Database Query Results : Silymarin (Milk Thistle) silibinin, , NF-kB

SIL, Silymarin (Milk Thistle) silibinin: Click to Expand ⟱
Features:
Silymarin (Milk Thistle) Flowering herb related to daisy and ragweed family.
Silibinin (INN), also known as silybin is the major active constituent of silymarin, a standardized extract of the milk thistle seeds.
-a flavonoid combination of 65–80% of seven flavolignans; the most important of these include silybin, isosilybin, silychristin, isosilychristin, and silydianin. Silybin is the most abundant compound in around 50–70% in isoforms silybin A and silybin B

-Note half-life 6hrs?.
BioAv not soluble in water, low bioAv (1%). 240mg yielded only 0.34ug/ml plasma level. oral administration of SM (equivalent to 120 mg silibinin), total (unconjugated + conjugated) silibinin concentration in plasma was 1.1–1.3 μg/mL, so can not achieve levels used in most in-vitro studies.
Pathways:
- results for both inducing and reducing ROS in cancer cells. In normal cell seems to consistently lower ROS. Reports show both ROS↑ and ROS↓ in cancer models; systemic pro-oxidant effects may require higher exposures than typical oral dosing, but local or combination contexts may differ. (level in GUT could be much higher (800uM).
- ROS↑ related: MMP↓(ΔΨm), Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓">NF-kB↓, COX2↓, p38↓(context-dependent; often stress-activated), Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, FAK↓, NF-κB↓, CXCR4↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, GRP78↑(ER stress), Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi1↓, β-catenin↓, Notch2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS / redox buffering + mitochondrial protection Often ↑ stress susceptibility; can support apoptosis when survival signaling is blocked ↓ oxidative stress; mitochondrial protection P, R, G Context-selective redox modulation Silymarin is classically cytoprotective/antioxidant in normal tissues (notably liver), while in tumors it can weaken pro-survival adaptation and increase vulnerability to stressors and therapy.
2 Intrinsic apoptosis (mitochondria → caspases) ↑ apoptosis signaling; ↑ caspase activation ↔ minimal activation G Cell death execution Common downstream outcome in cancer models: apoptosis increases after earlier signaling/redox shifts and/or checkpoint disruption.
3 Cell-cycle control (cyclins/CDKs; checkpoints) ↑ arrest (G1/S or G2/M depending on model) ↔ G Cytostasis Typically observed as reduced proliferation with checkpoint engagement; timing usually later than kinase phosphorylation changes.
4 NF-κB inflammatory transcription ↓ NF-κB activity; ↓ inflammatory/pro-survival tone ↔ or protective anti-inflammatory effect R, G Anti-inflammatory / anti-survival transcription NF-κB suppression can reduce tumor-promoting inflammation and blunt stress-adaptive survival programs.
5 JAK/STAT3 axis (incl. PD-L1 / immune escape programs in some models) ↓ STAT3 signaling (context); may ↓ PD-L1 in certain tumor contexts ↔ R, G Reduced survival + immune-evasion signaling Reported to attenuate STAT3-driven tumor programs and, in some contexts, reduce immune-suppressive signaling (model dependent).
6 PI3K → AKT → mTOR survival / growth signaling ↓ PI3K/AKT/mTOR signaling (context) ↔ R, G Growth/survival suppression Reduced PI3K/AKT/mTOR tone increases sensitivity to apoptosis and can reinforce cell-cycle arrest.
7 MAPK re-wiring (ERK/p38/JNK balance) Stress-MAPK shifts; ERK tone often reduced or re-patterned ↔ P, R, G Signal reprogramming Early phosphorylation shifts can precede later gene-expression changes; exact ERK direction is model and dose dependent.
8 Angiogenesis (VEGF and angiogenic factors) ↓ VEGF / angiogenesis outputs ↔ G Anti-angiogenic support Typically reflected in reduced pro-angiogenic expression/secretion and angiogenesis-related phenotypes over longer windows.
9 EMT / invasion / migration programs (incl. TGF-β/Smad-associated EMT in some systems) ↓ EMT markers; ↓ migration/invasion ↔ G Anti-invasive phenotype Often presents as restoration of epithelial markers and suppression of migration/invasion assays; commonly a later phenotype-level outcome.
10 Xenobiotic handling (Phase I/II enzymes; cytoprotection / chemoprevention framing) May alter carcinogen activation/detox balance ↑ detox / cytoprotection against xenobiotics G Chemopreventive protection A key “dual strategy” theme: protection of normal tissue from toxins/therapy while modulating tumor response pathways.
11 Drug resistance / efflux (MDR phenotype; P-gp-related resistance in some models) May ↓ functional MDR and ↑ chemo sensitivity (context) ↔ R, G Chemo-sensitization support Reported synergy with chemotherapy in resistant tumor settings; transporter direction can be context-specific, so present as “reported to reduce functional resistance” rather than a universal single-transporter claim.
12 Immune microenvironment signaling (cytokines / macrophage recruitment in some models) May ↓ pro-tumor cytokine programs and recruitment signals (context) ↔ G Anti-inflammatory tumor microenvironment shift Immune-modulatory effects are increasingly discussed, but they are more model-dependent and typically show on longer time scales.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/physical–chemical effects; rapid signaling / phosphorylation shifts)
  • R: 30 min–3 hr (redox signaling + acute stress-response signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
3314- SIL,    Silymarin: Unveiling its pharmacological spectrum and therapeutic potential in liver diseases—A comprehensive narrative review
- Review, NA, NA
*antiOx↑, silymarin, demonstrating remarkable antioxidant and hepatoprotective properties in extensive preclinical investigations.
*hepatoP↑, It can protect healthy liver cells or those that have not yet sustained permanent damage by reducing oxidative stress and mitigating cytotoxicity.
*Half-Life↑, The main ingredient in silymarin, silibinin, normally takes two to four hours to reach its peak plasma concentration after oral consumption, and it has a 6‐hour plasma half‐life
*ROS↓, silibinin has potent anti‐ROS qualities,
*GSH↑, silymarin, the precursor to silibinin, can increase glutathione production in the liver and hence increase the liver tissues' antioxidant capacity
*hepatoP↑, silymarin, the precursor to silibinin, can increase glutathione production in the liver and hence increase the liver tissues' antioxidant capacity
*lipid-P↓,
*TNF-α↓, inhibit the production of pro‐inflammatory cytokines, such as TNF‐α, IFN‐γ, IL‐2, and IL‐4, which are crucial in the inflammatory cascade
*IFN-γ↓,
*IL2↓,
*IL4↓,
*NF-kB↓, Silymarin's mechanism involves suppressing NF‐κB activation,
*iNOS↓, It downregulates inflammatory mediators like interleukins, TNF‐α, and iNOS, which are involved in various diseases.
*OATPs↓, Its inhibition of transporters, including OATPs and OCTs, may also affect members of the solute carrier family
*OCT4↓,
*Inflam↓, Silymarin may have anti‐inflammatory properties that limit the production of inflammatory mediators like NF‐B and inflammatory metabolites like prostaglandin E2 (PGE2)
*PGE2↓,
MMPs↓, Silymarin significantly inhibits matrix metalloproteinases (MMPs), essential for cancer metastasis,
VEGF↓, Additionally, silymarin down‐regulates VEGF expression, contributing to anti‐angiogenic effects, and has the potential to reverse STAT‐3‐associated cancer drug resistance.
angioG↓,
STAT3↓,
*ALAT↓, The research revealed improved liver function as seen by lower levels of ALT, AST, and alkaline phosphatase, as well as a considerably lower likelihood of developing DILI four weeks after starting silymarin treatment
*AST↓,
Dose↝, The suggested dosage of silymarin has been used in clinical trials for up to 48 weeks at a dose of 2100 mg/day and for up to 4 years at a dose of up to 420 mg/day.

