IBI Cancer Research Results

IBI, Intestinal Barrier Integrity: Click to Expand ⟱
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Intestinal Barrier Integrity (IBI) refers to the functional integrity of the gut mucosal barrier, including epithelial tight junctions, mucus protection, antimicrobial defenses, and control of luminal antigen and microbial translocation. Loss of intestinal barrier integrity increases permeability, promotes endotoxin and cytokine-driven inflammation, and can sustain tumor-supportive signaling through NF-κB, STAT3, oxidative stress, and immune dysregulation. In IBD, barrier disruption is a core pathogenic feature that amplifies chronic mucosal inflammation and tissue injury. In cancer, especially colorectal cancer, persistent barrier dysfunction may contribute to initiation, progression, and a pro-inflammatory microenvironment, although in some treatment contexts increased permeability can also alter drug exposure or immune interactions. Agents that improve intestinal barrier integrity may be relevant in IBD-associated carcinogenesis and in reducing inflammation-linked tumor promotion.

Related terms/synonyms: gut barrier, epithelial barrier, mucosal barrier, intestinal permeability, leaky gut.
Scientific Papers found: Click to Expand⟱
5932- CAR,    Carvacrol attenuates mucosal barrier impairment and tumorigenesis by regulating gut microbiome
- in-vivo, IBD, NA - in-vivo, Park, NA
*GutMicro↑, Carvacrol can regulate the gut microbiota. bundance of specific microbiota, such as Lactobacillus, Escherichia coli/Shigella, and Lachnoclostridium.
Risk↓, Carvacrol inhibits the development of colitis-associated colorectal cancer.
*Inflam↓, nti-inflammatory and antioxidant traits,
*antiOx↓,
*ZO-1↑, carvacrol significantly restored colonic length (p < 0.01) and re-established key tight junction proteins like ZO-1.
*iNOS↓, downregulated mRNA levels of inflammatory mediators such as iNOS and IL-6.
*IL6↓,
*NO↓, carvacrol has been shown to suppress nitric oxide and prostaglandin E2 production
*PGE2↓,
*memory↑, carvacrol improves memory deficits in Parkinson’s disease models
*TLR4↓, anti-inflammatory effects of carvacrol by inhibiting the TLR4/NF-κB signaling pathway
*NF-kB↓,
*IBI↑, Carvacrol improves intestinal barrier function
*CLDN3↑, expression levels of ZO-1, Claudin3, Claudin1, Occludin, and Mucin were significantly increased in the carvacrol group compared to the DSS group
*CLDN1↑,
*MUC1↑,
*OCLN↑,
*iNOS↑, carvacrol significantly inhibited the mRNA expression levels of iNOS, COX-2, Interferon-γ, IL-1β, and IL-6 in the intestinal tracts of colitis mice
*COX2/PTGS2↓,
*IFN-γ↓,
IL1β↓,
ADAM10?,

6023- CGA,    Pharmacological advances of the chlorogenic acids family: current insights and future research directions
- Review, AD, NA - Review, Park, NA - Review, IBD, NA
*Aβ↓, chlorogenic acid can reduce Aβ plaques in Alzheimer’s disease model mice by 37%, indicating its neuroprotective potential.
*neuroP↑,
*cardioP↑, Similarly, CGAs offer protection to the cardiovascular system, gastrointestinal tract, kidneys, and liver, while additionally preventing metabolic syndrome and displaying anticancer and antimicrobial capabilities.
*GastroP↑,
*RenoP↑,
*hepatoP↑,
*Obesity↓,
*Bacteria↓,
*BioAv↑, hydroxycinnamoyl-CoA quinate hydroxycinnamoyl transferase, HQT in tomatoes significantly enhances CGA accumulation without significantly altering the levels of other soluble phenolic botanical drugs.
*BioAv↑, Mechanistic studies have shown that dietary fats (such as soybean oil and coconut oil) can significantly enhance the permeability of CGA in the Caco-2 monolayer by increasing cell membrane fluidity
*BioAv↑, Following oral administration of CGA, the acidic environment in the stomach helps maintain the structural stability of CGA, with approximately one-third of the dose entering the blood system through passive diffusion in the small intestine, while the
*ROS↓, CGA pretreatment markedly diminished ROS caused by PD toxins
*GutMicro↑, CGA works with the gut microbiota and its metabolites to alleviate post-infectious irritable bowel syndrome (PI-IBS)
*IBI↑, CGA increases intestinal damage repair, decreases MCT-1 and TFF-3 expression, and suppresses NF-κB expression
*MCT1↓,
*NF-kB↓,
*DNMT1↓, Liver Cancer, DNMT1 protein expression↓

