IL4 Cancer Research Results

IL4, interleukin 4: Click to Expand ⟱
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Type:
A cytokine that regulates humoral and adaptive immunity, and is involved in allergies and regulates inflammation.
IL-4 produced by cancer cells promotes resistance to immune checkpoint blockade (ICB). The close correlation between interleukin-4 (IL-4) and tumor progression has been observed in plenty of studies.

IL-4 is expressed in various cancers, including breast cancer, lung cancer, colorectal cancer, and hematological malignancies. Its expression can vary depending on the tumor type and the immune context.
Elevated levels of IL-4 are often associated with the presence of tumor-infiltrating immune cells, particularly Th2 cells and other immune cells that produce IL-4.
IL-4 is often considered a pro-tumorigenic cytokine. It can promote tumor growth and survival by enhancing the proliferation and survival of cancer cells. IL-4 can activate signaling pathways such as the STAT6 pathway, which is associated with cell proliferation and survival.
In some cancers, IL-4 can also promote angiogenesis, the formation of new blood vessels, which is critical for tumor growth and metastasis.
Scientific Papers found: Click to Expand⟱
6462- 1,8-Cin,    Modes of Action of 1,8-Cineol in Infections and Inflammation
- Review, Var, NA - Review, AD, NA
*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation

3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, DHA exerts anticancer effects through various molecular mechanisms, such as inhibiting proliferation, inducing apoptosis, inhibiting tumor metastasis and angiogenesis, promoting immune function, inducing autophagy and endoplasmic reticulum (ER) stres
Apoptosis↑,
TumMeta↓,
angioG↓,
TumAuto↑,
ER Stress↑,
ROS↑, DHA could increase the level of ROS in cells, thereby exerting a cytotoxic effect in cancer cells
Ca+2↑, activation of Ca2+ and p38 was also observed in DHA-induced apoptosis of PC14 lung cancer cells
p38↑,
HSP70/HSPA5↓, down-regulation of heat-shock protein 70 (HSP70) might participate in the apoptosis of PC3 prostate cancer cells induced by DHA
PPARγ↑, DHA inhibited the growth of colon tumor by inducing apoptosis and increasing the expression of peroxisome proliferator-activated receptor γ (PPARγ)
GLUT1↓, DHA was shown to inhibit the activity of glucose transporter-1 (GLUT1) and glycolytic pathway by inhibiting phosphatidyl-inositol-3-kinase (PI3K)/AKT pathway and downregulating the expression of hypoxia inducible factor-1α (HIF-1α)
Glycolysis↓, Inhibited glycolysis
PI3K↓,
Akt↓,
Hif1a↓,
PKM2↓, DHA could inhibit the expression of PKM2 as well as inhibit lactic acid production and glucose uptake, thereby promoting the apoptosis of esophageal cancer cells
lactateProd↓,
GlucoseCon↓,
EMT↓, regulating the EMT-related genes (Slug, ZEB1, ZEB2 and Twist)
Slug↓, Downregulated Slug, ZEB1, ZEB2 and Twist in mRNA level
Zeb1↓,
ZEB2↓,
Twist↓,
Snail?, downregulated the expression of Snail and PI3K/AKT signaling pathway, thereby inhibiting metastasis
CAFs/TAFs↓, DHA suppressed the activation of cancer-associated fibroblasts (CAFs) and mouse cancer-associated fibroblasts (L-929-CAFs) by inhibiting transforming growth factor-β (TGF-β signaling
TGF-β↓,
p‑STAT3↓, blocking the phosphorylation of STAT3 and polarization of M2 macrophages
M2 MC↓,
uPA↓, DHA could inhibit the growth and migration of breast cancer cells by inhibiting the expression of uPA
HH↓, via inhibiting the hedgehog signaling pathway
AXL↓, DHA acted as an Axl inhibitor in prostate cancer, blocking the expression of Axl through the miR-34a/miR-7/JARID2 pathway, thereby inhibiting the proliferation, migration and invasion of prostate cancer cells.
VEGFR2/KDR/Flk1↓, inhibition of VEGFR2-mediated angiogenesis
JNK↑, JNK pathway activated and Beclin 1 expression upregulated.
Beclin-1↑,
GRP78/BiP↑, Glucose regulatory protein 78 (GRP78, an ER stress-related molecule) was upregulated after DHA treatment.
eff↑, results demonstrated that DHA-induced ER stress required iron
eff↑, DHA was used in combination with PDGFRα inhibitors (sunitinib and sorafenib), it could sensitize ovarian cancer cells to PDGFR inhibitors and achieved effective therapeutic efficacy
eff↑, DHA combined with 2DG (a glycolysis inhibitor) synergistically induced apoptosis through both exogenous and endogenous apoptotic pathways
eff↑, histone deacetylase inhibitors (HDACis) enhanced the anti-tumor effect of DHA by inducing apoptosis.
eff↑, DHA enhanced PDT-induced cell growth inhibition and apoptosis, increased the sensitivity of esophageal cancer cells to PDT by inhibiting the NF-κB/HIF-1α/VEGF pathway
eff↑, DHA was added to magnetic nanoparticles (MNP), and the MNP-DHA has shown an effect in the treatment of intractable breast cancer
IL4↓, downregulated IL-4;
DR5↑, Upregulated DR5 in protein, Increased DR5 promoter activity
Cyt‑c↑, Released cytochrome c from the mitochondria to the cytosol
Fas↑, Upregulated fas, FADD, Bax, cleaved-PARP
FADD↑,
cl‑PARP↑,
cycE/CCNE↓, Downregulated Bcl-2, Bcl-xL, procaspase-3, Cyclin E, CDK2 and CDK4
CDK2↓,
CDK4↓,
Mcl-1↓, Downregulated Mcl-1
Ki-67↓, Downregulated Ki-67 and Bcl-2
Bcl-2↓,
CDK6↓, Downregulated of Cyclin E, CDK2, CDK4 and CDK6
VEGF↓, Downregulated VEGF, COX-2 and MMP-9
COX2/PTGS2↓,
MMP9↓,

