurobehavioral models.
8 Acetylcholinesterase ↓ AChE ↑ cholinergic signaling Primarily biochemical/preclinical evidence; clinical magnitude is unknown.
9 Neuronal apoptosis and mitochondrial stress ↓ apoptosis; ↓ mitochondrial injury ↑ neuronal survival Opposite phenotypic direction from luteolin-induced apoptosis in many cancer models.
10 Clinical Translation Constraint Low free-luteolin exposure; limited human CNS data Uncertain clinical efficacy Human Alzheimer’s disease efficacy trials are insufficient; brain exposure and formulation remain unresolved.


Catalase, Catalase: Click to Expand ⟱
Source:
Type:
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA.

Catalase and Cancer
Oxidative Stress and Cancer:
Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis.
Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells.
Expression Levels in Different Cancers:
Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior.
Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis.
Prognostic Implications:
Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress.

Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched).
Scientific Papers found: Click to Expand⟱
8377- LT,    Luteolin: exploring its therapeutic potential and molecular mechanisms in pulmonary diseases
- Review, Asthma, NA
*PI3K↑, multiple molecular mechanisms; these include inhibition of activation of the PI3K/Akt-mediated Nuclear Factor kappa-B (NF-κB) and MAPK signaling pathways, as well as the promotion of regulatory T cell (Treg)
*Akt↑,
*Inflam↓, alleviating inflammation and oxidative stress response
*ROS↓,
*BioAv↓, Luteolin, a naturally occurring polyphenol, is poorly water-soluble. The oral route may be ineffective because the gut poorly absorbs this type of flavonoid.
*RenoP↑, renoprotective (Diniz et al., 2022; Oyagbemi et al., 2021; Xiong et al., 2020), cardioprotective (Liu Z. et al., 2022; Xu et al., 2012) and neuroprotective (Nabavi et al., 2015; Ashaari et al., 2018) properties.
*cardioP↑,
*neuroP↑,
*antiAll↑, anti-allergic (Liang et al., 2020), anti-diabetic (Pradhan and Kulkarni, 2024),
*AntiDiabetic↑,
*hepatoP↑, hepatoprotective (Yao et al., 2023) and antithrombotic (Choi et al., 2015)
*AntiThr↑,
*toxicity↓, Numerous studies have indicated that the toxicity of luteolin is minimal, showing no significant harmful effects in clinical trials
*IL10↓, anti-inflammatory effects of luteolin are associated with reduced IL-10 levels.
*Sepsis↓, Luteolin protects lung tissue from SALI and reduces the excessive accumulation of IL-10 in the lungs during sepsis
*TNF-α↓, Celebi and colleagues found that luteolin mainly reduces the expression of TNF-α mRNA, decreases oxidative stress,
*ROS↓,
*GSH↑, An increase in malondialdehyde (MDA) caused by free radicals formed during sepsis was normalized by luteolin treatment, which improved glutathione (GSH) levels, CAT, and superoxide dismutase (SOD) activity, and reduced MDA levels
*Catalase↑,
*SOD↑,
*MDA↓,
*lipid-P↓, counteracting lipid peroxidation.
*IL4↓, decreased the levels of interleukin-4 (IL-4) and interleukin-5 (IL-5) in the BALF, attenuating the asthmatic characteristics of the experimental mice
*IL5↓,
*PGE2↓, inhibiting the production of Prostaglandin E2 (PGE2) (Jin et al., 2009).
*PI3K↑, luteolin activated the PI3K/Akt/mTOR pathway in the lung tissues of asthmatic mice and inhibited the Beclin-1-PI3KC3 protein complex.
*Akt↑,
*mTOR↑,
*Beclin-1/ATG6↓,
*Mucositis↓, suppressing excessive mucus secretion.
*PLA2↓, Figure6
STAT3↓, Luteolin inhibits the STAT3 signaling pathway and the expression of PD-L1, thereby exposing tumor cells to T cells of the immune system (
PD-L1↓,
miR-34a↓, luteolin upregulates the expression of miR-34a, which may subsequently inhibit the proliferation of non-small cell lung cancer (NSCLC)
Casp3↑, activation of caspase-9 and caspase-3, decreases the expression of Bcl-2, increases the expression of BAX, increases the BAX/Bcl-2 ratio, and induces apoptosis
Casp9↑,
Bcl-2↓,
BAX↑,
Bax:Bcl2↑,
Apoptosis↑,
ROS↑, accumulation of ROS induced by luteolin
EMT↓, Luteolin has been demonstrated to inhibit EMT and downregulate E-cadheri
E-cadherin↓,
DR5↑, By increasing DR5 expression and Drp1-mediated mitochondrial fission, luteolin enhances the sensitivity of NSCLC cells to TRAIL
LIMK1↓, suppresses tumor growth by inhibiting LIMK1 activity
Pain↓, luteolin also possesses the ability to alleviate bone cancer pain

