IL5 Cancer Research Results

IL5, Interleukin-5: Click to Expand ⟱
Source:
Type:
Interleukin-5 (IL-5) is a cytokine that is primarily produced by activated CD4+ helper T cells, mast cells, and eosinophils. It is responsible for stimulating the functions of eosinophils, which are a type of white blood cell.

Protumorigenic Role: IL-5 can promote eosinophil survival and activation, which may contribute to tumor progression in certain cancers by enhancing inflammation and tissue remodeling.
Antitumorigenic Role: Conversely, in some settings, eosinophils activated by IL-5 may exert antitumor effects, highlighting the dual role of IL-5 in cancer.
Scientific Papers found: Click to Expand⟱
13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2/PTGS2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

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

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

7934- H2,    Hydrogen-generating silicon-based agent is effective in a mouse model of ovalbumin-induced allergic bronchial asthma
- in-vivo, Asthma, NA
*IgE↓, Silicon-based agent tended to decrease the total IgE concentration in serum
*antiOx↑, Hydrogen therapy, which involves the intake of hydrogen as an antioxidant, has been reported to be effective against various oxidative stress-related diseases.
*Eos↓, The administration in the diet of this Si-based agent to a model mouse of allergic bronchial asthma significantly suppressed eosinophil counts in the BALF and reduced inflammatory cell infiltration in the lungs
*BALF-Infl↓,
*IL5↓, the expressions of interleukins 5, and 13 and C–C motif chemokine 11 in lung tissue tended to decreased in the Si group compared with those in the control group
*IL13↓,
*CCL11↓,

3257- PBG,    The Potential Use of Propolis as a Primary or an Adjunctive Therapy in Respiratory Tract-Related Diseases and Disorders: A Systematic Scoping Review
- Review, Var, NA
CDK4↓, CAPE also induces G1 phase cell arrest by lowering the expression of CDK4, CDK6, Rb, and p-Rb. M
CDK6↓,
pRB↓,
ROS↓, Artepillin C, a bioactive component of Brazilian green propolis, reduces oxidative damage markers, namely 4-HNE-modified proteins, 8-OHdG, malonaldehyde, and thiobarbituric acid reactive substances in lung tissues with pulmonary adenocarcinoma
TumCCA↑, Propolin, a novel component of prenylflavanones in Taiwanese propolis, was demonstrated to have anti-cancer properties. Propolin H induces cell arrest at G1 phase and upregulates the expression of p21
P21↑,
PI3K↓, Propolin C also inhibits PI3K/Akt and ERK-mediated epithelial-to-mesenchymal transition by upregulating E-cadherin (epithelial cell marker) and downregulating vimentin
Akt↓,
EMT↓,
E-cadherin↑,
Vim↓,
*COX2/PTGS2↓, bioactive compounds such as CAPE, galangin significantly reduce the activity of lung cyclooxygenase (COX) and myeloperoxidase (MPO), and malonaldehyde (MDA), TNF-α, and IL-6 levels, while increasing the activity of catalase (CAT) and SOD
*MPO↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*Catalase↑,
*SOD↑,
*AST↓, Chrysin also reduces the expression of oxidative and inflammatory markers such as aspartate transaminase (AST), alanine aminotransferase (ALT), IL-1β, IL-10, TNF-α, and MDA levels and increases the antioxidant parameters such as SOD, CAT, and GPx
*ALAT↓,
*IL1β↓,
*IL10↓,
*GPx↓,
*TLR4↓, propolis also inhibits the expression of Toll-like receptor 4 (TLR4), macrophage infiltration, MPO activity, and apoptosis of lung tissues in septic animals
*Sepsis↓,
*IFN-γ↑, CAPE also significantly increases IFN-γ
*GSH↑, propolis significantly increased the level of GSH and the histological appearances of propolis-treated bleomycin-induced pulmonary fibrosis rats.
*NRF2↑, CAPE significantly increases the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)
*α-SMA↓, propolis significantly inhibits the expression of α- SMA, collagen fibers, and TGF-1β.
*TGF-β↓,
*IL5↓, Propolis also inhibits the expression of inflammatory cytokines and chemokines such as TNF-α, IL-5, IL-6, IL-8, IL-10, NF-kB, IFN-γ, PGF2a, and PGE2.
*IL6↓,
*IL8↓,
*PGE2↓,
*NF-kB↓,
*MMP9↓, downregulating the expression of TGF-1β, ICAM-1, α-SMA, MMP-9, IgE, and IgG1.