560- ART/DHA,    Dihydroartemisinin shift the immune response towards Th1, inhibit the tumor growth in vitro and in vivo
- in-vivo, NA, NA
IL4↓,
CD4+↓,
CD25+↓,
FoxP3+↓, Foxp3+
Treg lymp↓,

5680- BML,    Anticancer properties of bromelain: State-of-the-art and recent trends
- Review, Var, NA
*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2/PTGS2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju

2768- Bos,    Boswellic acids as promising agents for the management of brain diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, BAs-induced neuroprotection is proposed to be associated with the ability to reduce neurotoxic aggregates, decrease oxidative stress, and improve cognitive dysfunction.
*ROS↓,
*cognitive↓,
TumCP↓, BAs have been suggested as potential agents for the treatment of brain tumors due to their potential to attenuate cell proliferation, migration, metastasis, angiogenesis, and promote apoptosis during both in vitro and in vivo studies
TumCMig↓,
TumMeta↓,
angioG↓,
Apoptosis↑,
*Inflam↓, The anti-inflammatory activities of BAs have been investigated in many preclinical and clinical trials
IL1↓, BAs inhibit the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-4, IL-6, and tumor necrosis factor-α (TNF-α) in several experimental studies.
IL2↓,
IL4↓,
IL6↓,
TNF-α↓,
P53↑, AKBA has been reported to induce apoptosis in pancreatic and gastric cancers, through tumor suppressor protein 53 (p53)-independent pathway, while reducing expression of protein kinase (PK) B and NF-kb
Akt↓,
NF-kB↓,
DNAdam↑, DNA fragmentation, and activation of caspase cascade
Casp↑,
COX2/PTGS2↓, regulated genes such as cyclooxygenase-2 (COX-2), matrix metallopeptidase-9 (MMP-9), C-X-C motif chemokine receptor 4 (CXCR4), and vascular endothelial growth factor (VEGF)
MMP9↓,
CXCR4↓,
VEGF↓,
*SOD↑, BAs against oxidative injury has been shown in several cell lines and animal models [12], [13], [21]. BAs exert protective effects through the normalization of antioxidant enzyme levels, such as superoxide dismutase (SOD), catalase, and glutathione p
*Catalase↑,
*GPx↑,
*NRF2↑, Moreover, it can activate nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant response element-regulated pathways

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2/PTGS2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓, treatment with CUR enhances pro-oxidant levels, antioxidant enzymes activities and anti-inflammatory cytokine production and decreases apoptotic cells in AlCl3-exposed hippocampus rats.
*BBB↑, CUR is able to cross the blood–brain barrier
*NRF2↑, CUR was shown to provide neuroprotection by inducing the upregulation of the transcription of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and by suppression of NF-κB activation
*NF-kB↓,
*cognitive↑, CUR Protects against AlCl3-Induced Cognitive Impairment
*ROS↓, Co-treatment with CUR significantly attenuated oxidative stress in the hippocampus by decreasing levels of MDA and enhancing SOD and catalase activities, when compared to AlCl3-treated animals.
*MDA↓,
*SOD↑,
*Catalase↑,
*INF-γ↓, CUR significantly reduced INF-γ concentration,
*IL4↓, our results showed that co- and post-treatments of CUR reduce IL-4 concentration.
*memory↑, CUR treatments protect rats against deterioration of spatial memory and
*TNF-α↓, CUR modulated the inflammatory status by the (i) inhibition of TNF-α and IL-1β production in the rat brain
*IL1β↓,