8382- LT,    Luteolin as a dietary flavonoid for brain health: modulating neuroinflammation and cognitive decline in neurodegenerative disorders
- Review, AD, NA - Review, Park, NA
*neuroP↑, been recognized as a potentially effective neuroprotective nutraceutical because of its remarkable anti-inflammatory, antioxidant, and neurotrophic properties.
*Inflam↓,
*antiOx↑,
*NF-kB↓, Luteolin significantly inhibits microglial activation, reduces pro-inflammatory cytokine production, modulates the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, and enhances Nrf2-mediated antioxidant
*NRF2↑,
*BDNF↑, promotes synaptic plasticity through brain-derived neurotrophic factor (BDNF)-associated pathways
*cognitive↑, Preclinical studies consistently demonstrate substantial improvements in cognitive function, motor performance, demyelination, and neuronal viability in models of AD, PD, MS, and HD.
*motorD↑,
*BBB↑, Accumulating preclinical and nascent clinical evidence indicates that luteolin is able to cross the blood-brain barrier (BBB), reducing neuroimmune activation, promoting neuronal viability, and enhancing cognitive performance in models of AD, PD, and
*BioAv↓, The absolute oral bioavailability of luteolin is quite low due to its limited solubility and rapid metabolism; yet, its metabolites preserve considerable biological activity that may enhance its neuroprotective properties
*NO↓, curtails the production of nitric oxide and reactive oxygen species (ROS)
*ROS↓,
*NRF2↑, Numerous investigations reveal that luteolin stimulates the Nrf2/ARE pathway, enhancing the production of phase II antioxidant enzymes and thus fortifying cellular endurance against ROS
*ARE↑,
*MMP↑, At the mitochondrial level, luteolin protects membrane potential, decreases ROS generation, and limits permeability transition; these actions collectively support ATP synthesis
*BDNF↑, luteolin may elevate the levels of brain-derived neurotrophic factor (BDNF) and amplify the downstream tropomyosin receptor kinase B signaling,
*Learn↑, protective actions converge to enhance learning and memory across various animal models exhibiting cognitive deficits.
*memory↑,
*cognitive↑,
*p‑JNK↓, Luteolin (80 mg/kg/day, i.c.v.) AD mice (Aβ1-42 oligomers injected) Cognitive impairment ↓, p-JNK ↓, p38 MAPK ↓, GFAP ↓, Iba-1 ↓, TNF-α ↓, IL-1β ↓, Bax ↓, Bcl-2 ↑, Caspase-3 ↓, Cox-2 ↓, BACE-1 ↓, Aβ1-42 ↓, PSD-95 ↑, SN
*GFAP↓,
*AIF1/Iba-1↓,
*TNF-α↓,
*IL1β↓,
*BAX↓,
*COX2/PTGS2↓,
*BACE/β-secretase↓,
*Aβ42↓,
*PSD95↑,
*SNAP25↑, SNAP-25 ↑
*lipid-P↓, Luteolin (5, 10, 15, 20 μM in diet) Transgenic Drosophila expressing human Aβ42 Lifespan ↑, climbing ability ↑, activity ↑, LPO ↓, PCC ↓, GST ↓, GSH ↑, SOD ↓, CAT ↓, AChE ↓, caspase-3/9 ↓, Aβ42 plaque ↓
*GSTs↓,
*GSH↑,
*SOD↓,
*Catalase↓,
*AChE↓,
*Casp3↓,
*Casp9↓,

8403- LT,    Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
- in-vitro, CRC, HT-29
tumCV↓, Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC).
selectivity↑,
Apoptosis↑, Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells
Casp↑,
MMP↓, Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol
Ca+2↑,
BAX↑,
Bcl-2↓,
Cyt‑c↑,
Casp9↑, increased the levels of the active forms of caspase-9 and caspase-3
Casp3↑,
ROS↓, Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells.
SOD↑,
Catalase↑,
GSH↑, Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis.
antiOx↑, luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.
MAPK↑,