3328- SIL,    Modulatory effect of silymarin on inflammatory mediators in experimentally induced benign prostatic hyperplasia: emphasis on PTEN, HIF-1α, and NF-κB
- in-vivo, BPH, NA
*NF-kB↓, SIL attenuated testosterone-induced nuclear factor-kappa B (NF-κB), cyclooxygenase-II (COX-II), and inducible nitric oxide synthase (iNOS) upregulation
*Hif1a↓, Testosterone-induced downregulation of phosphatase and tensin homolog (PTEN) and upregulation of hypoxia-inducible factor 1α (HIF-1α) were alleviated by SIL.
*PTEN↑,
*Weight↓, Concomitant administration of SIL (50 mg/kg) significantly decreased the prostate weight and prostate index induced by testosterone by 0.64-fold and 0.68-fold, respectively
*NO↓, co-treatment with SIL significantly ameliorated testosterone-induced rise in NO
*IL6↓, SIL-treated group significantly down- regulated mRNA expression of IL-6 and IL-8 compared to testosterone-treated group
*IL8↓,
*COX2↓, SIL suppressed NF-κB, COX-II, and iNOS expressions as well as nitric oxide level in several experimental models
*iNOS↓,

3324- SIL,    Silymarin prevents NLRP3 inflammasome activation and protects against intracerebral hemorrhage
*ROS↓, Silymarin (200 mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status.
*TAC↑,
*NF-kB↓, Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions.
*IL2↓,
*NRF2↑, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection.
*HO-1↑,
*neuroP↑, silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury.
*Inflam↓,
*NLRP3↓, The NLRP3 mediated inflammatory responses were down regulated during silymarin treatment post ICH injury compared to ICH group

3323- SIL,    Anticancer therapeutic potential of silibinin: current trends, scope and relevance
- Review, Var, NA
Inflam↓, Silibinin has been shown to have anti-inflammatory, anti-angiogenic, antioxidant, and anti-metastatic properties
angioG↓,
antiOx↑,
TumMeta↓,
TumCP↓, silibinin helps in preventing proliferation of the tumor cells, initiating the cell cycle arrest, and induce cancer cells to die
TumCCA↑,
TumCD↑,
α-SMA↓, figure
p‑Akt↓,
p‑STAT3↓,
COX2↓,
IL6↓,
MMP2↓,
HIF-1↓,
Snail↓,
Slug↓,
Zeb1↓,
NF-kB↓,
p‑EGFR↓,
JAK2↓,
PI3K↓,
PD-L1↓,
VEGF↓,
CDK4↓,
CDK2↓,
cycD1/CCND1↓,
E2Fs↓,