6358- DRE,    Dandelion root extracts and taraxasterol inhibit LPS‑induced colorectal cancer cell viability by blocking TLR4‑NFκB‑driven ACE2 and TMPRSS2 pathways
- in-vitro, CRC, NA
TLR4↓, Mechanistically, dandelion root extracts or TS may inhibit the LPS-promoted toll-like receptor 4 (TLR4)/NFκB-p65 pathway and transcription levels of pro-inflammatory genes (TNFα, IL4 and IL6).
NF-kB↓,
TNF-α↓,
IL4↓,
IL6↓,
tumCV↓, Dandelion root extracts and TS inhibit the LPS-induced viability of colorectal cancer cells

6356- Eug,  Cin,    Investigating the Molecular Mechanisms of the Anticancer Effects of Eugenol and Cinnamaldehyde Against Colorectal Cancer (CRC) Cells In Vitro
- in-vitro, CRC, SW-620 - in-vitro, CRC, Caco-2 - in-vitro, Nor, NCM460
P21↑, In CRC cell lines, p21 levels were significantly increased only by EU 600 μM treatment.
ChemoSen↑, CN yielded a stronger anti-inflammatory action. We confirmed that EU and CN are promising natural candidates in CRC prevention and treatment, even in association with chemotherapeutic drugs.
Casp3↑, EU treatment (600 μM) induced an increase in active caspase-3 while in Caco-2 cells
IL4↓, EU and CN, individually and in combination, especially at higher concentrations, effectively reduced the levels of IL-4 and IL-8 in both CRC cell lines
IL8↓,
ROS↑, cytotoxic effects probably through a mitochondria-dependent apoptotic mechanism, which becomes evident mainly at concentrations that induce ROS-mediated cell death
NRF2↑, In Caco-2 cells, where the basal inflammatory tone is low, EU can activate the Nrf2–HO-1 pathway, a redox-regulated cytoprotective system that limits oxidative stress and restrains inflammatory signaling
HO-1↑,
EMT↓, EU predominantly acts by attenuating survival and migration pathways and by reducing EMT-associated transcriptional signatures rather than by directly modulating inflammatory signaling.

7482- H2,    Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA - Review, Sepsis, NA - Review, AD, NA
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.

7929- H2,    Hydrogen-rich saline reduces airway remodeling via inactivation of NF-κB in a murine model of asthma
- NA, Asthma, NA
*IL4↓, The results showed that hydrogen-rich saline reduced cell counts and levels of cytokines IL-4, IL-5, IL-13 and TNF-α in BALF.
*IL5↓,
*IL13↓,
*TNF-α↓,
*AirwayM↓, Hydrogen-rich saline treatment also significantly decreased mucus index, collagen deposition, and expression of MUC5AC, collagen III and VEGF.
*MUC5AC↓,
*COL3A1↓,
*VEGF↓,
*NF-kB↓, The ratio of phospho-NF-κB p65 to total NF-κB p65 was much lower in mice treated with hydrogen-rich saline than in untreated mice.
*Inflam↓, These effects of hydrogen-rich saline on airway inflammation and remodeling were dose-dependent

7927- H2,    Hydrogen gas (XEN) inhalation ameliorates airway inflammation in asthma and COPD patients
- Human, Asthma, NA
*IL8↓, decreased IL-8 level only in asthma group
*IL4↓, IL-4 and IL-6 levels in EBC were significantly lower after inhalation in the COPD (0.80–0.64 pg/mL, P = 0.025) and asthma (0.06–0.05 pg/mL, P = 0.007) group, respectively.
*IL6↓,
*Inflam↓, A single inhalation of hydrogen for 45 min attenuated inflammatory status in airways in patients with asthma and COPD
*Sepsis↓, has been demonstrated that hydrogen could provide protection against various diseases, including sepsis, stroke and ischemia-reperfusion injury
*Stroke↓,
*antiOx↑, Hydrogen, which exhibits anti-oxidative and anti-inflammation effects, was proved to be relatively safe for inhalation in diving.9
*toxicity↓,

7926- H2,    Hydrogen gas inhalation enhances alveolar macrophage phagocytosis in an ovalbumin-induced asthma model
- in-vivo, Asthma, NA
*Dose↝, Hydrogen gas was delivered to the mice through inhalation twice a day (2 h once) for 7 consecutive days
*Airway↓, Hydrogen gas inhalation significantly alleviated OVA-induced airway hyperresponsiveness, inflammation and goblet cell hyperplasia, diminished TH2 response and decreased IL-4 as well as IgE levels, reduced malondialdehyde (MDA) production
*BALF-Infl↓,
*Th2↓,
*IL4↓,
*IgE↓,
*MDA↓,
*SOD↑, increased superoxide dismutase (SOD) activity
*NF-kB↓, hydrogen gas inhalation inhibited NF-κB activation and markedly activated Nrf2 pathway in OVA-induced asthmatic mice.
*NRF2↑,

