Database Query Results : Silymarin (Milk Thistle) silibinin, , neuroP

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 bioA (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 on acheive 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. Given low bioavailability seems unlikely one could acheieve levels in vivo to raise ROS(except 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↓, COX2↓, p38↓, 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↓, OXPHOS↓, GRP78↑, 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


neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
3330- SIL,    Mechanistic Insights into the Pharmacological Significance of Silymarin
- Review, Var, NA
*neuroP↑, silymarin is employed significantly as a neuroprotective, hepatoprotective, cardioprotective, antioxidant, anti-cancer, anti-diabetic, anti-viral, anti-hypertensive, immunomodulator, anti-inflammatory, photoprotective and detoxification agent
*hepatoP↑,
*cardioP↑,
*antiOx↓,
*NLRP3↓, Zhang et al. (2018) observed that silybin significantly impedes NLR family pyrin domain containing 3 (NLRP3) inflammasome activation in NAFLD by elevating NAD+ levels,
*NAD↑,
ROS↓, MDA-MB-231: it was observed that silybin treatment also abolishes activation of the NLRP3 inflammasome through repression of ROS generation, resulting in reduced tumor cell migration and invasion
NLRP3↓,
TumCMig↓,
*COX2↓, mpairing several enzymes (COX-2, iNOS, SGPT, SGOT, MMP, MPO, AChE, G6Pase, MAO-B, LDH, Telomerase, FAS and CK-MB)
*iNOS↓,
*MPO↓,
*AChE↓,
*LDH↓,
*Telomerase↓,
*Fas↓,

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

3321- SIL,    Silymarin (Milk thistle)
- Review, AD, NA
*neuroP↝, Although silymarin is effective in several Alzheimer’s animal models, most of the proposed mechanisms of action are similar to approved drugs or drugs that have been ineffective for Alzheimer’s.
*Dose↝, Large variability in doses used, but commonly 200-600mg/day
*Half-Life?, Half-life: Six hours
*BioAv↝, (oral absorption is ~23-47%)
*cognitive↑, silibinin and silymarin improved cognition in an Alzheimer’s mouse model
*Aβ↓, Silymarin was also reported to slightly reduce Aβ plaques, Aβ oligomers, and insoluble (but not soluble) Aβ, reduce microglial inflammation, and improve cognition in an Alzheimer’s mouse model
*Inflam↓,
*OS↑, silymarin increased mean lifespan of worms by 10.1% and 24.8% at 25μM and 50μM, respectively, but had no effect at 100μM
*memory↑, (50mg/kg/day intramuscular injection) improved memory performance

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

3317- 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
*neuroP↑, protective effects against NDs such as Alzheimer's disease, Parkinson's disease, and depression.

3316- SIL,  Chemo,    Silymarin Nanoparticles Counteract Cognitive Impairment Induced by Doxorubicin and Cyclophosphamide in Rats; Insights into Mitochondrial Dysfunction and Nrf2/HO-1 Axis
Inflam↓, Silymarin was reported to possess anti-inflammatory, antioxidant, and neuroprotective impacts.
antiOx↓,
neuroP↑,
cognitive↑, recent study shed light on the neuroprotective attributes of silymarin against cognitive dysfunction instigated in rats with doxorubicin/cyclophosphamide combination
NRF2↑, additionally, caspase-3 augmentation and of nuclear factor erythroid 2-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1) pathway disturbance were found following chemotherapy treatment.
HO-1↑,
memory↑, Silymarin treatment opposed such effects via enhancing memory function, preserving brain architecture, and reducing acetylcholinesterase activity and caspase-3 level.
AChE↓,
Casp3↓,