3320- SIL,    Neuroprotective Potential of Silymarin against CNS Disorders: Insight into the Pathways and Molecular Mechanisms of Action
- Review, AD, NA
*hepatoP↑, Apart from the hepatoprotective nature, which is mainly due to its antioxidant and tissue regenerative properties,
*neuroP↑, Silymarin has recently been reported to be a putative neuroprotective agent against many neurologic diseases including Alzheimer's and Parkinson's diseases, and cerebral ischemia
*ROS↓, capacity to inhibit oxidative stress in the brain,
*β-Amyloid↓, additional advantages by influencing pathways such as β‐amyloid aggregation, inflammatory mechanisms, cellular apoptotic machinery, and estrogenic receptor mediation.
*Inflam↓,
*Aβ↓, Silymarin on inhibition of Aβ fibril formation and aggregation in animal and cellular models of AD
*NF-kB↓, By inhibiting the production of inflammatory agents such as NF‐κB, TNF‐α, TNF‐β, iNOS, NO, COX, Silymarin impedes neuroinflammation
*TNF-α↓,
*TNF-β↓,
*iNOS↓,
*NO↓,
*COX2↓,

3319- SIL,    Silymarin and neurodegenerative diseases: Therapeutic potential and basic molecular mechanisms
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, Silymarin can be used as a neuroprotective therapy against AD, PD and CI
*ROS↓, Silymarin prohibit oxidative stress, pathologic protein aggregation.
*Inflam↓, Silymarin inhibit neuroinflammation, apoptosis, and estrogenic receptor modulation.
*Apoptosis↓,
*BBB?, Silymarin, as a polyphenolic complex, can cross the blood-brain barrier (BBB)
*tau↓, inhibitory action of Silibinin on tau protein phosphorylation in the hippocampus and cortical region of the brain could describe an important neuro-protective effect against AD progression
*NF-kB↓, inhibiting the NF-κB pathway leading to attenuating the activity of NF-κB (
*IL1β↓, inhibition of inflammatory responses such as IL-1β and TNF-α mRNA gene
*TNF-α↓,
*IL4↓, enhance the production of IL-4 in the hippocampal region
*MAPK↓, down-regulation of MAPK activation
*memory↑, Silibinin exhibited its beneficial effect on improvement of memory impairment in rats
*cognitive↑, Silymarin was able to alleviated the impairment in cognitive, learning and memory ability caused by Aβ aggravation through making a reduction in oxidative stress in the hippocampal region
*Aβ↓,
*ROS↓,
*lipid-P↓, eduction in lipid peroxidation, controlling the GSH levels and then cellular anti-oxidant status improvement,
*GSH↑,
*MDA↓, Silymarin could reduce MDA content and significantly increased the reduced activity level of antioxidant enzyme, including SOD, CAT and GSH in the brain tissue induced by aluminum
*SOD↑,
*Catalase↑,
*AChE↓, Silibinin/ Silymarin, as a strong suppressor of AChE and BChE activity, exerted a positive effect against AD symptoms via increasing the ACh level in the brain
*BChE↓,
*p‑ERK↓, Silibinin could inhibit increased level of phosphorylated ERK, JNK and p38 (p-ERK, p-JNK and p-p38, respectively
*p‑JNK↓,
*p‑p38↓,
*GutMicro↑, demonstrated in APP/PS1 transgenic mice model of AD which was associated with controlling of the gut microbiota by both Silymarin and Silibinin
*COX2↓, Inhibition of the NF-κB pathway/ expression, Inhibition of IL-1β, TNF-α, COX_2 and iNOS level/ expression
*iNOS↓,
*TLR4↓, suppress TLR4 pathways and then subsequently diminished elevated level of TNF-α and up-regulated percentage of NF-κB mRNA expression
*neuroP↑, neuro-protective mechanisms on cerebral ischemia (CI)
*Strength↑, Silymarin decreased the loss of grip strength in the experimental rats
*AMPK↑, In SH-SY5Y cells, Silibinin blocked OGD/re-oxygenation- induced neuronal degeneration via AMPK activation as well as suppression in both ROS production and MMP reduction and even reduced neuronal apoptosis and necrosis.
*MMP↑,
*necrosis↓,
*NRF2↑, Silymarin up-regulated Nrf-2/HO-1 signaling (Yuan et al., 2017
*HO-1↑,

3318- SIL,    Pharmaceutical prospects of Silymarin for the treatment of neurological patients: an updated insight
- Review, AD, NA - Review, Park, NA
*hepatoP↑, widely studied as a hepatoprotective drug for various liver disorders.
*neuroP↑, research studies have shown its putative neuroprotective nature against various brain disorders, including psychiatric, neurodegenerative, cognitive, metabolic and other neurological disorders
*TLR4↓, Silymarin treatment has shown anti-inflammatory action in AD models by suppressing toll-like receptor 4 (TLR4) pathways and decreasing the increased mRNA levels of TNF-α, IL-1β and NF-κB
*TNF-α↓,
*IL1β↓,
*NF-kB↓,
*memory↑, improvement in memory los
*cognitive↑, finally leading to normal cognitive functions
*NRF2↑, upregulating the Nrf-2/HO-1 signaling in mice model
*HO-1↑,
*ROS↓, inhibition of oxidative stress in the brain
*Akt↑, Figure 4
*mTOR↑,
*SOD↑,
*Catalase↑,
*GSH↑,
*IL10↑,
*IL6↑,
*NO↓,
*MDA↓,
*AChE↓,
*MAPK↓,
*BDNF↑, Silymarin supplementation improved learning and memory in diabetes-induced cognitively impaired rats by elevating BDNF levels

