Luteolin / Inflam 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↑,
- lowers Inflam">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.


Inflam, inflammation: Click to Expand ⟱
Source:
Type:
Cancer and inflammation are closely linked, with chronic inflammation contributing to the development and progression of cancer. Various inflammatory mediators and cells are involved in this process.
Scientific Papers found: Click to Expand⟱
7815- Api,  LT,  NarG,  QC,  MOR  The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer’s disease: a narrative review
- Review, AD, NA
*Inflam?, 13 natural flavonoids (apigenin, luteolin, naringenin, quercetin, morin, kaempferol, fisetin, isoquercitrin, astragalin, rutin, icariin, mangiferin, and anthocyanin) derived from plants or medicinal herbs on neuroinflammation in Alzheimer’s diseas

8375- LT,    Luteolin, a flavone ingredient: Anticancer mechanisms, combined medication strategy, pharmacokinetics, clinical trials, and pharmaceutical researches
- Review, Var, NA
TumCP↓, luteolin executes multiple anticancer effects mainly by dampening proliferation and invasion, spurring apoptosis, intercepting cell cycle, regulating autophagy and immune, inhibiting inflammatory response, inducing ferroptosis, and pyroptosis
TumCI↓,
Apoptosis↑,
TumCCA↑,
Inflam↓,
Ferroptosis↑,
Pyro↑,
ChemoSen↑, Luteolin can be applied in combination with numerous clinical anticarcinogens and natural ingredients to synergistically enhance the therapeutic efficacy of malignancies while reducing adverse reactions.
chemoP↑,
*BioAv↓, luteolin has an unfavorable oral bioavailability, it mainly persists in plasma as glucuronides and sulfate-conjugates after being metabolized,
OATPs↓, regarded as potent inhibitors of OATP1B1 and OATP2B1

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

8379- LT,    Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*neuroP↑, Luteolin, a natural flavonoid abundant in medicinal plants, fruits, and vegetables, exerts multifaceted neuroprotective effects across diverse experimental disease models.
*Inflam↓, attenuate inflammatory mediator release, reduce oxidative stress-induced neuronal damage, and inhibit apoptosis, thereby counteracting neuroinflammation-driven pathology
*ROS↓,
*Apoptosis↓,
*BioAv↓, notably limited oral bioavailability and restricted blood-brain barrier (BBB) permeability
*BBB∅,
Ferroptosis↑, In colon cancer, luteolin promotes ferroptosis in tumor cells by facilitating the accumulation of ROS/Fe2+, lipid peroxidation, elevated MDA, GSH depletion, and downregulation of GPX4.
ROS↑,
Iron↑,
lipid-P↑,
MDA↑,
GSH↓,
GPx4↓,
*Aβ↓, Similarly, combined treatment with luteolin and exercise reverses the increase in Aβ conten
*memory↑, reducing neuroinflammation and thereby slowing the progression of memory dysfunction in AD
*neuroG↑, Luteolin treatment promotes hippocampal neurogenesis, improves dendritic spine maturation and the dendritic arborization of hippocampal and cortical neurons
*NRF2↑, luteolin significantly enhances the expression of Nrf2 while concurrently downregulating NLRP3 inflammasome activation.
*NLRP3↓,
*ROS↓, This attenuates oxidative stress, inflammatory responses, and neuronal degeneration, exerting a protective effect by inhibiting the NLRP3 inflammasome
JAK2↓, Research has found that in lung adenocarcinoma, luteolin binds to PRDX2, inhibiting the JAK2/STAT3 pathway, reducing PD-L1 expression, and promoting the release of perforin and granzyme B by CD8+ T cells.
STAT3↓,
PD-L1↓,
Perforin↝,
GranB/GZMB↝,
hepatoP↑, In esophageal cancer, combination therapy with luteolin and paclitaxel mitigates paclitaxel-induced hepatotoxicity,
*Learn↑, studies have demonstrated that in AD, luteolin treatment dose-dependently improves spatial learning and memory deficits in AD mouse models.
*TNF-α↓, (evidenced by reduced levels of TNF-α, IL-1β, IL-6, NO, COX-2, and iNOS protein)
*IL1β↓,
*IL6↓,
*NO↓,
*COX2/PTGS2↓,
*iNOS↓,
*ER Stress↓, luteolin decreases the expression of ER stress markers GRP78 and IRE1α in brain tissue.
*GRP78/BiP↓,
*IRE1↓,
*cognitive↑, thereby contributing to cognitive improvement
*BAX↓, Bax, Bcl-2, Caspase-3, and Cox-2 is significantly diminished, while the expression of synaptic markers like PSD-95 and SNAP-25 is markedly increased.
*Bcl-2↓,
*Casp3↓,
*PSD95↑,
*SNAP25↑,
*JNK↓, luteolin may attenuate Aβ-related neuroinflammation and neurodegeneration, potentially through the inhibition of JNK signaling
*eff↑, Combinatorial therapy with DHA, luteolin, and UA has shown enhanced efficacy in inhibiting Aβ pathology
*mtDam↓, By reversing mitochondrial swelling and restoring mitochondrial transmembrane potential, it augments antioxidant capacity and exerts neuroprotective effects following cerebral ischemia
*MMP↑,
*Stroke↓,
*TJ↑, Luteolin also inhibited the degradation of tight junction proteins and decreased MMP9 expression, thereby ameliorating BBB permeability
*MMP9↓,
*BBB∅,
*NeuroI↓, luteolin may provide neuroprotection following cerebral ischemia-reperfusion injury by inhibiting neuroinflammation and oxidative stress.

