antiPs Cancer Research Results
antiPs, antiPsoriatic: Click to Expand ⟱
| Source: |
| Type: |
| antiPsoriatic
|
Scientific Papers found: Click to Expand⟱
*cognitive↑, wound healing,ulcer-protective, psychoneuro-pharmacological (cognitive effects), antinociceptive, anti-inflammatory, antimicrobial, immunomodulayory, antiproliferative, antimutagenic, angiogenetic, antioxidant of the Centella extracts or asiaticosid
*Inflam↓,
*AntiBio↑,
*Imm↑,
*antiOx↑,
*Wound Healing↑, Alcoholic Centella extracts when topically applied accelerate wound healing stimulating epithelisation
and increasing the rate of wound contraction.
*cardioP↑, cardio protective effect of Centella asiatica on myocardial marker enzymes and antioxidant enzymes in adriamycin induced cardiomyopathy was inve
*SOD↑, (SOD, CAT, GPx, GST). Treatment with Centella asiatica (200 mg/kg of body wt/oral) extract significantly prevented these alterations and restored the enzyme activities to near normal levels
*Catalase↑,
*GPx↑,
*GSTs↑,
*MDA↓, lower MDA levels than did the other rats, which indicates decreased lipid peroxidation in these rats.
*lipid-P↓,
*ROS↓, Centella asiatica extract and powder may ameliorate H2 O2 -induced oxidative stress by decreasing lipid peroxidation via alteration of the antioxidant defence system of the rats
*memory↑, Only the aqueous extract of whole plant (200 mg/kg for 14 days) showed an improvement in learning
and memory of male Wistar rats
*GABA↑, The alcoholic Centella asiatica extract dose-dependently increased the GABA level in rats.
*antiPs↑, Centella asiatica extracts as a topical anti-psoriatic agent
*BioAv↝, After oral or subcutaneous administration of madecassoside, asiaticoside, asiatic acid and madecassic acid in rats, the bio-availability is varying between 30% and 50%, respectively.
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
PSA, |
NA |
|
|
|
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;
*NF-kB↓, GA Inhibits Signaling of Nuclear Factor-Kappa B (NF-jB)
PI3K↓, GA Inhibits Phosphatidylinositol 3′-Kinase/Protein Kinase B (PI3K/Akt)
Akt↓,
STAT3↓, table 15.1 GA Inhibits Signal Transducer and Activator of Transcription-3 (STAT-3) Pathways
STAT5↓,
IL6↓,
COX2/PTGS2↓, GA Inhibits COX-2
iNOS↓, GA Inhibits iNOS
MMPs↓,
Src↓, GA Inhibits Src
PKA↓,
CXCR4↑, GA Inhibits Chemokine X-Receptor 4 (CXCR4) and Downstream Signaling Pathways
VEGF↓,
Bcl-2↓, GA Inhibits the Expression of Bcl-2 Family Proteins
Bcl-xL↓,
IAP1↓,
Mcl-1↓,
survivin↓,
cycD1/CCND1↓, GA Inhibits Expression of Cyclin D1
HSP90↓,
HSP70/HSPA5↓,
MAPK↓, GA Inhibits Mitogen-Activated Protein Kinase (MAPK)
HATs↓, GA Inhibits CBP/p300 Histone Aceyltransferase (HAT) and Histone Deacetylase (HDAC)
HDAC↓,
FAK↓, GA Inhibits the Activation of Focal Adhesion Kinase (FAK)
ROS↑, GA Induces the Production of Reactive Oxygen Species (ROS)
MMP7↓, GA Inhibits Matrix Metalloproteinase 7 & 9 (MMP-7 & 9)
MMP9↓,
α-tubulin↑, GA Inhibits Tubulin
cl‑PARP↑, GA Induces Cleavage of Poly(ADP-Ribose) Polymerases (PARPs)
TNF-α↓, GA Inhibits Tumor Necrosis Factor-a (TNF-a)
BID↑, GA Induces BID
BAD↑, GA Induces BAD
Cyt‑c↑, GA, induces the expression of cytochrome c in colorectal cancer HT-29, bladder cancer T24 and UMUC3, breast cancer MDA-MB-231, and human hepatocellular carcinoma cells
Casp3↑, GA Induces the Activation of Caspase-3 and Caspase-9
Casp9↑,
*AntiArt↑, GA inhibits RA by inhibiting the levels of cytokines and key inflammatory molecules [
*antiPs↑, recent study showed that GA could be used as an anti-psoriatic agent
| - |
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.
*BioAv↓, Although ISLT has been globally recognized for its health benefits, its oral administration is still restricted by sparing water solubility, poor bioavailability, and slow dissolution in the intestine.
GlucoseCon↓, ISLT (MGC803 cells: 40 μM, SGC7901 cells: 50 µM) downregulated the expression of glucose transporter four and reduced the uptake of glucose by GC cells.
LDH↓, demonstrated that it suppressed the activity of lactate dehydrogenase and pyruvate dehydrogenase kinase 1 and reduced the production of glycolytic products.
PDK1↓,
Glycolysis↓,
mt-OXPHOS↓, It impaired mitochondrial function while simultaneously suppressing glycolysis and inhibiting mitochondrial oxidative phosphorylation, ultimately leading to energy metabolic collapse in GC cells.
