RNS Cancer Research Results
RNS, reactive nitrogen species: Click to Expand ⟱
| Source: |
| Type: |
Reactive nitrogen species (RNS) are chemically reactive molecules that contain nitrogen and can play significant roles in cellular signaling and homeostasis. Like reactive oxygen species (ROS), RNS can have both beneficial and detrimental effects in the context of cancer.
|
Scientific Papers found: Click to Expand⟱
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,
*antiOx↑, multiple activities of berberine, including antioxidant, acetylcholinesterase and butyrylcholinesterase inhibitory,
*AChE↓, inhibit AChE with an IC50 of 0.44 μM
*BChE↓, BChE inhibitor and the corresponding IC50 was estimated to be 3.44 μM
*MAOA↓, inhibitory activity on MAO-A with an IC50 value of 126 μM
*Aβ↓, monoamine oxidase inhibitory, amyloid-b peptide level-reducing and cholesterol-lowering activities.
*LDL↓, effectively reduce serum cholesterol and LDL-cholesterol levels in hyperlipidemic hamsters and human hypercholesterolemic patients
*ROS↓, First, it was reported that berberine can scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*lipid-P↓, Secondly, berberine can inhibit lipid peroxidation
*Dose↝, berberine can inhibit AChE with an IC50 of 0.44 μM
*MAOB↓, inhibition of berberine against MAO-B: IC50 was estimated to be 98.4 μM
*memory↑, beneficial effect of berberine in ameliorating memory dysfunction in a rat model of streptozotocin-induced diabetes
*toxicity↓, Berberine is generally considered to be non-toxic at doses used in clinical situations and lacks genotoxic, cytotoxic or mutagenic activity
*BBB↑, Berberine can be administered orally [67] and pass through the blood-brain barrier
*cognitive↝, Clinical studies are mixed regarding curcumin’s effects on cognitive deficits.
*BioAv↑, Ways to improve curcumin’s bioavailability are required.
*Inflam↓, anti-inflammatory activity can be attributed to the suppression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes via down-regulation of nuclear factor kappa B (NF-κB)
*COX2↓,
*iNOS↓,
*NF-kB↓,
*TNF-α↓, nhibition of several inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-a) or interleukin (IL) -1, -2, -6, -8, and -12 (
*IL1↓,
*IL2↓,
*IL6↓,
*IL8↓,
*IL12↓,
*ROS↓, Curcumin’s ability to scavenge free radicals, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), provides its antioxidant capacity
*RNS↓,
*antiOx↑,
*BBB↑, Multiple studies in rodents and humans have shown that curcumin crosses the blood brain barrier (BBB)
*BioAv↓, drawback is the low bioavailability due to poor solubility, low absorption, rapid metabolism, and rapid excretion
*cognitive↑, The researchers detected a significant cognitive improvement at both doses compared to the untreated group, while a significant dose-response effect was found throughout time with higher doses of curcumin producing greater cognitive improvement
*memory↑, supplementation may improve memory and result in a number of biochemical alternations leading to suppressed tau aggregation
*tau↓,
*eff↑, Combined curcumin and piperine showed superiority, in a dose dependent manner,
ROS↑, Nano EGCG exhibited increased ROS/RNS levels and decreased mitochondrial membrane potential
RNS↓,
MMP↓,
NRF2↑, EGCG exhibited an increased expression of Nrf2 and Keap1 that could regulate apoptosis in A549 cells.
Keap1↓,
*AntiCan↑, EGCG’s therapeutic potential in preventing and managing a range of chronic conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes
*cardioP↑,
*neuroP↑,
*BioAv↝, Factors such as fasting, storage conditions, albumin levels, vitamin C, fish oil, and piperine have been shown to affect plasma concentrations and the overall bioavailability of EGCG
*BioAv↓, Conversely, bioavailability is reduced by processes such as air oxidation, sulfation, glucuronidation, gastrointestinal degradation, and interactions with Ca2+, Mg2+, and trace metals,
*BioAv↓, EGCG’s oral bioavailability is generally low, with marked differences observed across species, for example, bioavailability rates of 26.5% in CF-1 mice and just 1.6% in Sprague Dawley rats
*Dose↝, plasma concentrations exceeded 1 μM only when doses of 1 g or higher were administered.
*Half-Life↝, Specifically, a dose of 1600 mg yielded a Cmax of 3392 ng/mL (range: 130–3392 ng/mL), with peak levels observed between 1.3 and 2.2 h, AUC (0–∞) values ranging from 442 to 10,368 ng·h/mL, and a half-life (t1/2z) of 1.9 to 4.6 h.