7925- H2,    Inhalation of hydrogen gas attenuates airway inflammation and oxidative stress in allergic asthmatic mice
- in-vivo, Asthma, NA
*Dose?, received inhalation of 67% high concentration of hydrogen gas for 60 min once a day for 7 consecutive days after OVA or PBS challenge respectively
*IL4↓, Increased level of IL-4, IL-13, TNF-α and CXCL15 in the BALF and IL-4 in the serum were decreased significantly after inhalation.
*IL13↓,
*TNF-α↓,
*CXCL15↓,
*SOD↑, Hydrogen gas inhalation markedly upregulated the activity of decreased superoxide dismutase
*MDA↓, and significantly attenuated the increased level of malondialdehyde and myeloperoxidase
*MPO↓,
*ROS↓, Hydrogen gas inhalation improves lung function and protects established airway inflammation in the allergic asthmatic mice model which may be associated with the inhibition of oxidative stress process.
*antiOx↑, therapeutic effects of molecular hydrogen on various diseases have been investigated regarding its antioxidation capability [4] and its anti-inflammation [5] and anti-apoptosis
*Inflam↓,
*Apoptosis↓,
*toxicity↓, it is sufficiently mild that it does not disturb metabolic oxidation-reduction reactions or ROS-mediated cell signalling. Thus, it may be a safe and effective antioxidant for pulmonary diseases
*Stroke↓, , accumulating evidence has demonstrated various types of diseases involving oxidative stress, including ischaemic heart disease [7], stroke [8], acute lung injury [9] and inflammatory bowel disease
*Airway↓, Hydrogen gas inhalation decreased lung resistance in the asthmatic mice model
*Neut↓, There was a significant increase in the number of total cells, neutrophils , eosinophils , lymphocytes . Hydrogen gas inhalation resulted in significant reduction in the number of total cells
*Eos↓,
*BALF-Lym↓,
*BALF-Infl↓, Hydrogen gas inhalation attenuated the elevated levels of inflammatory cytokines present in BALF from the asthmatic mouse model
*AirwayM↓, In our study, we found the hydrogen gas inhalation significantly alleviated the pathologic inflammation degree and mucus content in the lung tissue.

7932- H2,    Hydrogen Gas Inhalation Alleviates Airway Inflammation and Oxidative Stress on Ovalbumin-Induced Asthmatic BALB/c Mouse Model
- in-vivo, Asthma, NA
*antiOx↑, Molecular hydrogen (H2) has recently been recognized for its antioxidant and anti-inflammatory properties
*Inflam↓,
*ROS↓, inhaled H2 significantly reduced inflammatory cell infiltration, OS markers, and pro-inflammatory cytokine expression while upregulating antioxidant enzyme activity.
*TAC↑,
*IgE↓, Furthermore, H2 also significantly decreased serum IgE levels, a marker of allergic inflammation.
*Dose↝, 3% H2 gas inhalation on OVA-induced inflammatory airway conditions, body and lung weights were recorded in mice.
*NLR↓, Our results also demonstrated a significant decline in the NLR in the HT group compared to the NT group
*IL4↓, Conversely, the levels of IL-4 (p < 0.001; Figure 4A), IL-5 (p < 0.001; Figure 4B), IL-13 (p < 0.01; Figure 4C), and GM-CSF (p < 0.01; Figure 4F) were significantly lower in the HT group than in the NC group
*IL5↓,
*IL13↓,
*GM-CSF↓,
*NO↓, NO (p < 0.05; Figure 5B) levels were reduced in the HT group compared with those in the NC group
*GPx↑, treatment with 3% H2 significantly increased the GPx activity in the HT group compared to that in the NC group
*Eos↓, In our study, we observed that H2 inhalation reduced neutrophils in the OVA-induced asthmatic BALB/c mouse model

7933- H2,    Hydrogen inhalation ameliorates lung inflammation in mice with asthma
- in-vivo, Asthma, NA
*antiOx↑, Hydrogen has been shown to exhibit antioxidant and anti-inflammatory properties that are beneficial for a range of diseases.
*Inflam↓,
*IL4↓, Hydrogen inhalation attenuated the immune response; decreased the levels of IL-4, IL-5 and IL-13;
*IL5↓,
*IL13↓,
*IL10↑, and further increased the mRNA expression levels of Treg-associated cytokines, namely, IL-10 and TGF-β1, thereby bolstering the body's inflammatory resistance mechanisms.
*TGF-β1↑,
*IgE↓, it also reduced total serum IgE levels and malondialdehyde (MDA) production and increased superoxide dismutase (SOD) secretion in lung tissue.
*MDA↓,
*SOD↑,
*Airway↓, Inhalation of hydrogen decreases airway resistance in asthmatic mice