7429- CS,    Functional and Therapeutic Potential of Cynara scolymus in Health Benefits
- Review, Nor, NA - Review, IBD, NA - Review, AD, NA
*Inflam↓, C. scolymus exhibits anti-inflammatory, antioxidant, liver-protective, bile-expelling, antimicrobial, and lipid-lowering neuroprotective properties.
*antiOx↑, Of particular interest is the abundance of chlorogenic acid, a type of caffeoylquinic acid known also by its antioxidant activity.
*hepatoP↑,
*lipid-P↓,
*TNF-α↓, Pectins from artichoke reduced the expression of inflammatory markers such as TNF-α, ICAM-I, IL-1β, and IL-6 in mice. This has resulted in a decrease in iNOS and TLR4 expression in favor of reducing inflammation.
*ICAM-1↓,
*IL1β↓,
*IL6↓,
*MUC1↑, artichoke pectin increased the intestinal barrier genes expression, MUC-1 and Occludin.
*OCLN↑,
*IBI↑, artichoke pectin has the potential to improve IBD by inhibiting inflammation and promoting the expression of genes involved in intestinal barrier function
*ROS↓, The beneficial components derived from artichoke have shown important scavenging activity against reactive oxygen species (ROS) and free radicals.
*cardioP↑, Moreover, artichoke leaf extracts supplementation has also decreased the cardiac markers and increased the antioxidant enzyme SOD, GPx, and GSH activities [80].
*SOD↑,
*GPx↑,
*GSH↑,
*TG/TAG↓, resulting in lower triglyceride (TG) levels
*LDL↓, 8 weeks with artichoke leaf extracts (administered as two daily doses of 250 mg). This treatment significantly reduced total cholesterol (TC), LDL cholesterol (LDL-c),
*neuroP↑, Growing evidence highlights the neuroprotective role of polyphenols
*5HT↑, Polyphenols have been shown to improve mood by increasing serotonin levels in the brain, stimulating the production of brain-derived neurotrophic factor (BDNF), and reducing inflammation
*BDNF↑,

7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7006- Fuc,    Seaweeds in the Oncology Arena: Anti-Cancer Potential of Fucoidan as a Drug—A Review
- Review, Var, NA
*toxicity↓, Fucoidan is a versatile, nontoxic marine-origin heteropolysaccharide that has received much attention due to its beneficial biological properties and safety.
*AntiViral↑, ucoidan has been demonstrated to exhibit a variety of conventional bioactivities, such as antiviral, antioxidant, and immune-modulatory characteristics, and anticancer activity against a wide range of malignancies has also recently been discovered.
*antiOx↑,
*Imm⇅,
AntiCan↑,
TumCCA↑, Fucoidan inhibits tumorigenesis by prompting cell cycle arrest and apoptosis, blocking metastasis and angiogenesis, and modulating physiological signaling molecules.
Apoptosis↑,
TumMeta↓,
angioG↓,
antiNeop↑, Fucoidans’ capacity to bind to Toll-like receptors and intervene with the action of vascular endothelial growth factors (VEGF) and matrix metalloproteinases (MMPs) could explain their anti-neoplastic properties
VEGF↓,
MMPs↓,
BioAv↑, Low molecular weight fractions (LMWF), in particular, are thought to be more biocompatible [47]
BioAv↑, in rats, following topical administration of fucoidan (MW 750 kDa) from Fucus vesiculosus demonstrated fine skin-penetrating characteristics.
ROS⇅, Induction/inhibition of reactive oxygen species (ROS), mitochondrial instability, and caspase and poly (ADP-ribose) polymerase (PARP) cleavage are all aspects of it
cl‑PARP↑, fucoidan treatment causes PARP cleavage and caspase-3/7 activation in MCF-7 cells, which are hallmarks of apoptosis [
Casp3↑,
Casp7↑,
ROS↑, human hepatoma SMMC-7721 cells, fucoidan therapy caused noteworthy growth inhibition and ROS-mediated apoptosi
GSH↓, lower glutathione consumption (GSH), mitochondrial swelling, and depolarization of the mitochondrial membrane potential
MMP↓,
PI3K↓, Fucoidan inhibits PI3K, suppressing ERK and activates MAPK, limiting cancer cell proliferation and decreasing Bcl-2 to Bax ratio, inducing caspase-dependent apoptosis in BEL-7402 and LM3 cell lines
ERK↓,
MAPK↑,
TumCP↓,
Bax:Bcl2↑,
TJ↑, Meanwhile, dietary fucoidan progressively restores intestinal villi by upregulating the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1, and Claudin-8 via p38 MAPK and ERK1/2 activation.
ZO-1↑,
OCLN↑,
CLDN1↑,
IBI↑, fucoidan supplementation improves intestinal barrier function by enhancing intestinal microbiota diversity
GutMicro↑,
NK cell↑, ↑NK cell-mediated anticancer immunity
STAT3↓, Inhibits STAT3 Signaling
eff↑, Astragalus polysaccharide as a topical mucosal adjuvant to boost the anticancer efficacy of immune checkpoint inhibitors