8390- LT,    Luteolin in Inflammatory Bowel Disease and Colorectal Cancer: A Disease Continuum Perspective
- Review, IBD, NA - Review, CRC, NA
*Diff↝, luteolin regulates immune cell differentiation, mitigates inflammation and oxidative stress, modulates gut microbiota, and restores intestinal mucosal barrier function in IBD.
*Inflam↓,
*ROS↓, Reduction in the Inflammatory Response and Reactive Oxygen Species (ROS)
*GutMicro↑,
*IBI↑,
TumCP↓, In the context of CRC, luteolin demonstrates significant anti-tumor effects by inhibiting cancer cell proliferation, inducing apoptosis, and suppressing cell migration and invasion.
Apoptosis↑,
TumCMig↓,
TumCI↓,
*BioAv↑, such as the use of polymer micelles and responsive nanoparticles, have greatly improved the bioavailability and efficacy of luteolin.
*iNOS↓, It effectively mitigates the inflammatory response by decreasing the expression of inflammatory mediators such as inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF-α), and interleukin-6 (IL-6).
*TNF-α↓,
*IL6↓,
*MDA↓, luteolin lowered colonic dialdehyde (MDA) levels, a biomarker of lipid peroxidation, indicating its antioxidant effects
*lipid-P↓,
*antiOx↑,
*NRF2↑, The antioxidant properties of luteolin are associated with its activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway.
*HO-1↑, This pathway activation enhances the expression of antioxidant enzymes, including heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1), which are crucial for maintaining intracellular redox balance
*NQO1↑,
*SOD↑, Luteolin treatment also increased the activities of colonic superoxide dismutase (SOD) and catalase (CAT), key components of the cellular antioxidant defense system that help mitigate oxidative stress damage
*Catalase↑,
*5HT↓, Luteolin reduced the generation of 5-HT by inhibiting TPH-1 expression and the MAPK/ERK signaling pathway, thus producing an inhibitory effect on intestinal inflammation
*TPH1↓,
*MAPK↓,
*ERK↓,
*Inflam↓,
cycD1/CCND1↓, luteolin downregulates the expression of Cyclin D1 and CDK4, blocking the transition of CRC cells from the G1 phase to the S phase, thereby reducing cell proliferation
CDK4↓,
TumCCA↑,
Casp3↑, luteolin activates Caspase-3 and Caspase-9, triggering the mitochondrial pathway to promote cell death.
Casp9↑,
PI3K↓, luteolin inhibits the activation of the PI3K/Akt signaling pathway, reducing the phosphorylation of Akt and mTOR, thus inhibiting CRC cell survival
Akt↓,
p‑Akt↓,
p‑mTOR↓,
E-cadherin↑, enhancement of E-cadherin levels while simultaneously reducing N-cadherin and Vimentin
N-cadherin↓,
Vim↓,

2907- LT,    Protective effect of luteolin against oxidative stress‑mediated cell injury via enhancing antioxidant systems
- in-vitro, Nor, NA
*ROS↓, Intracellular ROS levels and damage to cellular components such as lipids and DNA in H2O2-treated cells were significantly decreased by luteolin pretreatment.
*Casp9↓, Luteolin suppressed active caspase-9 and caspase-3 levels while increasing Bcl-2 expression and decreasing Bax protein levels.
*Casp3↓,
*Bcl-2↑,
*BAX↓,
*GSH↑, luteolin restored levels of glutathione that was reduced in response to H2O2.
*SOD↑, luteolin enhanced the activity and protein expressions of superoxide dismutase, catalase, glutathione peroxidase, and heme oxygenase-1.
*Catalase↑,
*GPx↑,
*HO-1↑,
*antiOx↑, upregulating antioxidant enzymes.
*lipid-P↓, protective effect of luteolin against lipid peroxidation
*p‑γH2AX↓, showed that luteolin pretreatment diminished expression levels of phospho-H2A.X in H2O2-exposed cells
eff↑, promising therapeutic agent for management and treatment of conditions such as COPD and pulmonary fibrosis.