2521- H2,    Oxyhydrogen Gas: A Promising Therapeutic Approach for Lung, Breast and Colorectal Cancer
- Review, CRC, NA - Review, Lung, NA - Review, BC, NA
Inflam↑, Oxyhydrogen gas, a mixture of 66% molecular hydrogen (H2) and 33% molecular oxygen (O2) has shown exceptional promise as a novel therapeutic agent due to its ability to modulate oxidative stress, inflammation, and apoptosis.
ROS↓, neutralises reactive oxygen and nitrogen species
ChemoSen↑, enhancing existing treatments and reducing harmful oxidative states in cancer cells. boosting the effectiveness of conventional therapies
p‑PI3K↓, inhibiting the PI3K/Akt phosphorylation cascade.
p‑Akt↓,
QoL↑, Similar results have been observed in breast cancer, where patients reported improved quality of life.
GutMicro↑, improves intestinal microflora dysbiosis.
chemoP↑, reduced oxidative stress and mitigated tissue damage, suggesting its potential as a cytoprotective agent in cancer patients undergoing radiation therapy or chemotherapy
radioP↑,
*NRF2↑, documented role in activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.
*Catalase↑, consequently, hydrogen can enhance the expression of endogenous antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GPx), haem oxygenase (e.g., HO-1), and superoxide dismutase (SOD) [45]
*GPx↑,
*HO-1↑,
*SOD↑,
*TNF-α↓, reducing the expression of proinflammatory mediators such as chemokines (e.g., CXCL15), cytokines (e.g., TNF-α), interleukins (e.g., IL-4, IL-6)
*IL4↓,
*IL6↓,
ChemoSen↑, further research demonstrates that oxyhydrogen gas enhanced the sensitivity of lung cancer cells to chemotherapy drugs, suggesting its potential as an adjuvant therapy
Appetite↑, inhaled oxyhydrogen gas over a minimum of 3 months. The results indicated substantial improvements in appetite, cognition, fatigue, pain, and sleeplessness
cognitive↑,
Pain↓,
Sleep↑,
other?, It is recommended that hydrogen should not exceed 4.6% in air or 4.1% by volume in pure oxygen gas (explosion risk)

1041- Lyco,  immuno,    Lycopene improves the efficiency of anti-PD-1 therapy via activating IFN signaling of lung cancer cells
- in-vivo, Lung, NA
TumVol↓, combined lycopene and anti-PD-1 reduced the tumor volume and weight compared to control treatment.
TumW↓,
eff↑, lycopene could assist anti-PD-1 to elevate the levels of interleukin (IL)-1 and interferon (IFN) γ while reduce the levels of IL-4 and IL-10
IL1↑,
IFN-γ↑,
IL4↓,
IL10↓,

1672- PBG,    The Potential Use of Propolis as an Adjunctive Therapy in Breast Cancers
- Review, BC, NA
ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT/TERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1/CCND1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.

1164- PI,    Inhibition of T cell activation by the phytochemical piperine
- in-vitro, Nor, NA
*other↓, inhibited T cell proliferation in a dose-dependent manner without affecting T cell viability.
*CD25+↓,
*IFN-γ↓,
*IL2↓,
*IL4↓,
*IL17↓,
*CD69↓,
*CTLA-4↓,
*p‑ERK↓,
*IKKα↓,

3597- PI,    Chronic diseases, inflammation, and spices: how are they linked?
- Review, AD, NA - Review, Park, NA - Review, Var, NA
*NF-kB↓, downregulation of inflammatory pathways such as NF-κB, MAPK, AP-1, COX-2, NOS-2, IL-1β, TNF-α, PGE2, STAT3
*MAPK↓,
*AP-1↓,
*COX2/PTGS2↓,
*NOS2↓,
*IL1β↓, Parkinson’s disease ↓IL-1β, ↓TNF-α
*TNF-α↓,
*PGE2↓,
*STAT3↓,
*IL10↑, Arthritis ↑IL-10
*IL4↓, Asthma ↓IL-4, -5, ↓NF-κB
*IL5↓,
P53↑, Breast cancer ↑p53, ↓MMP-9,-2, ↓c-Myc, ↓VEGF
MMP9↓,
MMP2↓,
cMyc↓,
VEGF↓,
STAT3↓, Gastric cancer ↓STAT3
survivin↓, Triple negative breast cancer ↓Survivin, ↓p65
p65↓,

3927- PTS,    Effects of Pterostilbene on Cardiovascular Health and Disease
- Review, AD, NA - Review, Stroke, NA
*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2/PTGS2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1/CCL2↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke

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/PTGS2↓, NSCLC ↓ NF-kB activation; ↓COX-2; ↑apoptosis; ↑doxorubicin efficacy
Apoptosis↑,
ChemoSen↑,
PGE2↓, ↓prostaglandin E 2
VEGF↓, ↓VEGF

3646- SIL,    "Silymarin", a promising pharmacological agent for treatment of diseases
- Review, NA, NA
*P-gp/ABCB1↓, The possible known mechanisms of action of silymarin protection are blockade and adjustment of cell transporters, p-glycoprotein, estrogenic and nuclear receptors.
*Inflam↓, silymarin anti-inflammatory effects through reduction of TNF-α, protective effects on erythrocyte lysis and cisplatin-induced acute nephrotoxicity
*hepatoP↑, first usage of Milk thistle, however, was for its hepatoprotectant and antioxidant activities
*antiOx↑,
*GSH↑, increasing the glutathione concentrations
*BioAv↑, Milk thistle extract is now marketing as silymarin and silybinin capsules and tablets with an improved bioavailability under the trade names like Livergol, Silipide and Legalon
*SOD↑, increases the superoxide dismutase activity within the erythrocytes and lymphocytes (
*IFN-γ↓, enhances the IFN-γ, IL-4 and IL-10 secretion in cultures containing lymphocytes.
*IL4↓,
*IL10↓,
*Half-Life↓, Silymarin has a short half-life and quick conjugation in the liver and principal excretion in bile.
*TNF-α↓, Silybinin inhibits elevated intra-hepatic messenger RNA (mRNA) levels of IL-2, IL-4, IFN-γ, and TNF-α significantly
*ALAT↓, reduces the alanine aminotransferase and aspartate aminotransferase levels and suppressed the apoptosis in hepatocytes
*AST↓,
Akt↓, HepG2 -cells death occurs via inhibition of Akt kinase stimulated by palmitate exposure and silymarin prevents this inhibition as it has hepatoprotective activity different from its antioxidant property
chemoP↑, Silymarin can be applied as a co-treatment with the other chemotherapeutics agents while silybin is mainly useful as a hepatoprotective substance against chemotherapeutics-induced oxidative stress.
β-catenin/ZEB1↓, silymarin inhibits β-catenin increase, which will suppress the proliferation of hepatocellular carcinoma HepG2 cells.
TumCP↓,
MMP↓, mitochondrial membrane potential of HepG2 cells decreases by silymarin that causes disruption of membrane permeability so that cytochrome C transfers from the intermembrane space to the cytoplasm
Cyt‑c↑,
*RenoP↑, Renal protection
*BBB↑, silymarin has antioxidant activities in the central nervous system, which enables it to enter the CNS via the blood–brain barrier (BBB)

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/PTGS2↓, 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↑,

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.

7938- TQ,    The effect of single dose of thymoquinone, the main constituents of Nigella sativa, in guinea pig model of asthma
*Dose↝, Thirty guinea pigs were randomly divided to 3 groups; control (C), sensitized (S) and pretreated group with (TQ); 3 mg/kg, IP (S+TQ)
*Eos↓, Administration of TQ caused significant decline in eosinophil (p<0.001), basophil (p<0.05) and condensable increment in neutrophil, monocyte and lymphocyte count (p<0.001 for all cases) in comparison with S group.
*IFN-γ↑, Treatment with TQ caused a significant increase in blood IFN-γ in the S +TQ group (124.93±2.31) compared to that in the S group
*Inflam↓, The preventive effect of TQ may be due to its ability to suppress airway inflammation which is indicated by Hajhashemi in 2004.
*IL4↓, In the present study, asthma induction increased IL-4 and IFN-γ and TQ administration decreased IL-4 and increased IFN-γ compared with sensitized group.
*antiOx↑, TQ has been shown to have strong antioxidant properties25-28 and to suppress the expression of inducible nitric oxide (NO) synthesis in rat macrophages
*NO↓,
*COX2/PTGS2↓, It has been shown that TQ has inhibitory effects on both the cyclooxygenase and the 5-lipoxygenase pathways of arachidonic acid metabolism and on membrane lipid peroxidation.
*5LO↓,

7939- TQ,    Effects of Nigella sativa and its constituents on inflammatory markers in ovalbumin-induced asthma model: a preclinical systematic review and meta-analysis
- Review, Asthma, NA
*IL4↓, The findings from the meta-analysis indicated that N. sativa and its constituents significantly reduced the levels of interleukin (IL)-4, IL-5, IL-13, and IL-17
*IL5↓,
*IL13↓,
*IL17↓,
*IgE↓, Furthermore, there was a notable decrease in immunoglobulin E (IgE) following the intervention with N. sativa and its active components.
*IFN-γ∅, However, the levels of interferon-gamma (IFN-γ) remained unchanged as a result of the intervention with N. sativa and its active ingredients.
*antiOx↑, modulate the asthma model induced by ovalbumin through their anti-inflammatory and antioxidant effects.
*Inflam↓,

