NOX4 Cancer Research Results

NOX4, NADPH oxidase 4: Click to Expand ⟱

Source:

Type:

NOX4 (NADPH oxidase 4) is a member of the NADPH oxidase (NOX) family of enzymes, which are responsible for generating reactive oxygen species (ROS) in various cell types. NOX4 is regulated by hypoxia, which can activate its expression and activity.
NOX4 (NADPH oxidase 4) is an enzyme that produces reactive oxygen species (ROS), particularly hydrogen peroxide (H₂O₂).
NOX4 is a cytoplasmic enzyme that catalyzes the transfer of electrons from NADPH to oxygen, resulting in the production of superoxide anion (O2-) and other ROS. NOX4 is expressed in a variety of tissues, including the kidney, lung, and vascular smooth muscle cells.
NOX4 is generally expressed in cancer.
In general, high NOX4 expression is associated with:
      Poor prognosis
      Increased tumor size
      Metastasis
      Resistance to chemotherapy and radiation therapy
      Poor response to treatment
Low NOX4 expression is associated with:
      Better prognosis
      Smaller tumor size
      Less metastasis
      Better response to chemotherapy and radiation therapy
      Better response to treatment

The combination of NOX4-driven ROS and available iron can lead to a synergistic increase in oxidative stress, setting the stage for ferroptotic cell death.

Scientific Papers found: Click to Expand⟱

3451-

ALA,

Alpha-lipoic acid ameliorates H2O2-induced human vein endothelial cells injury via suppression of inflammation and oxidative stress

in-vitro,

Nor,

HUVECs

(HUVECs) injury induced by hydrogen peroxide (H2O2)

*LDH↓, ALA reduces LDH release from H2O2-induced cells
*NOX4↓, ALA downregulates the expression of Nox4
*NF-kB↓, ALA inhibits H2O2-induced activation of the NF-κB signaling pathway
*iNOS↓, ALA suppresses the upregulation of iNOS, VCAM-1 and ICAM-1 in H2O2-induced HUVECs
*VCAM-1↓,
*ICAM-1↓,
*ROS↓, ALA protected HUVECs against oxidative damage induced by H2O2, as assessed by cell viability and LDH activity.
*cardioP↑, regulating Nox4 protein expression and play a protective role in cardiovascular disease.

1093-

And,

Andrographolide attenuates epithelial‐mesenchymal transition induced by TGF‐β1 in alveolar epithelial cells

in-vitro,

Lung,

A549

TGF-β↓,
TumCMig↓,
MMP2↓,
MMP9↓,
ECM/TCF↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,
p‑ERK↓,
ROS↓, reduced (TGF‐β1‐induced) intracellular ROS generation
NOX4↓,
SOD2↑,
SIRT1↑, Andro protects AECs from EMT partially by activating Sirt1/FOXO3‐mediated anti‐oxidative stress pathway
FOXO3↑,

2724-

BetA,

NOX4_by_betulinic_acid_protects_against_cerebral_ischemia-reperfusion_in_mice">Down-regulation of NOX4 by betulinic acid protects against cerebral ischemia-reperfusion in mice

in-vivo,

Nor,

mice

in-vivo,

Stroke,

AntiTum↑, Betulinic acid is mainly known for its anti-tumor and anti-inflammatory activities.
*Inflam↓,
*ROS↓, Our previous study showed that betulinic acid could decrease the reactive oxygen species (ROS) production by regulating the expression of NADPH oxidase.
*NOX4↓, Pre-treatment with betulinic acid (50 mg/kg/day for 7 days via gavage) prior to MCA occlusion prevented the ischemia/reperfusion-induced up-regulation of NOX4 and ROS production.
*Apoptosis↓, treatment with betulinic acid could markedly blunt the ischemia/reperfusion-induced neuronal apoptosis
neuroP↑, betulinic acid protects against cerebral ischemia/reperfusion injury in mice

3869-

Carno,

Carnosine, Small but Mighty—Prospect of Use as Functional Ingredient for Functional Food Formulation