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↓,

8367- LT,    Role of Luteolin in Prevention of Oral, Esophageal, Gastric, Pancreatic, and Colon Cancers: Recent Trends and Future Perspectives
- Review, Var, NA
*antiOx↑, The multifaceted protective mechanism/s offered by luteolin are contributed by its antioxidative, anti-inflammatory, and anti-proliferative properties, thus characterizing it as a potent drug candidate against gastrointestinal cancers.
ROS↓, Particularly, the impact of luteolin on limiting esophageal and gastric cancers is mediated by alleviating oxidative stress, inhibiting chronic inflammation, and significant induction of apoptosis
Inflam↓,
Apoptosis↑,

7825- LT,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, neuroprotective activity of luteolin was also observed in a transgenic Drosophila model.
*OS↑, showed that luteolin extend the life span of Drosophila, enhanced its antioxidative ability, and directly bound to Aβ42 and AChE to inhibit the Aβ aggregation and cholinergic deficits
*antiOx↑,
*Aβ42↓,
*AChE↓,
*Aβ↓,
*IRes↓, It was found that luteolin (50 mg/kg) reduced cerebral insulin resistance and tau hyperphosphorylation in a high fat diet (HFD
*p‑tau↓,
*ROS↓, neuroprotective activity in AD was achieved by inhibition of oxidative stress, apoptosis, neuroinflammation, AChE activity, cerebral insulin resistance, or iron imbalance.
*Apoptosis↓,
*Inflam↓,
*Iron↝,

4338- LT,    Luteolin: a natural product with multiple mechanisms for atherosclerosis
- Review, NA, NA
*Inflam↓, Figure 2
*ROS↓,
*PDGF↓, luteolin 7-glucoside (L7G) can inhibit PDGF-BB-induced VSMC proliferation and DNA synthesis by blocking the phosphorylation of PLC-γ1, Akt, and Erk1/2, ultimately inhibiting VSMC proliferation.
*lipid-P↓, luteolin prevents aortic lipid accumulation and atherosclerotic plaque formation in LDLR −/− mice induced by a Western diet.
*AMPK↑, luteolin prevents aortic lipid accumulation and atherosclerotic plaque formation in LDLR −/− mice induced by a Western diet.
*SIRT1↑,
*AntiAg↑,

4293- LT,    Regulatory Role of NF-κB on HDAC2 and Tau Hyperphosphorylation in Diabetic Encephalopathy and the Therapeutic Potential of Luteolin
- in-vivo, Diabetic, NA
*Inflam↓, luteolin, a natural flavonoid compound with anti-inflammatory, antioxidant, and neuroprotective properties.
*antiOx↑,
*neuroP↑,
*cognitive↑, results indicated that treatment with luteolin improved the degree of cognitive impairment in mice with DE.
*p‑mTOR↓, decreased the levels of phosphorylated mTOR, phosphorylated NF-κB, and histone deacetylase 2 (HDAC2) and increased the expression of brain-derived neurotrophic factor and synaptic-related proteins
*p‑NF-kB↓,
*HDAC2↓,
*BDNF↑,
*other↓, luteolin may also directly target HDAC2, as an HDAC2 inhibitor, to alleviate DE, complementing mTOR/NF-κB signaling inhibition
*p‑tau↓, HDAC2 and tau hyperphosphorylation are regulated by the mTOR/NF-κB signaling cascade in DE, and luteolin is found to reverse these effects, demonstrating its protective role in DE