2906- LT,    Luteolin, a flavonoid with potentials for cancer prevention and therapy
- Review, Var, NA
*Inflam↓, anti-inflammation, anti-allergy and anticancer, luteolin functions as either an antioxidant or a pro-oxidant biochemically
AntiCan↑,
antiOx⇅, With low Fe ion concentrations (< 50 μM), luteolin behaves as an antioxidant while high Fe concentrations (>100 μM) induce luteolin's pro-oxidative effect
Apoptosis↑, induction of apoptosis, and inhibition of cell proliferation, metastasis and angiogenesis.
TumCP↓,
TumMeta↓,
angioG↓,
PI3K↓, , luteolin sensitizes cancer cells to therapeutic-induced cytotoxicity through suppressing cell survival pathways such as phosphatidylinositol 3′-kinase (PI3K)/Akt, nuclear factor kappa B (NF-κB), and X-linked inhibitor of apoptosis protein (XIAP)
Akt↓,
NF-kB↓,
XIAP↓, luteolin inhibits PKC activity, which results in a decrease in the protein level of XIAP by ubiquitination and proteasomal degradation of this anti-apoptotic protein
P53↑, stimulating apoptosis pathways including those that induce the tumor suppressor p53
*ROS↓, Direct evidence showing luteolin as a ROS scavenger was obtained in cell-free systems
*GSTA1↑, Third, luteolin may exert its antioxidant effect by protecting or enhancing endogenous antioxidants such as glutathione-S-transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT)
*GSR↑,
*SOD↑,
*Catalase↑,
*other↓, luteolin may chelate transition metal ions responsible for the generation of ROS and therefore inhibit lipooxygenase reaction, or suppress nontransition metal-dependent oxidation
ROS↑, Luteolin has been shown to induce ROS in untransformed and cancer cells
Dose↝, It is believed that flavonoids could behave as antioxidants or pro-oxidants, depending on the concentration and the source of the free radicals
chemoP↑, may act as a chemopreventive agent to protect cells from various forms of oxidant stresses and thus prevent cancer development
NF-kB↓, We found that luteolin-induced oxidative stress causes suppression of the NF-κB pathway while it triggers JNK activation, which potentiates TNF-induced cytotoxicity in lung cancer cells
JNK↑,
p27/CDKN1B↑, Table 1
P21↑,
DR5↑,
Casp↑,
Fas↑,
BAX↑,
MAPK↓,
CDK2↓,
IGF-1↓,
PDGF↓,
EGFR↓,
PKCδ↓,
TOP1↓,
TOP2↓,
Bcl-xL↓,
FASN↓,
VEGF↓,
VEGFR2/KDR/Flk1↓,
MMP9↓,
Hif1a↓,
FAK↓,
MMP1↓,
Twist↓,
ERK↓,
P450↓, Recently, it was determined that luteolin potently inhibits human cytochrome P450 (CYP) 1 family enzymes such as CYP1A1, CYP1A2, and CYP1B1, thereby suppressing the mutagenic activation of carcinogens
CYP1A1↓,
CYP1A2↓,
TumCCA↑, Luteolin is able to arrest the cell cycle during the G1 phase in human gastric and prostate cancer, and in melanoma cells

2904- LT,    Luteolin from Purple Perilla mitigates ROS insult particularly in primary neurons
- in-vitro, Park, SK-N-SH - in-vitro, AD, NA
*ROS↓, Food-derived compound luteolin possesses multitarget actions including reactive oxygen species (ROS)-scavenging activit
*neuroP↑, Upon the ROS-insulted primary neurons, luteolin concentration-dependently enhanced neuronal cell survival with efficacy higher than and potency similar to vitamin E.
*MMP↑, prevented the decreases in activities of mitochondria, catalase, and glutathione in ROS-insulted primary neurons
*Catalase↑, decreases of catalase/glutathione activity by H 2O 2 were markedly reversed following luteolin treatment.
*GSH↑,
selectivity↑, Results showed that luteolin mildly inhibited the viability of SK-N-SH cells (50% inhibition at 68.7 uM) and relatively strongly inhibited that of HuH-7 cells (50% inhibition at 14.3 uM), but did not affect that of primary neurons
*eff↑, luteolin can be designated as a potent neuroprotectant as well as suggesting that it may be effective either in the treatment of neurodegenerative diseases, such as cerebral ischemia, Parkinsons, and AD, or in the improvement of brain aging
*Cyt‑c↓, reduction of cytochrome c release from mitochondria into cytosome,