7481- H2,  Rad,    Clinical Efficacy of Hydrogen Therapy on Acute Radiation Enteritis and Inflammatory Response in Patients with Cervical Cancer Undergoing Concurrent Chemoradiation Therapy
- Trial, Var, NA
Dose↝, The experimental group received inhalation therapy with a hydrogen-oxygen gas mixture (66.6% hydrogen, 33.3% oxygen; 3 L/min, 2 h/d) on each radiation therapy day.
CRP↓, experimental group showed significantly lower levels of C-reactive protein, neutrophil-to-lymphocyte ratio, interleukin 6, and fecal occult blood positivity rates
NLR↓,
IL6↓,
AntiTum∅, Importantly, no significant difference in tumor response was observed between groups based on the Response Evaluation Criteria in Solid Tumors
*toxicity↓, Hydrogen inhalation is a safe and effective adjunctive therapy that significantly alleviates inflammation and mitigates clinical symptoms of ARE in patients with cervical cancer who are undergoing CCRT, without compromising antitumor treatment outcom
Inflam↓,
radioP↑,
*IBI↑, significant reduction in fecal occult blood positivity in the hydrogen group (χ² = 16.278, P < .001), reinforcing its protective effect on intestinal mucosa integrity.
*ROS↓, Molecular hydrogen has demonstrated a unique capacity to selectively scavenge cytotoxic ROS

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.

7903- IVT,    Inhibition of advanced glycation end products by Isovitexin alleviates intestinal damage: Toward dietary strategies for gut health
- in-vivo, Nor, NA
*AGEs↓, Results demonstrated that ISV effectively inhibited AGEs formation in bovine serum albumin (BSA)-
*TAC↑, In C. elegans, ISV reduced AGEs accumulation, enhanced antioxidant capacity, and improved intestinal barrier function.
*IBI↑,
*TJ↑, upregulated tight junction proteins, and suppressed oxidative stress and apoptosis.
*ROS↓,
*Apoptosis↓,