8393- LT,    Progress, pharmacokinetics and future perspectives of luteolin modulating signaling pathways to exert anticancer effects: A review
- Review, Var, NA
TumCP↓, induce apoptosis, inhibition of tumor cell proliferation and metastasis, anti-angiogenesis, reversal of epithelial-mesenchymal transition, regulation of immune function, synergism with anti-cancer drugs and regulation of reactive oxygen species level
TumMeta↓,
angioG↓,
EMT↓,
Imm↝,
ChemoSen↑,
*Inflam↓, Luteolin are known for their natural anti-inflammatory properties,
*COX2/PTGS2↓, It inhibits the synthesis and activity of COX-2, a key enzyme in prostaglandins.
*NF-kB↓, luteolin can also inhibit the activation of nuclear factor Kappa-light-chain-enhancer of activated B cells (NF-κB)
MMP2↓, luteolin significantly decreased the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) whilst also inhibiting the phosphorylation of AKT and PI3K
MMP9↓,
p‑Akt↓,
p‑PI3K↓,
IGF-2↓, insulin-like growth factor 2 (IGF-2) and insulin growth factor receptor 1 (IGF-1R) were significantly reduced in human colon cancer cells (HT-29) treated with luteolin,
IGF-1R↓,
CXCL16↓, luteolin reduced the mRNA levels of CXC chemokine ligand 16 (CXCL16) to inhibit the PI3K/AKT pathway
NOTCH1↓, this anti-tumor effect may be associated with a reduction in key factors that promote tumor development such as Notch-1, Hes-1, VEGF, and MMPs
HES1↓,
VEGF↓,
ROS↑, Ju et al[86] found that Luteolin can lead to the accumulation of ROS,

8398- LT,    Luteolin: Nature's promising warrior against Alzheimer's and Parkinson's disease
- Review, AD, NA - Review, Park, NA
*antiOx↑, Luteolin is a flavone that possesses potent antioxidant and anti-inflammatory properties.
*Inflam↓,
*AntiBio↑, Luteolin has antiinflammatory, antimicrobial, antioxidant, anticancer, antiulcer, antiinfluenza, cytoprotective, hepatoprotective, neuroprotective, cardioprotective, neurogenesis, and neurotrophic activity, macrophage polarization, and detoxifying fr
*AntiCan↑,
*hepatoP↑,
*neuroP↑,
*cardioP↑,
*neuroG↑,
*BBB↑, In addition, luteolin can pass the blood–brain barrier and employ its neuroprotective effects.
*ROS↓, Luteolin decreases oxidative stress, suppresses inflammation, microglia activation, neurotoxicity, acetylcholinesterase (AChE), and tau phosphorylation, prevents the production of β‐amyloid plaques
*AChE↓,
*p‑T-cadherin↓,
*Aβ↓,
*memory↑, improves memory.
*TNF-α↓, inhibiting the release of pro‐inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin (IL)‐1β, as well as chemokines like CCL2 and CCL5 from human mast cells.
*IL1β↓,
*MCP1/CCL2↓,
*RANTES↓,
*BioAv↑, a recent study looked at how much luteolin is bioavailable in peanut hull extract (PHE). maximum concentration of luteolin in plasma reached 8.34 ± 0.98 μg/mL for PHE and 1.97 ± 0.15 μg/mL for luteolin.
*Half-Life↝, The time to attain the maximal plasma concentration was 0.520 ± 0.05 h for PHE and 1.02 ± 0.22 h for luteolin. Furthermore, the luteolin half‐life (t1/2) was 4.94 ± 1.2 h while the PHE t1/ 2 was 2.772 ± 0.54 h.
*toxicity↓, Luteolin is generally considered safe and lacks recognized toxicity
*BACE/β-secretase↓, Markers such as (BACE1), (Aβ1–42), Cox‐2, Bcl‐2, Caspase‐3, and Bax, were drastically decreased
*Aβ42↓,
*COX2/PTGS2↓,
*Bcl-2↓,
*Casp3↓,
*BAX↓,
*GSTs↓, reduced GST, LPO, AChE, PCC, CAT, caspase 3, and caspase 9 activity, reduced Aβ42 peptides expression
*lipid-P↓,
*Casp3↓,
*Casp9↓,
*memory↑, improved memory impairment and halted CA1 pyramidal cell layer shrinkage
*GSK‐3β↓, decreased levels of GSK‐3 activation, β‐amyloid deposition, pro‐inflammatory cytokines, and phosphorylated tau
*ChAT↑, increased activity of ChAT, SOD, GSH‐Px, inhibited oxidative injuries, enhanced activity of AchE was reversed and increased Ach content while MDA reduced
*SOD↑,
*GPx↑,
*MDA↓,
*ER Stress↓, decrease in the expression of estrogen receptor (ER) stress markers, including GRP78 and inositol‐requiring transmembrane kinase/ endoribonuclease 1α, in brain tissues.[
*GRP78/BiP↓,
*NRF2↑, figure 3
*motorD↑, improved motor asymmetry and motor impairment
*antiAll↑, Luteolin has also demonstrated antiallergic efficacy both in vitro as well as in vivo via several mechanisms, involving the release of histamine suppression.