986- LT,  doxoR,    Luteolin as a glycolysis inhibitor offers superior efficacy and lesser toxicity of doxorubicin in breast cancer cells
- in-vitro, BC, 4T1 - in-vitro, BC, MCF7
SOD↓, the activity of SOD and CAT was increased in serum and was decreased in tumor by Lu in vivo
Catalase↓,
Glycolysis↓, glycolytic inhibitor

2919- LT,    Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence
- Review, Var, NA
RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP/DDIT3↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration

2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, , by inactivating proteins; such as procaspase‐9, CDC2 and cyclin B or upregulation of caspase‐9 and caspase‐3, cytochrome C, cyclin A, CDK2, and APAF‐1, in turn inducing cell cycle
CDC2↓,
CycB/CCNB1↓,
Casp9↑,
Casp3↑,
Cyt‑c↑,
cycA1/CCNA1↑,
CDK2↓, inhibit CDK2 activity
APAF1↑,
TumCCA↑,
P53↑, enhances phosphorylation of p53 and expression level of p53‐targeted downstream gene.
BAX↑, Increasing BAX protein expression; decreasing VEGF and Bcl‐2 expression it can initiate cell cycle arrest and apoptosis.
VEGF↓,
Bcl-2↓,
Apoptosis↑,
p‑Akt↓, reduce expression levels of p‐Akt, p‐EGFR, p‐Erk1/2, and p‐STAT3.
p‑EGFR↓,
p‑ERK↓,
p‑STAT3↓,
cardioP↑, Luteolin plays positive role against cardiovascular disorders by improving cardiac function
Catalase↓, It can reduce activity levels of catalase, superoxide dismutase, and GS4
SOD↓,
*BioAv↓, bioavailability of luteolin is very low. Due to the momentous first pass effect, only 4.10% was found to be available from dosage of 50 mg/kg intake of luteolin
*antiOx↑, luteolin classically exhibits antioxidant features
*ROS↓, The antioxidant potential of luteolin and its glycosides is mainly due to scavenging activity against reactive oxygen species (ROS) and nitrogen species
*NO↓,
*GSTs↑, Luteolin may also have a role in protection and enhancement of endogenous antioxidants such as glutathione‐S‐transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT)
*GSR↑,
*SOD↑,
*Catalase↑,
*lipid-P↓, Luteolin supplementation significantly suppressed the lipid peroxidation
PI3K↓, inhibits PI3K/Akt signaling pathway to induce apoptosis
Akt↓,
CDK2↓, inhibit CDK2 activity
BNIP3↑, upregulation of BNIP3 gene
hTERT/TERT↓, Suppress hTERT in MDA‐MB‐231 breast cancer cel
DR5↑, Boost DR5 expression
Beclin-1/ATG6↑, Activate beclin 1
TNF-α↓, Block TNF‐α, NF‐κB, IL‐1, IL‐6,
NF-kB↓,
IL1↓,
IL6↓,
EMT↓, Suppress EMT essentially notable in cancer metastasis
FAK↓, Block EGFR‐signaling pathway and FAK activity
E-cadherin↑, increasing E‐cadherin expression by inhibiting mdm2
MDM2↓,
NOTCH↓, Inhibit NOTCH signaling
MAPK↑, Activate MAPK to inhibit tumor growt
Vim↓, downregulation of vimentin, N‐cadherin, Snail, and induction of E‐cadherin expressions
N-cadherin↓,
Snail↓,
MMP2↓, negatively regulated MMP2 and TWIST1
Twist↓,
MMP9↓, Inhibit matrix metalloproteinase‐9 expressions;
ROS↑, Induce apoptosis, reactive oxygen development, promotion of mitochondrial autophagy, loss of mitochondrial membrane potential
MMP↓,
*AChE↓, Reduce AchE activity to slow down inception of Alzheimer's disease‐like symptoms
*MMP↑, Reverse mitochondrial membrane potential dissipation
*Aβ↓, Inhibit Aβ25‐35
*neuroP↑, reduces neuronal apoptosis; inhibits Aβ generation
Trx1↑, luteolin against human bladder cancer cell line T24 was due to induction cell‐cycle arrest at G2/M, downregulation of p‐S6, suppression of cell survival, upregulation of p21 and TRX1, reduction in ROS levels.
ROS↓,
*NRF2↑, Luteolin reduced renal injury by inhibiting XO activity, modulating uric acid transporters, as well as activating Nrf2 HO‐1/NQO1 antioxidant pathways and renal SIRT1/6 cascade.
NRF2↓, Luteolin exerted anticancer effects in HT29 cells as it inhibits nuclear factor‐erythroid‐2‐related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway
*BBB↑, Luteolin can be used to treat brain cancer due to ability of this molecule to easily cross the blood–brain barrier
ChemoSen↑, In ovarian cancer cells, luteolin chemosensitizes the cells through repressing the epithelial‐mesenchymal transition markers
GutMicro↑, Luteolin was also observed to modulate gut microbiota which reduce the number of tumors in case of colorectal cancer by enhancing the number of health‐related microbiota and reduced the microbiota related to inflammation
*antiAll↑, Asthma Inhibit the mucus overproduction as well as suppress the GABAA receptors
*Mucositis↓,
*TregCell↑, Decrease inflammation in allergic asthma by activating Treg cells
*Beclin-1/ATG6↓, Inhibit autophagy in pulmonary tissues via restricting beclin1‐PI3KC3 protein complex and activating PI3K/Akt/mTOR signaling pathway
*PI3K↑,
*Akt↑,
*mTOR↑,