Review,

AD,

Review,

Stroke,

*ROS↓, carnosine scavenges reactive oxygen species (ROS)
*IronCh↑, it can chelate divalent metal ions: heavy metal chelating activity
*AntiAge↑, can slow down aging.
*antiOx↑, natural antioxidant [4] and has anti-inflammatory and neuroprotective properties
*Inflam↓,
*neuroP↑,
*lipid-P↓, Carnosine reduces lipid peroxidation, but also inhibits oxidative modification of protein exposed to hydroxyl radicals
*toxicity↓, carnosine can be recommended as a natural cure that has no side effects but is highly efficient
*NOX4↓, human kidney tubular epithelial (HK2) cells indicated that carnosine decreased NADPH oxidase (Nox) 4 expression and increased total superoxide dismutase (T-SOD) activity, thus reducing the production of intracellular ROS,
*SOD↑,
*HNE↓, Rising data indicate that carnosine acts as a scavenger of reactive and cytotoxic carbonyl species including 4-hydroxynonenal (HNE)
*IL6↓, anserine and/or carnosine supplementation significantly decreased IL-6, TNF-α, and IL-1β in pre-treated mice with MPTP-induced PD,
*TNF-α↓,
*IL1β↓,
*Sepsis↓, carnosine has a beneficial effect on reducing acute kidney injury due to septic shock
*eff↑, carnosine on ischemic stroke, there was a 29.4% average reduction in infarct volume with a clear dose-dependent effect (38.1% reduction on 1000 mg/kg dose compared with 13.2% for doses less than 500 mg/kg)
*GABA↝, In addition to the carnosine-histidine-histamine pathway, carnosine can also have a direct impact on CA1 pyramidal neurons [212] or act as a precursor for the neurotransmitter GABA
*Aβ↓, Several studies have reported that carnosine supplementation reduced β-amyloid cumulation in the hippocampus of a transgenic mouse model of AD
Glycolysis↓, carnosine has the ability to inhibit glycolysis and thus achieve an antitumor effect
AntiTum↑,
p‑Akt↓, significant reduction of Akt phosphorylation in the U87 glioblastoma cell line
TumCCA↑, Carnosine has an effect in bladder cancer by stopping the G1 phase cell cycle by increasing p21WAF1 expression and decreasing cyclin/CDK complexes
angioG↓, inhibits angiogenesis by suppressing VEGFR-2
VEGFR2/KDR/Flk1↓,
NF-kB↓, suppressing nuclear factor kB (NF-κB) signaling pathway activation in human colon cancer cells

2807-

CHr,

Evidence-based mechanistic role of chrysin towards protection of cardiac hypertrophy and fibrosis in rats

in-vivo,

Nor,

Wistar rats

*antiOx↑, antioxidant, anti-inflammatory, anti-fibrotic and anti-apoptotic
Inflam↓,
*cardioP↑, Pre-treatment with chrysin of 60 mg/kg reversed the ISO-induced damage to myocardium and prevent cardiac hypertrophy and fibrosis through various anti-inflammatory, anti-apoptotic, antioxidant and anti-fibrotic pathways
*GSH↑, CHY at the highest dose (60 mg/kg) significantly bolstered the antioxidant status :GSH, SOD and CAT
*SOD↑,
*Catalase↑,
*GAPDH↑, significant increase in GAPDH levels was observed in CHYP group in comparison with normal group
*BAX↓, Decrease in apoptotic (Bax), increase in anti-apoptotic (Bcl-2)
*Bcl-2↑,
*PARP↓, expression of downstream signalling proteins, that is, PARP, cytochrome-C and caspase-3 were following the similar pattern. however at CHY 60 mg/kg treatment group, the levels were remarkably (P < 0·001) reduced.
*Cyt‑c↓,
*Casp3↓,
*NOX4↓, Whereas, lower levels of Nox-4 and higher levels of Nrf-2, HO-1 and HSP-70 were observed in CHYP group
*NRF2↑,
*HO-1↑,
*HSP70/HSPA5↑,