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↓,

4292- LT,    Luteolin for neurodegenerative diseases: a review
- Review, AD, NA - Review, Park, NA - Review, MS, NA - Review, Stroke, NA
*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE/β-secretase↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*Synergy↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats

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

2921- LT,    Luteolin as a potential hepatoprotective drug: Molecular mechanisms and treatment strategies
- Review, Nor, NA
*hepatoP↑, Due to its excellent liver protective effect, luteolin is an attractive molecule for the development of highly promising liver protective drugs.
*AMPK↑, fig2
*SIRT1↑,
*ROS↓,
STAT3↓,
TNF-α↓,
NF-kB↓,
*IL2↓,
*IFN-γ↓,
*GSH↑,
*SREBP1/SREBF1↓,
*ZO-1↑,
*TLR4↓,
BAX↑, anti cancer
Bcl-2↓,
XIAP↓,
Fas↑,
Casp8↑,
Beclin-1/ATG6↑,
*TXNIP↓, luteolin inhibited TXNIP, caspase-1, interleukin-1β (IL-1β) and IL-18 to prevent the activation of NLRP3 inflammasome, thereby alleviating liver injury.
*Casp1↓,
*IL1β↓,
*IL18↓,
*NLRP3↓,
*MDA↓, inhibiting oxidative stress and regulating the level of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH)
*SOD↑,
*NRF2↑, luteolin promoted the activation of the Nrf2/ antioxidant response element (ARE) pathway and NF-κB cell apoptosis pathway, thereby reversing the decrease in Nrf2 levels(lead induced liver injury)
*ER Stress↓, down regulate the formation of nitrotyrosine (NT) and endoplasmic reticulum (ER) stress induced by acetaminophen, and alleviate liver injury
*ALAT↓, ↓ALT, AST, MDA, iNOS, NLRP3 ↑GSH, SOD, Nrf2
*AST↓,
*iNOS↓,
*IL6↓, ↓TXNIP, NLRP3, TNF-α, IL-6 ↑HO-1, NQO1
*HO-1↑,
*NQO1↑,
*PPARα↑, ↓TNF-α, IL-6 IL-1β, Bax ↑PPARα
*ATF4↓, ↓ALT, AST, TNF-α, IL-6, MDA, ATF-4, CHOP ↑GSH, SOD
*CHOP/DDIT3↓,
*Inflam↓, Luteolin ameliorates MAFLD through anti-inflammatory and antioxidant effects
*antiOx↑,
*GutMicro↑, luteolin could significantly enrich more than 10% of intestinal bacterial species, thereby increasing the abundance of ZO-1, down regulating intestinal permeability and plasma lipopolysaccharide

4231- LT,    Luteolin and its antidepressant properties: From mechanism of action to potential therapeutic application
- Review, AD, NA
*PSD95↑, upregulating the expression of synaptophysin, postsynaptic density protein 95, brain-derived neurotrophic factor, B cell lymphoma protein-2, superoxide dismutase, and glutathione S-transferase; and decreasing the expression of malondialdehyde, caspa
*BDNF↑,
*SOD↑,
*GSTA1↑,
*MDA↑,
*Casp3↓,
*Mood↑, antidepressant effects of luteolin are mediated by various mechanisms, including anti-oxidative stress, anti-apoptosis, anti-inflammation, anti-endoplasmic reticulum stress, dopamine transport, synaptic protection, hypothalamic–pituitary–adrenal axi
*antiOx↑,
*Apoptosis↓,
*Inflam↓,
*ER Stress↓,


Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx⇅, 1,   GPx4↓, 1,   GSH↓, 1,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   ROS↓, 1,   ROS↑, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FASN↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 5,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 2,   DR5↑, 2,   Fas↑, 2,   Ferroptosis↑, 2,   GranB/GZMB↝, 1,   Perforin↝, 1,   Pyro↑, 1,   XIAP↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 2,   p‑Akt↓, 2,   EGFR↓, 1,   ERK↓, 1,   IGF-1R↓, 1,   JAK2↓, 1,   JNK↑, 1,   LIMK1↓, 1,   MAPK↓, 1,   p‑mTOR↓, 1,   PI3K↓, 2,   p‑PI3K↓, 1,   PKCδ↓, 1,   STAT3↓, 3,  