2915- LT,    Luteolin promotes apoptotic cell death via upregulation of Nrf2 expression by DNA demethylase and the interaction of Nrf2 with p53 in human colon cancer cells
- in-vitro, Colon, HT29 - in-vitro, CRC, SNU-407 - in-vitro, Nor, FHC
DNMTs↓, luteolin inhibited the expression of DNA methyltransferases, a transcription repressor, and increased the expression and activity of ten-eleven translocation (TET) DNA demethylases,
TET1↑,
NRF2↑, luteolin decreased the methylation of the Nrf2 promoter region, which corresponded to the increased mRNA expression of Nrf2
HDAC↓, Recently, Zao et al. demonstrated that luteolin epigenetically activates the Nrf2 pathway by downregulating DNA methyltransferase (DNMT) and histone deacetylase (HDAC) expression
tumCV↓, Luteolin decreased the viability of all three cell lines in a dose-dependent manner
BAX↑, luteolin upregulated the expression of the apoptotic protein Bax, active caspase-9, and active caspase-3, while it downregulated the expression of the anti-apoptotic protein Bcl-2,
Casp9↑,
Casp3↑,
Bcl-2↓,
ROS↓, Luteolin promotes ROS scavenging by inducing the expression of antioxidant enzymes
GSS↑, luteolin increased the protein expression of the antioxidant enzymes GCLc, GSS, catalase, and HO-1 in a dose- and time-dependent manner
Catalase↑,
HO-1↑,
DNMT1↓, Luteolin markedly decreased the protein expression of DNMT1, DNMT3A, and DNMT3B in a dose- and time-dependent manner
DNMT3A↓,
TET1↑, In contrast, it markedly increased the protein expression of TET1, TET2, and TET3 in a dose- and time-dependent manner
TET3↑,
TET2↓,
P53↑, Luteolin upregulated the expression of p53 and its target p21 in a dose- and time-dependent manner
P21↑,


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   antiOx⇅, 1,   Catalase↓, 3,   Catalase↑, 2,   GPx↓, 1,   GSH↓, 2,   GSH↑, 1,   GSR↓, 1,   GSS↑, 1,   GSTs↓, 1,   HO-1↓, 1,   HO-1↑, 1,   NQO1↓, 1,   NRF2↓, 2,   NRF2↑, 1,   ROS↓, 3,   ROS↑, 4,   SOD↓, 3,   SOD↑, 1,   SOD2↓, 1,   Trx1↑, 1,   VitC↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FASN↓, 1,   Glycolysis↓, 1,   SIRT1↓, 1,  

Cell Death(tgid=5) ⓘ

AIF↑, 1,   APAF1↑, 1,   Apoptosis↑, 5,   ASC↓, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Bcl-xL↓, 1,   BNIP3↑, 1,   Casp↑, 2,   Casp1↓, 1,   Casp3↑, 6,   Casp8↑, 1,   Casp9↑, 5,   proCasp9↓, 1,   Cyt‑c↑, 3,   DR5↑, 4,   Fas↑, 2,   FasL↑, 1,   MDM2↓, 1,   p‑MDM2↓, 1,   p‑p38↑, 1,   XIAP↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 3,   p‑Akt↓, 3,   EGFR↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   HGF/c-Met↓, 1,   IKKα↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   LIMK1↓, 1,   MAPK↓, 2,   MAPK↑, 2,   mTOR↓, 1,   p‑mTOR↓, 1,   PI3K↓, 3,   p‑PI3K↓, 1,   PKCδ↓, 1,   PTEN↓, 1,   p‑Src↓, 1,   STAT3↓, 2,   p‑STAT3↓, 1,   p‑STAT6↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,   DNMTs↓, 1,   H3↓, 1,   H4↓, 1,   HDAC↓, 2,   miR-34a↓, 1,   TET3↑, 1,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   p‑eIF2α↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,   LC3II↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