7489-

H2,

Molecular Hydrogen in the Treatment of Respiratory Diseases

Review,

Asthma,

*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

7563-

HYP,

Hyperoside alleviates macrophages and microglia-mediated neuroinflammation and oxidative stress through activating PI3K/AKT and Nrf2/HO-1 signaling pathway post spinal cord injury

vitro+vivo,

Nor,

SCI mice were treated with HYP (10 mg/kg or 50 mg/kg) via intraperitoneal injection

*Inflam↓, Hyperoside (HYP), a bioactive flavonoid derived from traditional Chinese medicinal herbs, exhibits potent anti-inflammatory and antioxidant properties.
*antiOx↑,
*Dose↝, SCI mice were treated with HYP (10 mg/kg or 50 mg/kg) via intraperitoneal injection
*IL1β↓, HYP treatment significantly reduced the expression of pro-inflammatory mediators (IL-1β, IL-6, TNF-α, iNOS, and COX-2) and oxidative stress-related markers (NOX1, NOX2, and NOX4).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2/PTGS2↓,
*NOX4↓,
*NOX2↓,
*NOX1↓,
*PI3K↑, HYP enhanced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway and upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1)
*Akt↑,
*NRF2↑,
*HO-1↑,
*neuroP↑, our findings demonstrate that HYP confers neuroprotection by alleviating neural tissue damage and facilitating locomotor recovery after SCI

7878-

isoO,

Cisplatin,

Isoorientin Attenuates Cisplatin-Induced Nephrotoxicity Through the Inhibition of Oxidative Stress and Apoptosis via Activating the SIRT1/SIRT6/Nrf-2 Pathway

in-vivo,

Nor,

mice

*antiOx↑, Isoorientin (Iso) is a flavonoid-like compound known to have antioxidant effects.
*RenoP↑, Iso treatment significantly reduced CDDP-induced nephrotoxicity via attenuating cell damage in vitro and via ameliorating renal injury, as determined by biochemical markers, in mice.
*chemoP↑,
*SIRT1↑, Iso up-regulated the expression levels of SIRT1 and SIRT6 in vivo and in vitro.
*SIRT6↑, Iso treatment markedly enhanced the expression levels of SIRT1, SIRT6, Nrf2, HO-1, and NQO1 compared with that in the CDDP-exposed group
*NRF2↑, Iso activated Nrf2 translocation and the expression levels of its downstream antioxidant enzymes, such as HO-1 and NQO1,
*HO-1↑,
*NQO1↑,
*NOX4↓, whereas it inhibited the expression level of NOX4, thus decreasing oxidative stress.
*ROS↓,
*MPO↓, MPO and MDA levels were lowered by pretreatment with Iso
*MDA↓,
*SOD↑, SOD and GSH levels were significantly increased
*GSH↑,

7837-

ISQ,

Isoquercitrin Delays Denervated Soleus Muscle Atrophy by Inhibiting Oxidative Stress and Inflammation

in-vivo,

Nor,

*Dose↝, Isoquercitrin demonstrated the optimal protective effect at 20 mg/kg/d, which was the dose used in subsequent experiments.
*autophagy↓, Following isoquercitrin treatment, mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy-related proteins (ATG7, BNIP3, LC3B, and PINK1);
*ATG7↓,
*BNIP3↓,
*LC3B↓,
*PINK1↓,
*ROS↓, (ROS) in the target muscle was reduced, which might be associated with the upregulation of antioxidant factors (SOD1, SOD2, NRF2, NQO1, and HO1) and the downregulation of ROS production-related factors (Nox2, Nox4, and DUOX1).
*SOD1↑,
*SOD2↑,
*NRF2↑,
*NQO1↑,
*HO-1↑,
*NOX2↓,
*NOX4↓,
*DUOX1↓,
*IL1β↓, isoquercitrin treatment reduced the levels of inflammatory factors—interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)—in the target muscle and inactivated the JAK/STAT3 signaling pathway.
*IL6↓,
*TNF-α↓,
*JAK↓,
*STAT3↓,
*Inflam↓, via inhibition of oxidative stress and inflammatory response.