3315- SIL,    Silymarin alleviates docetaxel-induced central and peripheral neurotoxicity by reducing oxidative stress, inflammation and apoptosis in rats
- in-vivo, Nor, NA
neuroP↑, Silymarin protects against the brain and sciatic nerve injuries induced by docetaxel.
*NRF2↑, Silymarin activates Nrf2/HO-1, and suppresses Bax/Bcl2 signaling.
*HO-1↑,
*lipid-P↓, SLM significantly decreased brain lipid peroxidation level and ameliorated brain glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in DTX-administered rats
*GSH↑,
*SOD↑,
*Catalase↑,
*GPx↑,
*NF-kB↓, SLM attenuated levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α),
*TNF-α↓,
*JNK↓, decreased the expression of c-Jun N-terminal kinase (JNK) in the sciatic nerve
*Bcl-2↑, SLM markedly up-regulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and B-cell lymphoma-2 (Bcl-2) and downregulated the expression of Bcl-2 associated X protein (Bax) in the brain
*BAX↑,

4203- SIL,    Unlocking the Neuroprotective Potential of Silymarin: A Promising Ally in Safeguarding the Brain from Alzheimer’s Disease and Other Neurological Disorders
- Review, NA, NA
*MAPK↝, Silymarin utilizes a range of molecular mechanisms, including modulation of MAPK, AMPK, NF-κB, mTOR, and PI3K/Akt pathways
*AMPK↝,
*NF-kB↓,
*mTOR↝,
*PI3K↝,
*Akt↝,
*BioAv↝, silymarin faces challenges related to bioavailability and aqueous solubility, hindering its development as a clinical drug
*memory↑, silymarin dose-dependently improves the memory and expression of BDNF in TBI-induced mice along with a significant reduction in the level of glutamate and TNF-α, affirming that silymarin could be a potential therapeutic agent for addressing cognitiv
*BDNF↑,
*TNF-α↓,

3331- SIL,    The clinical anti-inflammatory effects and underlying mechanisms of silymarin
- Review, NA, NA
*Inflam↓, anti-inflammatory mechanisms of silymarin,
*NF-kB↓, inhibition of the NF-kB and NLRP3 signaling pathways and the suppression of COX-2 and inducible nitric oxide synthase (iNOS) expression
*NLRP3↓,
*COX2↓,
*iNOS↓,
*neuroP↑, silymarin offers neuroprotection by inhibiting the phosphorylation of ERK1/2, JNK, and p38 MAPK and reducing the expression of the epidermal growth factor receptor and glial fibrillary acidic protein
*p‑ERK↓,
*p38↓,
*MAPK↓,
*EGFR↓,
*ROS↓, By the way, silymarin was reported to curb the formation of oxygen radicals and lipid peroxides.
*lipid-P?,
*5LO↓, Its anti-inflammatory effects were shown by inhibiting 5-LOX activity and obstructing the lipid peroxidation pathway to prevent the generation of ROS involved in inflammatory responses.

3649- SIL,    Silymarin suppresses TNF-induced activation of NF-kappa B, c-Jun N-terminal kinase, and apoptosis
*Inflam↓, anti-inflammatory, cytoprotective, and anticarcinogenic effects.
*NF-kB↓, suppression of NF-kappa B,
*cJun↓, Silymarin also inhibited the TNF-induced activation of mitogen-activated protein kinase kinase and c-Jun N-terminal kinase and abrogated TNF-induced cytotoxicity and caspase activation.
*Casp↓,
*ROS↓, Silymarin suppressed the TNF-induced production of reactive oxygen intermediates and lipid peroxidation
*lipid-P↓,

3294- SIL,    Silymarin: a review on paving the way towards promising pharmacological agent
- Review, Nor, NA - Review, Arthritis, NA
*hepatoP↑, It improves hepatic function, lessens hepatotoxicity caused by high acetaminophen intake, and can lessen oxidative stress in experimental mice, according to a study on animals
*Inflam↓,
*chemoP↑, moreover reducing the side effect of chemotherapeutic agents.
*glucose↓, Silymarin is effective anti-diabetic as it lowers serum glucose levels thus preventing the development of diabetic nephropathy
*antiOx↑, Various studies revealed that Silymarin could exert antioxidant properties in several mechanisms, which includes direct hindrance in free radical production,
*ROS↓,
*ACC↓, down-regulation of acetyl-CoA carboxylase, fatty acid synthase, and peroxisome proliferator-activated receptor
*FASN↓,
*radioP↑, More studies have revealed radioprotective properties of Silymarin in the testis tissues of mice and rats
*NF-kB↓, Silymarin inhibits NF-kB, down-regulates TGF-ß1 mRNA
*TGF-β↓,
*AST↓, Silymarin significantly decreased the elevation of aspartate aminotransferase (AST), alanine aminotransferase, and alkaline phosphatase in serum, and also reversed the altered expressions of α-smooth muscle actin in fibrotic tissue
*α-SMA↝,
*eff↑, Okda et al.[Citation76] currently reported that silymarin with ginger has significantly decreased the severity and incidence of liver fibrosis.
*neuroP↑, Researchers demonstrated that silymarin inhibits microglia activation, and protects dopaminergic neurons from lipopolysaccharide (LPS)-induced neurotoxicity
eff↑, The Silymarin with a selenium dose of 570 mg/d, for 6 months caused no side effects and was effective in reducing prostate cancer growth
ROS↓, Silymarin shows anti-cancerous properties considered to be linked to oxidative stress inhibition, apoptosis induction, growth cycle arrest, and mitochondrial pathway inhibition