hTERT/TERT↓, 1,   P53↑, 3,   PARP↑, 1,   PCNA↓, 1,   TOP1↓, 1,   TOP2↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 3,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 2,   p27/CDKN1B↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD34↓, 1,   cFos↑, 1,   IGF-1↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   TumCP↓, 2,  

Migration(tgid=13) ⓘ

AXL↓, 1,   Ca+2↑, 1,   Cdc42↓, 1,   E-cadherin↓, 2,   E-cadherin↑, 2,   EMT↓, 3,   FAK↓, 3,   ITGB1↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin↓, 3,   PDGF↓, 1,   Rac1↓, 1,   Rho↓, 1,   Snail↓, 2,   TET1↑, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 1,   Twist↓, 2,   Tyro3↓, 1,   Vim↓, 2,   Vim↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 3,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

CLDN1↓, 1,   MMP↓, 2,   ZO-1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ICAM-1↓, 1,   IL1↓, 1,   IL2↑, 1,   IL6↓, 2,   NF-kB↓, 4,   NLRP3↓, 1,   p‑p65↓, 1,   PD-1↓, 1,   PD-L1↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   CYP1A1↓, 2,   CYP1A2↓, 1,   Dose↝, 1,   eff↑, 1,   P450↓, 1,   RadioS↑, 1,   selectivity↑, 2,   TET2↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↓, 1,   CEA↓, 1,   EGFR↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   hTERT/TERT↓, 1,   IL6↓, 2,   NSE↓, 1,   PD-L1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cachexia↓, 1,   cardioP↑, 1,   chemoP↑, 2,   Pain↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,  
Total Targets: 177

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 4,   ARE↑, 1,   Catalase↓, 1,   Catalase↑, 7,   GPx↑, 2,   GSH↑, 5,   GSR↑, 2,   GSTs↓, 1,   GSTs↑, 2,   HO-1↑, 2,   lipid-P↓, 6,   MDA↓, 2,   NQO1↑, 1,   NRF2↑, 4,   ROS↓, 8,   SOD↓, 1,   SOD↑, 6,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PLA2↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 2,   Bcl-2↑, 1,   Casp3↓, 3,   Casp9↓, 2,   Cyt‑c↓, 1,   iNOS↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↑, 3,   ERK↓, 1,   p‑JNK↓, 1,   MAPK↓, 1,   mTOR↑, 2,   PI3K↑, 3,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,   other↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↓, 2,  

DNA Damage & Repair(tgid=10) ⓘ

p‑γH2AX↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Diff↝, 1,  

Migration(tgid=13) ⓘ

TregCell↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   IBI↑, 1,   MMP↑, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

AIF1/Iba-1↓, 1,   COX2/PTGS2↓, 1,   IL10↓, 1,   IL10↑, 1,   IL1β↓, 2,   IL4↓, 1,   IL5↓, 1,   IL6↓, 1,   Inflam↓, 5,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 4,  

Cellular Microenvironment(tgid=17) ⓘ

GFAP↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   AChE↓, 2,   BDNF↑, 2,   PSD95↑, 1,   SNAP25↑, 1,   TPH1↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   Aβ42↓, 1,   BACE/β-secretase↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 3,   BioAv↑, 1,   eff↑, 2,   GSTA1↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 2,   AntiDiabetic↑, 1,   cardioP↑, 1,   cognitive↑, 2,   hepatoP↑, 1,   Learn↑, 1,   memory↑, 1,   motorD↑, 1,   Mucositis↓, 2,   neuroP↑, 4,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,   Sepsis↓, 1,  
Total Targets: 82

Scientific Paper Hit Count for: Catalase, Catalase
11 Luteolin
1 doxorubicin
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#:118  Target#:46  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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