Transcription & Epigenetics(tgid=7) ⓘ

HES1↓, 1,   miR-34a↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   TOP1↓, 1,   TOP2↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   p27/CDKN1B↑, 1,   TumCCA↑, 3,  

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

IGF-1↓, 1,   IGF-2↓, 1,   NOTCH1↓, 1,   TumCP↓, 4,  

Migration(tgid=13) ⓘ

E-cadherin↓, 1,   E-cadherin↑, 1,   EMT↓, 2,   FAK↓, 1,   MMP1↓, 1,   MMP2↓, 1,   MMP9↓, 2,   N-cadherin↓, 1,   PDGF↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumMeta↓, 2,   Twist↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   Hif1a↓, 1,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

OATPs↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CXCL16↓, 1,   Imm↝, 1,   Inflam↓, 2,   NF-kB↓, 3,   PD-L1↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   CYP1A1↓, 1,   CYP1A2↓, 1,   Dose↝, 1,   P450↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   PD-L1↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 2,   hepatoP↑, 1,   Pain↓, 1,  
Total Targets: 91

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 9,   ARE↑, 1,   Catalase↓, 1,   Catalase↑, 3,   GPx↑, 1,   GSH↑, 3,   GSR↑, 1,   GSTs↓, 2,   HO-1↑, 3,   Iron↝, 1,   lipid-P↓, 5,   MDA↓, 4,   MDA↑, 1,   NQO1↑, 2,   NRF2↑, 7,   ROS↓, 12,   SOD↓, 1,   SOD↑, 7,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 2,   ATP↑, 1,   GSK‐3β↓, 2,   PLA2↓, 1,   SIRT1↑, 2,   SREBP1/SREBF1↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 3,   BAX↓, 3,   Bax:Bcl2↓, 1,   Bcl-2↓, 2,   Casp1↓, 1,   Casp3↓, 6,   Casp9↓, 2,   Casp9↑, 1,   iNOS↓, 3,  

Kinase & Signal Transduction(tgid=6) ⓘ

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

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,   ATF4↓, 1,   HDAC2↓, 1,   other↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   ER Stress↓, 4,   GRP78/BiP↓, 2,   GRP78/BiP↑, 1,   IRE1↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↓, 1,  

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

Diff↝, 1,   neuroG↑, 2,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   MMP9↓, 1,   PDGF↓, 1,   p‑T-cadherin↓, 1,   TXNIP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,   BBB∅, 2,   IBI↑, 1,   MMP↑, 2,   TJ↑, 1,   ZO-1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

AIF1/Iba-1↓, 1,   COX2/PTGS2↓, 4,   IFN-γ↓, 1,   IL10↓, 1,   IL18↓, 1,   IL1β↓, 5,   IL2↓, 1,   IL33↓, 1,   IL4↓, 1,   IL5↓, 1,   IL6↓, 4,   IL8↓, 1,   Inflam?, 1,   Inflam↓, 14,   MCP1/CCL2↓, 1,   NeuroI↓, 1,   NF-kB↓, 3,   p‑NF-kB↓, 1,   NLRP3↓, 2,   PGE2↓, 1,   RANTES↓, 1,   TLR4↓, 1,   TNF-α↓, 6,  

Cellular Microenvironment(tgid=17) ⓘ

GFAP↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   AChE↓, 3,   BDNF↑, 5,   ChAT↑, 1,   PSD95↑, 3,   SNAP25↑, 2,   TPH1↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 4,   Aβ42↓, 3,   BACE/β-secretase↓, 3,   tau↓, 1,   p‑tau↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARα↑, 1,   PPARγ↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 2,   BioAv↝, 1,   eff↑, 1,   GSTA1↑, 2,   Half-Life↝, 1,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   IL6↓, 4,   IRes↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 2,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 2,   cognitive↑, 5,   hepatoP↑, 3,   Learn↑, 2,   memory↑, 5,   Mood↑, 1,   motorD↑, 2,   Mucositis↓, 1,   neuroP↑, 7,   OS↑, 1,   RenoP↑, 1,   Stroke↓, 1,   toxicity↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiBio↑, 1,   GutMicro↑, 2,   Sepsis↓, 1,  
Total Targets: 139

Scientific Paper Hit Count for: Inflam, inflammation
16 Luteolin
1 Apigenin (mainly Parsley)
1 Naringin
1 Quercetin
1 Morin
1 Mung Bean Sprouts
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#:953  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page