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↑,

3655- SIL,    Protective effect of silymarin on oxidative stress in rat brain
- in-vivo, AD, NA
*GSH↑, After SM administration GSH and AA significantly increase and SOD activity was significantly enhanced
*VitC↑,
*SOD↑,
*lipid-P↓, SM may to protect the SNC by oxidative damage for its ability to prevent lipid peroxidation and replenishing the GSH levels.
*ROS↓,
*hepatoP↑, Silybum marianum (L.) Gaertn., known as milk thistle, is one of the most popular herbal remedies for liver disease.
*neuroP↑, small number of reports of the SM effects on brain, concerning protective effect on fetal rat brain by ethanol induced injury

3654- SIL,    Effect of silymarin on biochemical parameters of oxidative stress in aged and young rat brain
- in-vivo, AD, NA
*ROS↓, Flavonoids are antioxidants found molecules capable of intercepting reactive oxygen species (ROS)
*neuroP↑, SM may contribute to the prevention of aged-related and pathological degenerative processes in the brain.
*GSH↑, silymarin induce an increase of GSH, AA levels, and SOD activity in brain of rats treated with 200 mg/kg/day for 3 day
*SOD↑,

3653- SIL,    Silibinin ameliorates Aβ25-35-induced memory deficits in rats by modulating autophagy and attenuating neuroinflammation as well as oxidative stress
- in-vivo, AD, NA
*hepatoP↑, Silibinin (silybin), a flavonoid derived from the herb milk thistle, is well known for its hepatoprotective activities.
*neuroP↑, neuroprotective effect of silibinin on Aβ25-35-injected rats
*cognitive↑, silibinin significantly attenuated Aβ25-35-induced memory deficits in Morris water maze and novel object-recognition tests.
*memory↑,
*Inflam↓, Silibinin attenuated the inflammatory responses, increased glutathione (GSH) levels and decreased malondialdehyde (MDA) levels, and upregulated autophagy levels in the Aβ25-35-injected rats.
*GSH↑,
*MDA↓,
*Inflam↓, potential candidate for AD treatment because of its anti-inflammatory, antioxidant and autophagy regulating activities.
*antiOx↓,

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.

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

3288- SIL,    Silymarin in cancer therapy: Mechanisms of action, protective roles in chemotherapy-induced toxicity, and nanoformulations
- Review, Var, NA
Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31↓,
Hif1a↓,
VEGFR2↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress

3307- SIL,    Flavolignans from Silymarin as Nrf2 Bioactivators and Their Therapeutic Applications
- Review, Var, NA
*NRF2↑, antioxidant and protective activities, which are probably related to the activation of the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2), known as a master regulator of the cytoprotector response.
*antiOx↑, many studies have been conducted in order to identify its different biological activities, such as antioxidant, chemoprotective, anti-inflammatory,
*chemoP↑,
*Inflam↓,
*BioAv↑, The design of silybinnano-emulsions using oil, surfactants, and co-surfactants (sefsol-218/Tween 80/ethanol) in oral administration was more capable of improving the SM hepatoprotective effect than SM alone [138].
eff↑, ↑ Induction of UGT1A7 with propolis, artichoke and SM (7.3, 5 and 4.5-fold respectively
*NQO1↑, ↑ activity of NQO1
TNF-α↓, ↑ SOD and GPx activity ↓ gastric inflammation: TNF- α, IL-6 and myeloperoxidase activity,
IL6↓,
*GSH↑, PC12 cells (normal) ↑ intracellular levels of GSH ↓ levels of ROS and MDA
*ROS↓,
*MDA↓,
eff↑, combination of SM with vitamin E and/or curcumin can be a good option for the treatment of liver injury induced by toxic substances
*hepatoP↑,
*GPx↑, 50 mg/kg of SM inhibits the synthesis of lipid peroxides, promotes the upregulation of Nrf2, and the enhancement of the activity of GPx and SOD enzymes, increasing antioxidant and cytoprotective defense, thus preventing gastric oxidative stress.
*SOD↑,
*Catalase↑, treatment with SM at 200 mg/kg for 3 days improved oxidative stress by reducing MDA and increasing the activity of SOD, Cat, and GPx in lung tissue
*HO-1↑, These results were related to the upregulation of Nrf2, HO-1, and NQO1 in male Sprague-Dawley rats.
*neuroP↑, SM can exert neuroprotection against acrylamide-induced damage