Bax:Bcl2↓, it decreased the Bcl-2/Bax ratio and upregulated cleaved caspase-3/caspase-9 to promote GC cell apoptosis.
cl‑Casp3↑,
cl‑Casp9↑,
Apoptosis↑,
Hif1a↓, hypoxia-inducible factor-1α was downregulated to regulate the energy metabolism and proliferative activity of GC cells
ROS↑, ISLT-17 increases the production of Reactive oxygen species (ROS) in GC cells, thereby inhibiting cell growth.
*AntiDiabetic↑, ISLT possesses therapeutic effects on various diseases such as diabetes, cardiovascular diseases, and kidney diseases by activating the Nrf2 pathway
*cardioP↑,
*RenoP↑, structure in patients with diabetic kidney disease, inhibited oxidative stress and reduced ROS levels, and suppressed the activation of NF-kappa B and NLRP3 inflammasomes and the occurrence of pyroptosis, which played a renal protective role
*ROS↓,
*NF-kB↓,
*NLRP3↓,
*Pyro↓,
*antiPs↑, ISLT (1 mg/kg/day and 2 mg/kg/day) ameliorates psoriasis by inhibiting IL-6 and IL-8 and inhibiting inhibitory nuclear factor-kappa B activity, resulting in a reduction in pro-inflammatory.
*IL6↓,
*IL8↓,
BioAv↑, Compared with traditional oral and injectable methods, transdermal administration possesses significant advantages, such as protection against first-pass effects, improved bioavailability, enhanced patient compliance, prolonged drug stability, and th
BioAv↑, Accordingly, transdermal drug delivery systems containing intercellular lipid components (ceramides) can effectively improve the transdermal efficiency of lipophilic drugs, including ISLT.
BioAv↑, ISLT@NPs possessed significantly higher targeted accumulation in the colon and improved tissue penetration than free DiR, suggesting higher oral bioavailability.
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
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) ⓘ
mt-OXPHOS↓, 1, ROS↑, 3,
Mitochondria & Bioenergetics(tgid=3) ⓘ
PGC-1α↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
GlucoseCon↓, 1, Glycolysis↓, 1, LDH↓, 1, PDK1↓, 1, SCD1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Apoptosis↑, 2, BAD↑, 1, Bax:Bcl2↓, 1, Bcl-2↓, 1, Bcl-xL↓, 1, BID↑, 1, Casp3↑, 2, cl‑Casp3↑, 1, Casp9↑, 2, cl‑Casp9↑, 1, Cyt‑c↑, 2, IAP1↓, 1, IAP2/BIRC3↓, 1, iNOS↓, 1, MAPK↓, 1, Mcl-1↓, 2, survivin↓, 1, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
EZH2↓, 1, HATs↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP70/HSPA5↓, 1, HSP90↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 1, cycD1/CCND1↓, 2, mitA↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↑, 1, HDAC↓, 1, PI3K↓, 2, Src↓, 1, STAT3↓, 1, STAT5↓, 1,
Migration(tgid=13) ⓘ
BACH1↓, 1, FAK↓, 1, LAMs↓, 1, MALAT1↓, 1, MMP7↓, 1, MMP9↓, 1, MMPs↓, 1, PKA↓, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 2, α-tubulin↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
EGFR↓, 1, Hif1a↓, 3, VEGF↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, CXCR4↑, 1, IL6↓, 1, NF-kB↓, 1, NK cell↑, 1, PD-1↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 2, Dose↝, 2, eff↑, 3, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, EZH2↓, 1, IL6↓, 1, LDH↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, NP/CIPN↓, 2, QoL↑, 1, radioP↑, 1, TumVol↓, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 2,
Total Targets: 88
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 1, compII↑, 1, Stroke↓, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, Catalase↑, 3, GPx↑, 3, GSH↑, 1, GSTs↑, 1, HO-1↓, 1, HO-1↑, 1, Keap1↝, 1, lipid-P↓, 1, MDA↓, 3, MPO↓, 1, NRF2↑, 2, ROS↓, 4, mt-ROS?, 1, SOD↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, ATP↑, 2, compIII↑, 1, Insulin↑, 1, MMP↑, 2, PGC-1α↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 2, glucose↓, 1, LDL↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Casp12↓, 1, Casp3↓, 1, GranB/GZMB↓, 1, p‑JNK↓, 1, p38↓, 1, Pyro↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
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) ⓘ
Beclin-1↑, 1, LC3‑Ⅱ/LC3‑Ⅰ↑, 1, LC3II↑, 1, p62↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
PARP1↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTOR↓, 1, PI3K↓, 1, PI3K↑, 1,
Migration(tgid=13) ⓘ
APP↓, 1, TGF-β↑, 1, VCAM-1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1,
Barriers & Transport(tgid=15) ⓘ
IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX2/PTGS2↑, 1, IFN-γ↓, 1, IL10↑, 1, IL18↓, 1, IL1β↓, 2, IL4↓, 1, IL6↓, 3, IL8↓, 1, Imm↑, 2, Inflam↓, 3, LPS↓, 1, pol-M2 MC↑, 1, NF-kB↓, 3, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 1, BDNF↑, 1, GABA↑, 1, NGF↑, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 2, Dose↝, 2, eff↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 2, AST↓, 2, creat↓, 1, GutMicro↑, 2, IL6↓, 3, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 2, antiPs↑, 5, cardioP↑, 3, chemoP↑, 1, cognitive↑, 3, hepatoP↑, 3, memory↑, 2, neuroP↑, 3, Obesity↓, 2, RenoP↑, 2, toxicity↓, 2, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1, Bacteria↓, 1, Sepsis↓, 1,
Total Targets: 104
Scientific Paper Hit Count for: antiPs, antiPsoriatic
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#:1509 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
Home Page