*BioAv↑, Studies on the distribution of EGCG have revealed that, despite its limited absorption, it is rapidly disseminated throughout the body or quickly converted into metabolites
*BBB↑, Additionally, EGCG can cross the blood–brain barrier, allowing it to reach the brain
*hepatoP↓, Several studies have documented liver damage linked to green tea consumption [48,49,50,51,52,53].
*other↓, EGCG has also been shown to inhibit the intestinal absorption of non-heme iron in a dose-dependent manner in a controlled clinical trial
*Inflam↓, EGCG has been widely recognized for its anti-inflammatory effects
*NF-kB↓, EGCG has been shown to suppress NF-κB activation, inhibit its nuclear translocation, and block AP-1 activity
*AP-1↓,
*iNOS↓, downregulation of pro-inflammatory enzymes like iNOS and COX-2 and scavenging of ROS/RNS, including nitric oxide and peroxynitrite
*COX2↓,
*ROS↓,
*RNS↓,
*IL8↓, EGCG has been shown to suppress airway inflammation by reducing IL-8 release, a cytokine involved in neutrophil aggregation and ROS production.
*JAK↓, EGCG blocks the JAK1/2 signaling pathway
*PDGFR-BB↓, downregulate PDGFR and IGF-1R gene expression
*IGF-1R↓,
*MMP2↓, reduce MMP-2 mRNA expression
*P53↓, downregulation of the p53-p21 signaling pathway and the enhanced expression of Nrf2
*NRF2↑,
*TNF-α↓, 25 to 100 μM reduced the levels of TNF-α, IL-6, and ROS while enhancing the expression of E2F2 and superoxide dismutases (SOD1 and SOD2), enzymes vital for cellular antioxidant defense.
*IL6↓,
*E2Fs↑,
*SOD1↑,
*SOD2↑,
Casp3↑, EGCG has been shown to activate key apoptotic pathways, such as caspase-3 activation, cytochrome c release, and PARP cleavage, in various cell models, including PC12 cells exposed to oxidative stress
Cyt‑c↑,
PARP↑,
DNMTs↓, (1) the inhibition of DNA hypermethylation by blocking DNA methyltransferase (DNMT)
Telomerase↓, (2) the repression of telomerase activity;
Hif1a↓, (3) the suppression of angiogenesis via the inhibition of HIF-1α and NF-κB;
MMPs↓, (4) the prevention of cellular metastasis by inhibiting matrix metalloproteinases (MMPs);
BAX↑, (5) the promotion of apoptosis through the activation of pro-apoptotic proteins like BAX and BAK
Bak↑,
Bcl-2↓, while downregulating anti-apoptotic proteins like BCL-2 and BCL-XL;
Bcl-xL↓,
P53↑, (6) the upregulation of tumor suppressor genes such as p53 and PTEN;
PTEN↑,
TumCP↓, (7) the inhibition of inflammation and proliferation via NF-κB suppression;
MAPK↓, (8) anti-proliferative activity through the modulation of MAPK and IGF1R pathways
HGF/c-Met↓, EGCG inhibits hepatocyte growth factor (HGF), which is involved in tumor migration and invasion
TIMP1↑, EGCG has also been shown to influence the expression of tissue inhibitors of metalloproteinases (TIMPs) and MMPs, which are involved in tumorigenesis
HDAC↓, nhibition of UVB-induced DNA hypomethylation and modulation of DNMT and histone deacetylase (HDAC) activities
MMP9↓, inhibiting MMPs such as MMP-2 and MMP-9
uPA↓, EGCG may block urokinase-like plasminogen activator (uPA), a protease involved in cancer progression
GlutMet↓, EGCG can exert antitumor effects by inhibiting glycolytic enzymes, reducing glucose metabolism, and further suppressing cancer-cell growth
ChemoSen↑, EGCG’s combination with standard chemotherapy drugs may enhance their efficacy through additive or synergistic effects, while also mitigating chemotherapy-related side effects
chemoP↑,
*antiOx↑, Resveratrol has shown strong antioxidant properties in many studies
*ROS↓,
*PTEN↑, resveratrol upregulated the phosphatase and tensin homolog (PTEN), which decreased Akt phosphorylation, leading to an upregulation of antioxidant enzyme mRNA levels such as catalase (CAT) and superoxide dismutase (SOD)
*Akt↓,
*Catalase↑,
*SOD↑,
*ERK↓, modulating antioxidant enzymes through downregulation of extracellular signal-regulated kinase (ERK)
*GSH↑, thus the levels of antioxidants like glutathione (GSH) increased, and free radicals were directly scavenged
*AMPK↑, resveratrol activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) to maintain the structural stability of forkhead box O1 (FoxO1)
*FOXO1↝,
*RNS↓, Generally, resveratrol protects against oxidative stress mainly by (i) reducing ROS/reactive nitrogen species (RNS) generation; (ii) directly scavenging free radicals; (iii) improving endogenous antioxidant enzymes (e.g., SOD, CAT, and GSH);
*Catalase↑,
*cardioP↑, In summary, the cardiovascular protective effects of resveratrol mainly depend on the capabilities of reducing oxidative stress and alleviating inflammation through Nrf2 and/or SIRT1 activation, PI3K/eNOS upregulation, and NF-κB downregulation.