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↓,

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↓,

4031- VitB3,    Nicotinamide Riboside-The Current State of Research and Therapeutic Uses
- Review, NA, NA
*cardioP↑, Accumulating evidence on NRs’ health benefits has validated its efficiency across numerous animal and human studies for the treatment of a number of cardiovascular, neurodegenerative, and metabolic disorders.
*neuroP↑,
*NAD↑, Oral supplementation with NR has been shown to increase NAD+ levels in multiple tissues, along with increased SIRT activity [10,11], improved mitochondrial function [37], and regenerative potential of stem cells
*SIRT1↑,
*NADPH↑, Furthermore, NR is one of the NAD+ intermediates that also serves as a precursor of NADH, as well as hepatic NADP+ and NADPH
*ROS↓, Moreover, SIRT1 inhibits effects of oxidative stress in T2D mice
*IL2↓, NR can similarly decrease IL-2, IL-5, IL-6, and TNFα
*IL5↓,
*IL6↓,
*TNF-α↓,
*Inflam↓, Targeting IL-6 has been recently proposed as a promising treatment to block the inflammatory storm
*BioAv↝, the apparent oral bioavailability of a 1000 mg dose of NR was highly variable among individuals
*BioAv↑, NR was able to increase NAD+ levels in the liver of mice, exhibiting greater oral bioavailability than NAM, which was, in turn, more orally bioavailable than NA


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

NRF2↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,   IR↓, 1,   PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   DR5↑, 1,   Fas↑, 1,   JNK↑, 1,   MAPK↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,   PAK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

pRB↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   P21↑, 1,   TumCCA↑, 1,  

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

EMT↓, 1,   FGF↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,   STAT1↓, 1,   STAT3↓, 2,   STAT4↓, 1,   STAT5↓, 1,  

Migration(tgid=13) ⓘ

ATPase↓, 1,   E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   PDGF↓, 1,   TGF-β↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1↓, 1,   IL12↓, 1,   IL18↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 1,   IL8↓, 1,   JAK↓, 1,   NF-kB↓, 1,   p65↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,   ER(estro)↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,  
Total Targets: 52

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Airway↓, 1,   AirwayM↓, 2,   BALF-Infl↓, 1,   CCL11↓, 1,   Eos↓, 3,   IgE↓, 5,   IgG1↓, 1,   IL13↓, 6,   MUC5AC↓, 1,   NLR↓, 1,   SLIT2↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 4,   Catalase↑, 1,   GPx↓, 1,   GPx↑, 1,   GSH↑, 1,   MDA↓, 2,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 2,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   NAD↑, 1,   NADPH↑, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   MAPK↓, 1,  

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

PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   CD31/PECAM-1↓, 1,   COL3A1↓, 1,   MMP9↓, 1,   TGF-β↓, 1,   TGF-β1↑, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

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

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   GM-CSF↓, 1,   IFN-γ↑, 2,   IFN-γ∅, 1,   IL10↓, 1,   IL10↑, 2,   IL17↓, 1,   IL1β↓, 2,   IL2↓, 1,   IL4↓, 7,   IL5↓, 10,   IL6↓, 3,   IL8↓, 1,   Inflam↓, 7,   NF-kB↓, 3,   PGE2↓, 2,   Th2↓, 1,   TLR4↓, 1,   TNF-α↓, 4,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioAv↝, 1,   Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   IL6↓, 3,   NOS2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 69

Scientific Paper Hit Count for: IL5, Interleukin-5
4 Hydrogen Gas
3 Thymoquinone
1 Curcumin
1 Propolis -bee glue
1 Piperine
1 Vitamin B3,Niacin
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

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