7940- TQ,    Anti-inflammatory effect of thymoquinone in a mouse model of allergic lung inflammation
- in-vivo, Asthma, NA
*Eos↓, TQ before airway challenge of ovalbumin (OVA)-sensitized mice resulted in a marked decrease in lung eosinophilia and the elevated Th2 cytokines observed after airway challenge with OVA antigen;
*Th2↓, TQ attenuates allergic airway inflammation by inhibiting Th2 cytokines and eosinophil infiltration into the airways; thus demonstrating its potential anti-inflammatory role during the allergic response in the lung.
*IgE↓, TQ also decreased the elevated serum levels of OVA-specific IgE and IgG1.
*IgG1↓,
*Inflam↓, TQ significantly inhibited allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells.
*AirwayM↓,
*IL4↓, While TQ showed a significant effect in inhibiting IL-4, IL-5 and IL-13 and some effect in inducing IFN-gamma production in the BAL fluid,
*IL5↓,
*IL13↓,
*IFN-γ↑,

7942- TQ,    Thymoquinone inhibits inflammation, neoangiogenesis and vascular remodeling in asthma mice
- in-vitro, Asthma, NA
*IL4↓, TQ inhibited the production of inflammatory factors interleukin-4/-5 (IL-4/-5) by enzyme-linked immunesorbent assay (ELISA).
*IL5↓,
*CD31/PECAM-1↓, platelet endothelial cell adhesion molecule-1, which is also known as CD31 and α-smooth muscle actinalpha (α-SMA) expression in asthma mice challenged by OVA was suppressed by TQ.
*VEGFR2/KDR/Flk1↓, TQ suppressed the activation of VEGFR2-PI3K-Akt pathway and up-regulated the expression of Slit glycoprotein-2 (Slit-2) both in vivo and in vitro
*PI3K↓,
*Akt↓,
*SLIT2↑,
*Inflam↓, Our study demonstrates that TQ attenuated the inflammatory reaction by antagonizing IL-4/-5 while the anti-neoangiogenesis effect of TQ is mediated by inhibition of vascular endothelial growth factor (VEGF)
*VEGF↓,


Showing Research Papers: 1 to 30 of 30

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 30

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CD47↓, 1,   miR-124-3p↓, 1,   PFS↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   GSH↓, 1,   HO-1↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 8,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   MMP↓, 2,   mtDam↑, 2,   OCR↓, 1,   PGC-1α↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4↑, 1,   cMyc↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   LDH↓, 3,   PFK↓, 1,   PKM2↓, 2,   PPARγ↑, 1,   SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis?, 1,   Apoptosis↑, 5,   BAX↓, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↓, 2,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 2,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   hTERT/TERT↓, 1,   IAP2/BIRC3↓, 1,   iNOS↓, 1,   iNOS↑, 1,   JNK↓, 2,   JNK↑, 1,   MAPK↓, 1,   Mcl-1↓, 1,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,   other?, 1,   other↓, 2,   other↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 2,   GRP78/BiP↑, 1,   HSP27↓, 1,   HSP70/HSPA5↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 2,   LC3I↑, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 3,   P53↑, 3,   cl‑PARP↑, 1,   TP53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 2,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↓, 1,   P21↑, 2,  

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

CD44↓, 1,   EMT↓, 2,   ERK↓, 1,   GSK‐3β↑, 1,   HDAC8↓, 1,   HH↓, 1,   PI3K↓, 2,   p‑PI3K↓, 1,   STAT3↓, 3,   p‑STAT3↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AXL↓, 1,   Ca+2↑, 1,   CAFs/TAFs↓, 1,   fascin↓, 1,   Ki-67↓, 1,   MALAT1↓, 1,   MMP2↓, 1,   MMP9↓, 4,   MMPs↓, 1,   Slug↓, 1,   Snail?, 1,   TGF-β↓, 2,   TIMP1↓, 1,   Treg lymp↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 4,   TumMeta↓, 2,   Twist↓, 1,   uPA↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 3,   eNOS↑, 1,   Hif1a↓, 2,   VEGF↓, 6,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↓, 1,   CD4+↓, 1,   COX2/PTGS2↓, 4,   CXCR4↓, 1,   FoxP3+↓, 1,   IFN-γ↓, 1,   IFN-γ↑, 1,   IL1↓, 1,   IL1↑, 1,   IL10↓, 3,   IL2↓, 2,   IL4↓, 8,   IL6↓, 2,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 1,   Inflam↑, 1,   M2 MC↓, 1,   NF-kB↓, 5,   NK cell↑, 1,   p65↓, 2,   PGE2↓, 1,   TLR4↓, 2,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,   CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↓, 1,   ChemoSen↑, 6,   Dose↝, 4,   Dose∅, 2,   eff↑, 17,   RadioS↑, 2,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 2,   Ki-67↓, 1,   LDH↓, 3,   TP53↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   Appetite↑, 1,   chemoP↑, 3,   cognitive↑, 1,   NP/CIPN↓, 1,   OS↑, 1,   Pain↓, 1,   QoL↑, 2,   radioP↑, 2,   Sleep↑, 1,   TumVol↓, 2,   TumW↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2,  
Total Targets: 174