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

Results for Effect on Cancer/Diseased Cells:
AChE↓,1,   Akt↓,1,   angioG↓,1,   antiOx↓,1,   APAF1↑,1,   BAX↑,1,   Bcl-2↓,1,   Bcl-xL↓,1,   BIM↓,1,   cardioP↑,1,   Casp↑,1,   Casp3↓,1,   Casp3↑,1,   CD31↓,1,   chemoP↑,1,   cMyc↓,1,   cognitive↑,1,   cycD1↓,1,   Cyt‑c↑,1,   eff↑,3,   EMT↓,1,   ERK↓,1,   GSH↑,1,   HATs↑,1,   HDAC↓,1,   hepatoP↑,1,   Hif1a↓,1,   HO-1↑,1,   IFN-γ↑,1,   IL10↓,1,   IL2↑,1,   IL6↓,1,   Inflam↓,2,   LC3II↑,1,   lipid-P↓,1,   MAPK↓,1,   MDSCs↓,1,   MEK↓,1,   memory↑,1,   MMP↓,1,   MMPs↓,1,   mTOR↓,1,   neuroP↑,3,   NLRP3↓,1,   NRF2↑,1,   P53↑,1,   PCNA↓,1,   PI3K↓,1,   Raf↓,1,   ROS↓,2,   survivin↓,1,   TNF-α↓,1,   TumCMig↓,1,   TumMeta↓,1,   uPA↓,1,   VEGF↓,1,   VEGFR2↓,1,   YAP/TEAD↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 59

Results for Effect on Normal Cells:
5LO↓,1,   ACC↓,1,   AChE↓,3,   Akt↑,1,   AMPK↑,1,   antiOx↓,2,   antiOx↑,2,   Apoptosis↓,1,   AST↓,1,   Aβ↓,3,   BAX↑,1,   BBB?,1,   BChE↓,1,   Bcl-2↑,1,   BDNF↑,1,   BioAv↓,1,   BioAv↑,1,   BioAv↝,1,   cardioP↑,1,   Catalase↑,4,   chemoP↑,2,   cognitive↑,4,   COX2↓,4,   Dose↝,1,   eff↑,1,   EGFR↓,1,   p‑ERK↓,2,   Fas↓,1,   FASN↓,1,   glucose↓,1,   GPx↑,2,   GSH↑,7,   GutMicro↑,1,   Half-Life?,1,   hepatoP↑,7,   HO-1↑,5,   IL10↑,1,   IL1β↓,2,   IL2↓,1,   IL4↓,1,   IL6↑,1,   Inflam↓,9,   iNOS↓,4,   JNK↓,1,   p‑JNK↓,1,   LDH↓,1,   lipid-P?,1,   lipid-P↓,3,   MAPK↓,3,   MDA↓,4,   memory↑,4,   MMP↑,1,   MPO↓,1,   mTOR↑,1,   NAD↑,1,   necrosis↓,1,   neuroP↑,13,   neuroP↝,1,   NF-kB↓,7,   NLRP3↓,3,   NO↓,2,   NQO1↑,1,   NRF2↑,5,   OS↑,1,   p38↓,1,   p‑p38↓,1,   radioP↑,1,   ROS↓,10,   SOD↑,6,   Strength↑,1,   TAC↑,1,   tau↓,1,   Telomerase↓,1,   TGF-β↓,1,   TLR4↓,2,   TNF-α↓,4,   TNF-β↓,1,   VitC↑,1,   α-SMA↝,1,   β-Amyloid↓,1,  
Total Targets: 80

Scientific Paper Hit Count for: neuroP, neuroprotective
16 Silymarin (Milk Thistle) silibinin
1 Chemotherapy
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:154  Target#:1105  State#:%  Dir#:%
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