3290- SIL,    A review of therapeutic potentials of milk thistle (Silybum marianum L.) and its main constituent, silymarin, on cancer, and their related patents
- Analysis, Var, NA
hepatoP↑, well as hepatoprotective agents.
chemoP↑, silymarin could be beneficial to oncology patients, especially for the treatment of the side effects of anticancer chemotherapeutics.
*lipid-P↓, Silymarin has been shown to significantly reduce lipid peroxidation and exhibit anti-oxidant, antihypertensive, antidiabetic, and hepatoprotective effects
*antiOx↑,
tumCV↓, reduces the viability, adhesion, and migration of tumor cells by induction of apoptosis and formation of reactive oxygen species (ROS), reducing glutathione levels, B-cell lymphoma 2 (Bcl-2), survivin, cyclin D1, Notch 1 intracellular domain (NICD),
TumCMig↓,
Apoptosis↑,
ROS↑,
GSH↓,
Bcl-2↓,
survivin↓,
cycD1/CCND1↓,
NOTCH1↓,
BAX↑, as well as enhancing the amount of Bcl-2-associated X protein (Bax) level (
NF-kB↓, The suppression of NK-κB-regulated gene products (e.g., cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF), and interleukin-1 (IL-1)) mediates the anti-inflammatory effect of silymarin
COX2↓,
LOX1↓,
iNOS↓,
TNF-α↓,
IL1↓,
Inflam↓,
*toxicity↓, Silymarin is also safe for humans, hence at therapeutic doses patients demonstrated no negative effects at the high dose of 700 mg, three times a day, for 24 weeks
CXCR4↓, fig 2
EGFR↓,
ERK↓,
MMP↓, reduction in mitochondrial transmembrane potential due to an increase in cytosolic cytochrome complex (Cyt c) levels.
Cyt‑c↑,
TumCCA↑, Moreover, silymarin increased the percentage of cells in the gap 0/gap 1 (G0/G1) phase and decreased the percentage of cells in the synthesis (S)-phase,
RB1↑, concomitant up-regulation of retinoblastoma protein (Rb), p53, cyclin-dependent kinase inhibitor 1 (p21Cip1), and cyclin-dependent kinase inhibitor 1B (p27Kip1)
P53↑,
P21↑,
p27↑,
cycE/CCNE↓, and down-regulation of cyclin D1, cyclin E, cyclin-dependent kinase 4 (CDK4), and phospho-Rb
CDK4↓,
p‑pRB↓,
Hif1a↓, silibinin inhibited proliferation of Hep3B cells due to simultaneous induction of apoptosis and prevented the accumulation
cMyc↓, Silibinin also reduces cellular myelocytomatosis oncogene (c-MYC) expression, a key regulator of cancer metabolism in pancreatic cancer cells
IL1β↓, Silymarin can also inhibit the production of inflammatory cytokines, such as interleukin-1beta (IL-1β), interferon-gamma (IFNγ),
IFN-γ↓,
PCNA↓, ilymarin suppresses the high proliferative activity of cells started with a carcinogen so that it significantly inhibits proliferating cell nuclear antigen (PCNA) and cyclin D1 labeling indices
PSA↓, In another patent, S. marianum has been used as an estrogen receptor β-agonist and an inhibitor of PSA for treating prostate cancer
CYP1A1↓, Silymarin prevents the expression of CYP1A1 and COX-2

3289- SIL,    Silymarin: a promising modulator of apoptosis and survival signaling in cancer
- Review, Var, NA
*BioAv↝, silymarin’s poor bioavailability and limited thérapeutic efficacy have been overcome by encapsulation of silymarin into nanoparticles
*BioAv↓, Silymarin is barely 20–50% absorbed by the GIT cells and has an absolute oral bioavailability of 0.95%
Fas↑, silibinin, enhances the Fas pathway in most cancers cells by upregulating the Fas and Fas L
FasL↑,
FADD↑, silymarin triggered apoptosis via upregulating the expression of FADD (Fig. 2b), a downstream component of the death receptor pathway, subsequently leading to the cleavage of procaspase 8 and initiation of apoptotic cell death
pro‑Casp8↑,
Apoptosis↑,
DR5↑, silymarin promotes apoptosis through the death receptor-mediated pathway, contributing to its anticancer effects
Bcl-2↑, Bcl-2, an anti-apoptotic protein, was decreased
BAX↑, Bax is also upregulated and leads to the activation of caspase-3.
Casp3↑,
PI3K↓, Silibinin inhibits the PI3K activity, leading to the reduction of FoxM1 (Forkhead box M1) and the subsequent activation of the mitochondrial apoptotic pathway
FOXM1↓,
p‑mTOR↓, inhibiting phosphorylation of several key components in this pathway, such as mTOR, p70S6K and 4E-BP1
p‑P70S6K↓,
Hif1a↓, mTOR pathway signaling in turn may result in low levels of HIF-1α due to the unfavorable conditions of hypoxia.
Akt↑, silibinin activates the Akt pathway in cervical cancer cells. This activation of Akt could have some bearing on the overall antitumor activity of silibinin in cervical cancer cells.
angioG↓, silibinin inhibited STAT3, HIF-1α, and NF-κB, thereby reducing the population of lung macrophages and limiting angiogenesis
STAT3↓,
NF-kB↓,
lipid-P↓, silibinin delays the progression of endometrial carcinoma via inhibiting STAT3 activation and lowering lipid accumulation, which is regulated by SREBP1
eff↑, Sorafenib and silibinin work together to target both liver cancer cells and cancer stem cells. This combination operates by suppressing the STAT3/ERK/AKT pathways and decreasing the production of Mcl-1 and Bcl-2 proteins
CDK1↓, reducing the expression of CDK1, survivin, Bcl-xL, cyclinB1 and Mcl- 1 and simultaneously activate caspases 3 and 9
survivin↓,
CycB/CCNB1↓,
Mcl-1↓,
Casp9↑,
AP-1↓, hindered the activation of transcription factors NF-κB and AP-1
BioAv↑, Liang et al., created a chitosan-based lipid polymer hybrid nanoparticles that boosted the bioavailability of silymarin by 14.38-fold