3268-

Lyco,

Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders

Review,

AD,

*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1/SREBF1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,

3264-

Lyco,

Pharmacological potentials of lycopene against aging and aging‐related disorders: A review

Review,

Var,

Review,

AD,

Review,

Stroke,

*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.

3534-

QC,

Lyco,

Synergistic protection of quercetin and lycopene against oxidative stress via SIRT1-Nox4-ROS axis in HUVEC cells

in-vitro,

Nor,

HUVECs

*ROS↓, especially quercetin-lycopene combination (molar ratio 5:1), prevented the oxidative stress in HUVEC cells by reducing the reactive oxygen species (ROS) and suppressing the expression of NADPH oxidase 4 (Nox4), a major source of ROS production.
*NOX4↓, Quercetin-lycopene combination could interact with SIRT1 to inhibit Nox4 and prevent endothelial oxidative stress
*Inflam↓, quercetin-lycopene combination downregulated inflammatory genes induced by H2O2, such as IL-17 and NF-κB.
*NF-kB↓, NF-κB p65 was activated by H2O2 but inhibited by the quercetin-lycopene combination.
*p65↓,
*SIRT1↑, quercetin and lycopene combination promoted the thermostability of Sirtuin 1 (SIRT1) and activated SIRT1 deacetyl activity
*cardioP↑, The cardioprotective role of SIRT1
*IL6↓, LYP: Q = 1:5), interacted with deacetylase SIRT1 to inhibit NF-κB p65 and Nox4 enzyme, downregulated inflammatory cytokines such as IL-6 and pro-inflammatory enzymes such as COX-2, and suppressed ROS elevation activated by H2O2.
*COX2/PTGS2↓,

3012-

RosA,

Rad,

Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROSMYPT1TGFβ1 Signaling Via miR-19b-3p

in-vitro,

Nor,

IMR90

*Inflam↓, RA reduced X-ray-induced the expression of inflammatory related factors, and the level of reactive oxygen species.
*ROS↓,
*p‑NF-kB↓, RA down-regulated the phosphorylation of nuclear factor kappa-B (NF-κB).
*Rho↓, RA attenuated RhoA/Rock signaling through upregulating miR-19b-3p, leading to the inhibition of fibrosis
*ROCK1↓,
*radioP↑, RA attenuated radiation- induced damage by its capacity to relieve inflammation and regulate inflammatory factors.
*MCP1/CCL2↓, RA treatment reduced RNA levels of NF-kB target gene, including MCP-1, RANTES, and ICAM-1
*RANTES↓,
*ICAM-1↓,
*PGC1A↑, Western blot analysis showed that RA promoted the expression of PGC-1a and reduced the expression of NOX-4, this evidence further suggested that RA inhibits the generation of ROS
*NOX4↓,
*Dose↝, RA exerted strongly protective effects in the X-ray-induced inflammation at doses of 60 mg/kg, and treat- ment with a higher dose (120 mg/kg) do not enhance its anti- inflammatory effect.

966-

RT,

Antioxidant Mechanism of Rutin on Hypoxia-Induced Pulmonary Arterial Cell Proliferation

vitro+vivo,

Nor,

hypoxia-induced

*ROS↓, (NAC), a scavenger of ROS, abolished or diminished the capability of rutin in repressing hypoxia-induced cell proliferation. ****
*NOX4↓, rutin decreased the up-regulation of Nox4 induced by hypoxia
*Hif1a↓, Upregulated Expression of HIF-1α Induced by Hypoxia Was Depressed by Rutin
*α-tubulin↓, Rutin reversed this increasing expression of α-tubulin, and the reversed effect was attenuated after scavenging ROS with NAC.