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Airway↓, 3,   AirwayM↓, 3,   BALF-Infl↓, 2,   BALF-Lym↓, 1,   compII↑, 1,   CXCL15↓, 1,   Eos↓, 4,   IgE↓, 5,   IgG1↓, 1,   IL13↓, 6,   MUC5AC↓, 1,   NLR↓, 1,   SLIT2↑, 1,   Stroke↓, 3,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 11,   Catalase↑, 8,   GPx↑, 5,   GSH↑, 6,   GSR↓, 1,   GSR↑, 1,   GSTs↑, 1,   H2O2↓, 1,   HO-1↑, 3,   lipid-P↓, 6,   MDA↓, 7,   MPO↓, 2,   NRF2↑, 8,   ROS↓, 11,   SOD↑, 12,   TAC↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↑, 2,   compIII↑, 1,   MMP↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 4,   AMPK↑, 1,   LDH↓, 1,   LDL↓, 2,   NADPH↓, 1,   PPARα↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 3,   Casp12↓, 1,   Casp3↓, 1,   Casp9↓, 1,   GranB/GZMB↓, 1,   iNOS↓, 3,   p‑JNK↓, 2,   MAPK↓, 3,   MAPK↝, 1,   necrosis↓, 1,   p38↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↓, 1,   other↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

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

ERK↓, 1,   p‑ERK↓, 2,   GSK‐3β↓, 2,   mTOR↓, 1,   OCT4↓, 1,   PI3K↓, 1,   PI3K↑, 1,   STAT↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   AP-1↓, 1,   APP↓, 1,   CD31/PECAM-1↓, 1,   COL3A1↓, 1,   E-sel↓, 1,   MMPs↓, 1,   TGF-β↑, 1,   TGF-β1↑, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   NO↓, 3,   VEGF↓, 2,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB?, 1,   BBB↑, 4,   IBI↑, 1,   OATPs↓, 1,   P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↓, 1,   CD4+↑, 1,   CD69↓, 1,   COX2/PTGS2↓, 5,   CTLA-4↓, 1,   GM-CSF↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 5,   IFN-γ↑, 2,   IFN-γ∅, 1,   IKKα↓, 1,   IL10↓, 1,   IL10↑, 4,   IL17↓, 2,   IL1β↓, 7,   IL2↓, 4,   IL4↓, 22,   IL5↓, 7,   IL6↓, 6,   IL8↓, 2,   Imm↑, 1,   INF-γ↓, 2,   Inflam↓, 20,   LPS↓, 1,   MCP1/CCL2↓, 1,   MUC2↓, 1,   Neut↓, 1,   NF-kB↓, 9,   PGE2↓, 4,   Th2↓, 2,   TLR4↓, 1,   TNF-α↓, 12,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BChE↓, 1,   tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 2,   BACE/β-secretase↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 4,   BioAv↝, 1,   Dose?, 1,   Dose↝, 5,   eff↑, 1,   Half-Life↓, 1,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 4,   AST↓, 4,   creat↓, 1,   GutMicro↑, 2,   IL6↓, 6,   LDH↓, 1,   MUC19↓, 1,   NOS2↓, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiPs↑, 1,   cardioP↑, 2,   cognitive↓, 1,   cognitive↑, 4,   hepatoP↑, 6,   memory↑, 2,   neuroP↑, 7,   Obesity↓, 1,   Pain↓, 1,   RenoP↑, 2,   Strength↑, 1,   toxicity↓, 3,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 2,   Diar↓, 1,   Sepsis↓, 2,  
Total Targets: 163

Scientific Paper Hit Count for: IL4, interleukin 4
8 Hydrogen Gas
4 Silymarin (Milk Thistle) silibinin
4 Thymoquinone
2 Artemisinin
2 Curcumin
2 Piperine
1 1,8-Cineole
1 Bromelain
1 Boswellia (frankincense)
1 Dandelion Root
1 Eugenol
1 Cinnamon
1 Lycopene
1 immunotherapy
1 Propolis -bee glue
1 Pterostilbene
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#:%  Target#:561  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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