3282- SIL,    Role of Silymarin in Cancer Treatment: Facts, Hypotheses, and Questions
- Review, NA, NA
hepatoP↑, This group of flavonoids has been extensively studied and they have been used as hepato-protective substances
AntiCan↑, however, silymarin compounds have clear anticancer effects
TumCMig↓, decreasing migration through multiple targeting, decreasing hypoxia inducible factor-1α expression, i
Hif1a↓, In prostate cancer cells silibinin inhibited HIF-1α translation
selectivity↑, antitumoral activity of silymarin compounds is limited to malignant cells while the nonmalignant cells seem not to be affected
toxicity∅, long history of silymarin use in human diseases without toxicity after prolonged administration.
*antiOx↑, as an antioxidant, by scavenging prooxidant free radicals
*Inflam↓, antiinflammatory effects similar to those of indomethacin,
TumCCA↑, MDA-MB 486 breast cancer cells, G1 arrest was found due to increased p21 and decreased CDKs activity
P21↑,
CDK4↓,
NF-kB↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
ERK↓, human prostate carcinoma cells, silymarin decreased ligand binding to Erb1 135 and NF-kB expression was strongly inhibited by silymarin in hepatoma cell
PSA↓, Treating prostate carcinoma cells with silymarin the levels of PSA were significantly decreased and cell growth was inhibited through decreased CDK activity and induction of Cip1/p21 and Kip1/p27. 1
TumCG↓,
p27↑,
COX2↓, such as anti-COX2 and anti-IL-1α activity, 140 antiangiogenic effects through inhibition of VEGF secretion, upregulation of Insulin like Growth Factor Binding Protein 3 (IGFBP3), 141 and inhibition of androgen receptors.
IL1↓,
VEGF↓,
IGFBP3↑,
AR↓,
STAT3↓, downregulation of the STAT3 pathway which was seen in many cell models.
Telomerase↓, silymarin has the ability to decrease telomerase activity in prostate cancer cells
Cyt‑c↑, mitochondrial cytochrome C release-caspase activation.
Casp↑,
eff↝, Malignant p53 negative cells show only minimal apoptosis when treated with silymarin. Therefore, one conclusion is that silymarin may be useful in tumors with conserved p53.
HDAC↓, inhibit histone deacetylase activity;
HATs↑, increase histone acetyltransferase activity
Zeb1↓, reduce expression of the transcription factor ZEB1
E-cadherin↑, increase expression of E-cadherin;
miR-203↑, increase expression of miR-203
NHE1↓, reduce activation of sodium hydrogen isoform 1 exchanger (NHE1)
MMP2↓, target β catenin and reduce the levels of MMP2 and MMP9
MMP9↓,
PGE2↓, reduce activation of prostaglandin E2
Vim↓, suppress vimentin expression
Wnt↓, inhibit Wnt signaling
angioG↓, Silymarin inhibits angiogenesis.
VEGF↓, VEGF downregulation
*TIMP1↓, Silymarin has the capacity to decrease TIMP1 expression166–168 in mice.
EMT↓, found that silibinin had no effect on EMT. However, the opposite was found in other malignant tissues160–162 where it showed inhibitory effects.
TGF-β↓, Silibinin reduces the expression of TGF β2 in different tumors such as triple negative breast, 174 prostate, and colorectal cancers.
CD44↓, Silibinin decreased CD44 expression and the activation of EGFR (epidermal growth factor receptor)
EGFR↓,
PDGF↓, silibinin had the ability to downregulate PDFG in fibroblasts, thus decreasing proliferation.
*IL8↓, Flavonoids, in general, reduce levels of IL-8. Curcumin, 200 apigenin, 201 and silybin showed the ability to decrease IL-8 levels
SREBP1↓, Silymarin inhibited STAT3 phosphorylation and decreased the expression of intranuclear sterol regulatory element binding protein 1 (SREBP1), decreasing lipid synthesis.
MMP↓, reduced membrane potential and ATP content
ATP↓,
uPA↓, silibinin decreased MMP2, MMP9, and urokinase plasminogen activator receptor level (uPAR) in neuroblastoma cells. uPAR is also a marker of cell invasion.
PD-L1↓, Silibinin inhibits PD-L1 by impeding STAT5 binding in NSCLC.
NOTCH↓, Silybin inhibited Notch signaling in hepatocellular carcinoma cells showing antitumoral effects
*SIRT1↑, Silymarin can also increase SIRT1 expression in other tissues, such as hippocampus, 221 articular chondrocytes, 222 and heart muscle
SIRT1↓, Silymarin seems to act differently in tumors: in lung cancer cells SIRT downregulated SIRT1 and exerted multiple antitumor effects such as reduced adhesion and migration and increased apoptosis.
CA↓, Silymarin has the ability to inhibit CA isoforms CA I and CA II.
Ca+2↑, ilymarin increases mitochondrial release of Ca++ and lowers mitochondrial membrane potential in cancer cell
chemoP↑, Silymarin: Decreasing Side Effects and Toxicity of Chemotherapeutic Drugs
cardioP↑, There is also evidence that it protects the heart from doxorubicin toxicity, however, it is less potent than quercetin in this effect.
Dose↝, oral administration of 240 mg of silybin to 6 healthy volunteers the following results were obtained 377 : maximum\,plasmaconcentration0.34±0.16⁢𝜇⁢g/m⁢L
Half-Life↝, and time to maximum plasma concentration 1.32 ± 0.45 h. Absorption half life 0.17 ± 0.09 h, elimination half life 6.32 ± 3.94 h
BioAv↓, silymarin is not soluble in water and oral administration shows poor absorption in the alimentary tract (approximately 1% in rats,
BioAv↓, Our conclusion is that, from a bioavailability standpoint, it is much easier to achieve migration inhibition, than proliferative reduction.
BioAv↓, Combination with succinate: is available on the market under the trade mark Legalon® (bis hemisuccinate silybin). Combination with phosphatidylcholine:
toxicity↝, 13 g daily per os divided into 3 doses was well tolerated. The most frequent adverse event was asymptomatic liver toxicity.
Half-Life↓, It may be necessary to administer 800 mg 4 times a day because the half-life is short.
ROS↓, its ability as an antioxidant reduces ROS production
FAK↓, Silibinin decreased human osteosarcoma cell invasion through Erk inhibition of a FAK/ERK/uPA/MMP2 pathway