5934- TV,    Protective Effects of Natural Antioxidants on Inflammatory Bowel Disease: Thymol and Its Pharmacological Properties
- Review, Var, NA
*Inflam↓, anti-inflammation, anti-oxidation, anti-bacteria, anti-fungal, and anti-tumor potential
*antiOx↑,
*Bacteria↓,
AntiTum↑,
*toxicity∅, A high dose of thymol up to 500 mg/kg diet has been shown to have no toxicity
*IBI↑, thymol improves intestinal integrity and alleviates intestinal injury via the regulation of the immune response and oxidation-reduction homeostasis
*ZO-1↑, increasing the expression of the tight junction protein zonula occludens-1 (ZO-1) and occludins
*OCLN↑,
*COX1↑, up-regulates cyclooxygenase-1 (COX1) activity
*TLR4↓, thymol inhibits TLR4 expression and then inhibits the activation of NF-κB signaling, which reduces the production of inflammatory cytokines, such as TNF-α and IL-1β [58,59]
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*TAC↑, Thymol Improves Anti-Oxidant Capacity in IBD
*NRF2↑, Studies have indicated that thymol activates Nrf2 signaling in different tissues
*GutMicro↑, Thymol Changes Gut Microbes and Prevents Pathogen Infection. thymol also promoted the colonization of beneficial bacteria, such as Clostridium, Lactobacillus, and Bacteroides, to improve gut health


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

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

Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,   ROS⇅, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   PGC-1α↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 2,   Bax:Bcl2↑, 1,   Casp3↑, 1,   Casp7↑, 1,   IAP2/BIRC3↓, 1,   MAPK↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   TumCCA↑, 1,  

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

ERK↓, 1,   PI3K↓, 2,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

CLDN1↑, 1,   MALAT1↓, 1,   MMPs↓, 1,   TJ↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   ZO-1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CRP↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   NK cell↑, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

ADAM10?, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   ChemoSen↑, 1,   Dose↝, 3,   eff↑, 3,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

CRP↓, 1,   EZH2↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 1,   AntiTum↑, 1,   AntiTum∅, 1,   chemoP↑, 1,   NP/CIPN↓, 1,   QoL↑, 1,   radioP↑, 2,   Risk↓, 1,   TumVol↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2,  
Total Targets: 66

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 1,   compII↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 5,   Catalase↑, 2,   GPx↑, 3,   GSH↑, 1,   HO-1↑, 2,   lipid-P↓, 2,   MDA↓, 2,   MPO↓, 1,   NRF2↑, 3,   ROS↓, 6,   SOD↑, 3,   TAC↑, 2,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   compIII↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   LDL↓, 2,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 1,   Casp12↓, 1,   GranB/GZMB↓, 1,   iNOS↓, 1,   iNOS↑, 1,   p‑JNK↓, 1,   MAPK↓, 1,   MCT1↓, 1,   p38↓, 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) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   DNMT1↓, 1,  

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

ERK↑, 1,   mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,   CLDN1↑, 1,   COL1↓, 1,   Fibrosis↓, 1,   MUC1↑, 2,   RAGE↓, 1,   TGF-β↑, 1,   TGF-β1↓, 1,   TJ↑, 2,   ZO-1↑, 2,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

CLDN3↑, 1,   GastroP↑, 1,   IBI↑, 8,   OCLN↑, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX1↑, 1,   COX2/PTGS2↓, 1,   HMGB1↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 2,   IL10↑, 1,   IL1β↓, 3,   IL4↓, 1,   IL6↓, 3,   Imm↑, 1,   Imm⇅, 1,   Inflam↓, 5,   JAK2↓, 1,   LPS↓, 1,   NF-kB↓, 4,   PGE2↓, 1,   TLR4↓, 2,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   BDNF↑, 1,  

Protein Aggregation(tgid=19) ⓘ

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

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioAv↝, 1,   Dose↝, 3,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   creat↓, 1,   GutMicro↑, 5,   IL6↓, 3,   RAGE↓, 1,   TG/TAG↓, 1,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiPs↑, 1,   cardioP↑, 3,   cognitive↑, 1,   hepatoP↑, 4,   memory↑, 1,   neuroP↑, 4,   Obesity↓, 2,   RenoP↑, 3,   toxicity↓, 2,   toxicity∅, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 2,   Sepsis↓, 1,  
Total Targets: 120

Scientific Paper Hit Count for: IBI, Intestinal Barrier Integrity
2 Fucoidan
2 Hydrogen Gas
1 Carvacrol
1 Chlorogenic acid
1 Cynara scolymus/Globe Artichoke/Artichoke Extract
1 Radiotherapy/Radiation
1 Isovitexin
1 Thymol-Thymus vulgaris
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#:1462  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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