*PI3K↑,
*eNOS↑,
hepatoP↑, Resveratrol has shown its protective impacts on several liver diseases in some studies
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
Diabetic, |
NA |
|
|
|
- |
Review, |
Obesity, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Arthritis, |
NA |
|
|
|
*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol
| - |
in-vitro, |
Nor, |
RAW264.7 |
|
|
|
- |
in-vitro, |
AML, |
PLB-985 |
|
|
|
*antiOx↑, widely publicized as a universal anti-oxidant
*ROS↓, H-atom donors or radical scavengers (AA, vitamins E, Q, glutathione, etc.) present in aerobic cells regulate reactive oxygen and nitrogen species (ROS and RNS) by quenching them to avoid RNS and ROS-induced profound damages to surrounding cells and t
*RNS↓,
ROS↑, PLB‑985(cancer) cells that exhibited enhanced ROS production following AA treatment
Showing Research Papers: 1 to 8 of 8
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, H2O2↑, 1, Keap1↓, 1, lipid-P↑, 1, NRF2↑, 2, RNS↓, 2, ROS↑, 3, i-ROS↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, MMP↓, 2,
Core Metabolism/Glycolysis ⓘ
GlutMet↓, 1, LDL↓, 1,
Cell Death ⓘ
APAF1↑, 1, Apoptosis↑, 1, Bak↑, 1, BAX↑, 3, Bcl-2↓, 2, Bcl-xL↓, 1, Casp3↑, 2, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 2, HGF/c-Met↓, 1, MAPK↓, 1, Telomerase↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, DNMTs↓, 1, P53↑, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, HDAC↓, 1, PTEN↑, 1,
Migration ⓘ
Ca+2↑, 2, MMP2↓, 1, MMP9↓, 2, MMPs↓, 1, PKCδ↓, 1, TIMP1↑, 1, TumCMig↓, 1, TumCP↓, 2, uPA↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 2,
Clinical Biomarkers ⓘ
BP↓, 1,
Functional Outcomes ⓘ
AntiTum↑, 1, chemoP↑, 2, cognitive↑, 1, hepatoP↑, 2, memory↑, 1, radioP↑, 1, RenoP↑, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 56
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 5, Catalase↑, 3, GPx↑, 2, GSH↑, 2, GSTs↑, 1, H2O2↓, 1, HDL↑, 1, lipid-P↓, 1, MDA↓, 1, NADH↓, 1, NRF2↑, 1, RNS↓, 6, ROS↓, 6, SOD↑, 3, SOD1↑, 1, SOD2↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, LDL↓, 2,
Cell Death ⓘ
Akt↓, 1, iNOS↓, 2,
Transcription & Epigenetics ⓘ
other↓, 2, other↑, 1,
DNA Damage & Repair ⓘ
P53↓, 1,
Cell Cycle & Senescence ⓘ
E2Fs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, FOXO1↝, 1, IGF-1R↓, 1, PI3K↑, 1, PTEN↑, 1,
Migration ⓘ
AntiAg↑, 1, AP-1↓, 1, MMP2↓, 1,
Angiogenesis & Vasculature ⓘ
eNOS↑, 1, NO↓, 1, PDGFR-BB↓, 1,
Barriers & Transport ⓘ
BBB↑, 3, GastroP↑, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 3, IL1↓, 1, IL12↓, 1, IL2↓, 1, IL6↓, 2, IL8↓, 2, Imm↑, 1, Inflam↓, 3, JAK↓, 1, NF-kB↓, 2, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 2, BChE↓, 2, MAOA↓, 1, tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 1, MAOB↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 4, BioAv↝, 2, Dose↝, 2, eff↑, 2, Half-Life↝, 2,
Clinical Biomarkers ⓘ
BP↓, 1, IL6↓, 2, NOS2↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 3, cognitive↑, 2, cognitive↝, 1, hepatoP↓, 1, memory↑, 2, neuroP↑, 1, Obesity↓, 1, toxicity↓, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 75
Scientific Paper Hit Count for: RNS, reactive nitrogen species
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#:276 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page