3295- SIL,    Hepatoprotective effect of silymarin
- Review, NA, NA
*hepatoP↑, The hepatoprotective and antioxidant activity of silymarin is caused by its ability to inhibit the free radicals that are produced from the metabolism of toxic substances such as ethanol, acetaminophen, and carbon tetrachloride.
*ROS↓,
*GSH↑, Silymarin enhances hepatic glutathione and may contribute to the antioxidant defense of the liver.
*BioAv↝, For example, the level of silymarin absorption is between 20% and 50%. low solubility in water, low bioavailability, and poor intestinal absorption reduce its efficacy
ERK↓, treatment of melanoma cells with silybin attenuated the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 and RSK2,
NF-kB↓, silybin resulted in the reduced activation of nuclear factor-kappa B (NF-κB), activator protein-1, and STAT3
STAT3↓,
COX2↓, cytoprotective effect in liver is also caused by the inhibition of the cyclooxygenase cycle
Inflam↓, These affects reduce inflammation
IronCh↑, chelating iron, and slowing calcium metabolism,
lipid-P↓, Silymarin also affects intracellular glutathione, which prevents lipoperoxidation of membranes
ALAT↓, led to significantly reduced levels of alanine aminotransferase (ALT) and aspartame aminotransferase (AST) (AST/ALT < 1)
AST↓,
TNF-α↓, It also reduced the level of TNF-α, which reduces inflammation.
*α-SMA↓, There was also a reduction in FR and reduced markers of fibrosis such as alpha smooth muscle actin, collagen α 1(I), and in the caspase cytotoxicity marker.
*SOD↑, The activity of the enzymes superoxide dismutase (SOD) and glutathione-S-transferase (GST) increased significantly.

978- SIL,    A comprehensive evaluation of the therapeutic potential of silibinin: a ray of hope in cancer treatment
- Review, NA, NA
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.

3309- SIL,    Silymarin as a Natural Antioxidant: An Overview of the Current Evidence and Perspectives
- Review, NA, NA
*ROS↓, (1) Direct scavenging free radicals and chelating free Fe and Cu are mainly effective in the gut.
*IronCh↑,
*MMP↑, (2) Preventing free radical formation by inhibiting specific ROS-producing enzymes, or improving an integrity of mitochondria in stress conditions, are of great importance.
*NRF2↑, (3) Maintaining an optimal redox balance in the cell by activating a range of antioxidant enzymes and non-enzymatic antioxidants, mainly via Nrf2 activation
*Inflam↓, (4) Decreasing inflammatory responses by inhibiting NF-κB pathways is an emerging mechanism of SM protective effects in liver toxicity and various liver diseases.
*hepatoP↑,
*HSPs↑, (5) Activating vitagenes, responsible for synthesis of protective molecules, including heat shock proteins (HSPs), thioredoxin and sirtuins
*Trx↑,
*SIRT2↑, increased expression of protective molecules (GSH, Thioredoxins, heat shock proteins (HSPs), sirtuins, etc.)
*GSH↑,
*ROS↑, Similarly, production of O2− and NO in isolated rat Kupffer cells were inhibited by silibinin in a dose-dependent manner, with IC50 80 μM
*NADPH↓, It also decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue.
*iNOS↓,
*NF-kB↓,
*BioAv↓, active free silibinin concentration in plasma after oral consumption of SM, depending on dose of supplementation, could be in the range 0.2–2.0 μM.
*Dose↝, healthy volunteers, after an oral administration of SM (equivalent to 120 mg silibinin), total (unconjugated + conjugated) silibinin concentration in plasma was 1.1–1.3 μg/mL
*BioAv↑, For example, silibinin concentration in the gut could reach 800 μM