3405-

TQ,

doxoR,

Protective effect of thymoquinone against doxorubicin-induced cardiotoxicity and the underlying mechanism

vitro+vivo,

NA,

mice

*cardioP↑, thymoquinone can alleviate doxorubicin-induced cardiac toxicity in mice.
*NRF2↑, alleviate iron death in mouse cardiomyocytes by activating the Nrf2/HO-1 signaling pathway
*HO-1↑,
*ROS↓, Thymoquinone can also alleviate oxidative stress in mouse cardiomyocytes
*NQO1↑, similar effects on the expression levels of NQO1, COX-2, and NOX4
*COX2/PTGS2↓, implied
*NOX4↓, implied
*GPx4↑,
*FTH1↑, Reduces free iron, limiting ferroptosis
*p‑mTOR↓,
*TGF-β↓,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

autophagy↓, 1, DUOX1↓, 1, NOX1↓, 1, NOX2↓, 2, SpO2↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 7, Catalase↑, 4, Fenton↓, 1, GPx4↑, 1, GSH↑, 4, GSTs↑, 1, HNE↓, 1, HO-1↑, 8, lipid-P↓, 3, MDA↓, 4, MPO↓, 2, NOX4↓, 13, NQO1↑, 4, NRF2↑, 8, RNS↓, 1, ROS↓, 12, SOD↑, 6, SOD1↑, 1, SOD2↑, 1, TAC↑, 1, TBARS↓, 1, VitE↓, 1,

Metal & Cofactor Biology(tgid=2) ⓘ

FTH1↑, 1, IronCh↑, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

PINK1↓, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1, ALAT↓, 1, ATG7↓, 1, CRM↑, 1, FASN↓, 1, GAPDH↑, 1, LDH↓, 1, NADPH↓, 1, PGC1A↑, 1, SIRT1↑, 2, SREBP1/SREBF1↓, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 2, Apoptosis↓, 2, BAX↓, 1, Bcl-2↑, 2, Bcl-xL↑, 1, Casp3↓, 2, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 3,

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

BNIP3↓, 1, LC3B↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 2, PARP↓, 1, SIRT6↑, 1,

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

ERK↓, 1, p‑mTOR↓, 1, PI3K↑, 2, STAT3↓, 2, STAT3↑, 1,

Migration(tgid=13) ⓘ

Ca+2↓, 1, Ki-67↓, 1, MMP2↑, 1, Rho↓, 1, ROCK1↓, 2, TGF-β↓, 1, Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1, VCAM-1↓, 2, α-tubulin↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1, NO↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1, CD4+↑, 1, COX2/PTGS2↓, 3, FOXP3↑, 1, HMGB1↓, 1, ICAM-1↓, 4, IL1↓, 1, IL10↑, 1, IL1β↓, 5, IL22↓, 1, IL4↑, 1, IL6↓, 6, IL8↓, 1, Inflam↓, 8, JAK↓, 1, JAK2↑, 1, M2 MC↑, 1, MCP1/CCL2↓, 2, NF-kB↓, 5, p‑NF-kB↓, 1, p65↓, 1, PGE2↓, 1, RANTES↓, 1, TLR2↓, 1, TLR4↓, 1, TNF-α↓, 6,

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

GABA↝, 1, tau↓, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, Dose↓, 1, Dose↑, 2, Dose↝, 6, eff↑, 2, P450↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, AST↓, 1, BP↓, 1, creat↓, 1, IL6↓, 6, Ki-67↓, 1, LDH↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 1, cardioP↑, 5, chemoP↑, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 4, OS↑, 1, radioP↑, 1, RenoP↑, 2, toxicity↓, 1, toxicity∅, 1, Weight↑, 1,

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,
Total Targets: 135

Scientific Paper Hit Count for: NOX4, NADPH oxidase 4

3 Lycopene
1 Alpha-Lipoic-Acid
1 Andrographis
1 Betulinic acid
1 Carnosine
1 Chrysin
1 Hydrogen Gas
1 Hyperoside
1 isoorientin
1 Cisplatin
1 isoquercitrin
1 Quercetin
1 Rosmarinic acid
1 Radiotherapy/Radiation
1 Rutin
1 Thymoquinone
1 doxorubicin

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#:644  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

NOX4 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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