3300- SIL,    Toward the definition of the mechanism of action of silymarin: activities related to cellular protection from toxic damage induced by chemotherapy
- Review, Var, NA
*ROS↓, silymarin and silibinin protect the liver from oxidative stress and sustained inflammatory processes, mainly driven by Reactive Oxygen Species (ROS) and secondary cytokines
*SOD↑, Silymarin administered to patients with chronic alcoholic liver disease significantly enhanced the low SOD activity measured in the patients’ erythrocytes and lymphocytes.
*hepatoP↑,
*AST↓, Wistar albino rats 50 mg/kg oral silymarin ↓ AST, ALT; ↓MDA (lipid peroxidation); ↑SOD, GSH, CAT; ↑GST and GR
*ALAT↓,
*lipid-P↓,
*GSH↑,
*Catalase↑,
*GSTs↑,
*GSR↑,
*TNF-α↓, ↓hepatic TNF, IFN-γ, IL-4, IL-2; ↓hepatic NF-kB activation; ↑hepatic IL-10
*IFN-γ↓,
*IL4↓,
*IL2↓,
*NF-kB↓,
*IL10↑,
*Inflam↓, Anti-Inflammatory
COX2↓, NSCLC ↓ NF-kB activation; ↓COX-2; ↑apoptosis; ↑doxorubicin efficacy
Apoptosis↑,
ChemoSen↑,
PGE2↓, ↓prostaglandin E 2
VEGF↓, ↓VEGF


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

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP1A1↓, 1,   GSH↓, 1,   lipid-P↓, 2,   ROS↓, 2,   ROS↑, 2,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   cMyc↓, 1,   SIRT1↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 1,   Bcl-2↑, 1,   BID↑, 1,   Casp↑, 1,   Casp3↑, 2,   pro‑Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   FasL↑, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   p27↑, 2,   survivin↓, 3,   Telomerase↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

HATs↑, 1,   miR-21↓, 1,   p‑pRB↓, 1,   tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   P53↑, 2,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   cycE/CCNE↓, 1,   E2Fs↓, 1,   P21↑, 2,   RB1↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   EMT↓, 1,   ERK↓, 4,   FOXM1↓, 1,   HDAC↓, 1,   IGFBP3↑, 1,   p‑mTOR↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   p‑P70S6K↓, 1,   PI3K↓, 3,   STAT3↓, 4,   p‑STAT3↓, 1,   STAT5↓, 1,   TumCG↓, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Akt2↓, 1,   AP-1↓, 2,   CA↓, 1,   Ca+2↑, 1,   E-cadherin↑, 1,   FAK↓, 1,   miR-155↓, 1,   miR-203↑, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   PDGF↓, 1,   Slug↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 1,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 2,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   EGFR↓, 2,   p‑EGFR↓, 2,   HIF-1↓, 1,   Hif1a↓, 3,   LOX1↓, 1,   VEGF↓, 5,  

Barriers & Transport ⓘ

NHE1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   CXCR4↓, 1,   IFN-γ↓, 1,   IL1↓, 2,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   JAK2↓, 2,   NF-kB↓, 6,   PD-L1↓, 2,   PGE2↓, 2,   PSA↓, 2,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALAT↓, 1,   AR↓, 1,   AST↓, 1,   EGFR↓, 2,   p‑EGFR↓, 2,   FOXM1↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   PD-L1↓, 2,   PSA↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   chemoP↑, 2,   hepatoP↑, 2,   neuroP↑, 1,   toxicity↝, 1,   toxicity∅, 1,  
Total Targets: 142

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 4,   GPx↑, 1,   GSH↑, 7,   GSR↑, 1,   GSTs↑, 1,   HO-1↑, 4,   lipid-P?, 1,   lipid-P↓, 6,   MDA↓, 2,   NRF2↑, 5,   ROS↓, 12,   ROS↑, 1,   SOD↑, 5,   TAC↑, 1,   Trx↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ALAT↓, 2,   AMPK↑, 1,   AMPK↝, 1,   FASN↓, 1,   glucose↓, 1,   NADPH↓, 1,   SIRT1↑, 1,   SIRT2↑, 1,  

Cell Death ⓘ

Akt↑, 1,   Akt↝, 1,   Apoptosis↓, 1,   BAX↑, 1,   Bcl-2↑, 1,   Casp↓, 1,   iNOS↓, 6,   JNK↓, 1,   p‑JNK↓, 1,   MAPK↓, 3,   MAPK↝, 1,   necrosis↓, 1,   p38↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,  

Protein Folding & ER Stress ⓘ

HSPs↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 2,   mTOR↑, 1,   mTOR↝, 1,   OCT4↓, 1,   PI3K↝, 1,   PTEN↑, 1,  

Migration ⓘ

5LO↓, 1,   TGF-β↓, 1,   TIMP1↓, 1,   α-SMA↓, 1,   α-SMA↝, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   Hif1a↓, 1,   NO↓, 3,  

Barriers & Transport ⓘ

BBB?, 1,   OATPs↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   IFN-γ↓, 2,   IL10↑, 2,   IL1β↓, 2,   IL2↓, 3,   IL4↓, 3,   IL6↓, 1,   IL6↑, 1,   IL8↓, 2,   Inflam↓, 10,   NF-kB↓, 13,   PGE2↓, 1,   TLR4↓, 2,   TNF-α↓, 7,   TNF-β↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 1,   BDNF↑, 2,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   NLRP3↓, 2,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALAT↓, 2,   AST↓, 3,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   cognitive↑, 2,   hepatoP↑, 8,   memory↑, 3,   neuroP↑, 7,   radioP↑, 1,   Strength↑, 1,   toxicity↓, 1,   Weight↓, 1,  
Total Targets: 102

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
19 Silymarin (Milk Thistle) silibinin
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#:154  Target#:214  State#:%  Dir#:%
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