SOD Cancer Research Results

SOD, superoxide dismutase: Click to Expand ⟱
Source:
Type:
SOD, or superoxide dismutase, is an important antioxidant enzyme that plays a crucial role in protecting cells from oxidative stress. It catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide.
SOD Isoforms: There are three main isoforms of SOD:
SOD1 (cytosolic): Often found to be overexpressed in certain tumors, which may help cancer cells survive in oxidative environments.
SOD2 (mitochondrial): Plays a critical role in protecting mitochondria from oxidative damage. Its expression can be upregulated in some cancers, contributing to tumor growth and resistance to therapy.
SOD3 (extracellular): Its role in cancer is less well understood, but it may have implications in the tumor microenvironment and metastasis.
The expression levels of SOD can serve as a prognostic indicator in some cancers. For example, high levels of SOD expression have been associated with poor prognosis in certain types of tumors, potentially due to their role in promoting tumor cell survival and resistance to therapies.
Scientific Papers found: Click to Expand⟱
2725- BetA,    Betulinic acid protects against renal damage by attenuation of oxidative stress and inflammation via Nrf2 signaling pathway in T-2 toxin-induced mice
- in-vivo, Nor, NA
*RenoP↑, BA pretreatment alleviated excessive glomerular hemorrhage and inflammatory cell infiltration in kidneys caused by T-2 toxin.
*SOD?, Moreover, pretreatment with BA mitigated T-2 toxin-induced renal oxidative damage by up-regulating the activities of SOD and CAT, and the content of GSH, while down-regulating the accumulation of ROS and MDA
*Catalase↑,
*GSH↑,
*ROS↓,
*MDA↓,
*IL1β↓, decreasing the mRNA expression of IL-1β, TNF-α and IL-10, and increasing IL-6 mRNA expression
*TNF-α↓,
*IL10↓,
*IL6↑,
*NRF2↑, pretreatment with BA could activate Nrf2 signaling pathway.

7565- HYP,    Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review
- Review, AD, NA
*Inflam↓, exhibits a multitude of biological functions including anti-inflammatory, antidepressant, antioxidative, vascular protective effects and neuroprotective effects,
*antiOx↑,
*neuroP↑,
*lipid-P↓, Anti-oxidant Saccharomyces Cerevisiae 5, 20 mg/L Decreased LPO and the level of ROS
*ROS↓,
*IL1β↓, HT22 cells 20 μM Alleviates the level of IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax, and caspase-3; increases the expression of CAT, SOD, GSH, Bcl-2, BDNF, TrkB, and NGF.
*IL6↓,
*IL8↓,
*TNF-α↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Catalase↑,
*SOD↑,
*GSH↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*BDNF↑, Male Albino Swiss mice 0.94 mg/kg, 3.75 mg/kg Mediated by monoaminergic system and the upregulation of BDNF level
*NF-kB↓, Inhibited the activation of NF-κB, lessened the expression of iNOS,
*AChE↓, ICR mice 2.5 mg/kg Inhibited AchE activity
*H2S↑, SD rats 1, 10, 100 μM Upregulation of H2S,
Casp3↑, Anti-lung cancer A549 cells, Balb/c-nude mice 15, 20, 25 μM in vitro 15, 20, 25 mg/kg in vivo Activation of caspase-3 to motivate apoptosis and inactivation of NF-κB to inhibit inflammatory
Apoptosis↑,
NF-kB↓,
AMPK↑, A549 cells 10, 50, 100 μM Upregulation of AMPK signal pathway and HO-1 expression to suppressed the survival and proliferation of A549 cells
HO-1↑,
MAPK↑, A549 cells, H466 cells, C57BL/6J mice – Upregulated the expression of p38 MAPK, caspase 3, caspase 9, cleaved caspase 3, cleaved caspase 9 and Bax, downregulated the expression of Cu/Zn SOD, CAT, Nrf2, NQO1, HO-1 and Bcl-2
cl‑Casp3↑,
cl‑Casp9↑,
BAX↑,
SOD?,
Catalase↓,
NRF2↓,
NQO1↓,
HO-1↓,
Bcl-2↓,
TumCCA↑, A549 cells 10, 20, 50, 100, 200, 400 μg/mL Inhibited the process of G1/S phase to inhibit proliferation
FOXO1↑, NCI-H1975 cells, PC-9 cells, Nude male mice 30, 60, 90, 120, 150 μM in vitro, 25 mg/kg in vivo Upregulation of FoxO1
TumAuto↑, A549 cells 0.5, 1, 2 mM Induced autophagy through inhibiting the Akt/mTOR/p70S6K signal pathway
Akt↓,
mTOR↓,
P70S6K↓,
BMP7/OP1↓, HepG2 cells 5, 10, 20, 40, 80 μM Inhibiting the BMP-7
*cardioP↑, Cardiovascular Protective Effect
*hepatoP↑, Hepatoprotective
*antiCG↑, The report indicates hyperoside possesses antithrombotic activities and offer bases for development of a novel anticoagulant
*AntiThr↑,
*Diar↓, Antidiarrheal Activity
*AntiFungal↑, Antifungal Activity
*CYP2D6↓, hyperoside is a potent selective CYP2D6 inhibitor in HLMs, and might cause herb-drug interactions when co-administrated with CYP2D substrates.
*PDGFR-BB↓, In diabetic rats’ model, hyperoside inhibited the platelet-derived growth factor-BB (PDGF-BB)/platelet-derived growth factor-B receptor (PDGFR-β) ligand binding
*PDGFRB↓,
*toxicity↓, In research conducted in Wistar rats, the researchers demonstrated that in a long-term oral administration lasted for 6 months, hyperoside has a good safety. And the possible target organ of toxicity is kidney and the damage is reversible
*Half-Life↑, hyperoside also showed a long half-life for 4 hours and the safety experiments also proves that it has good safety.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

BMP7/OP1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 1,   HO-1↓, 1,   HO-1↑, 1,   NQO1↓, 1,   NRF2↓, 1,   SOD?, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   cl‑Casp9↑, 1,   MAPK↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

FOXO1↑, 1,   mTOR↓, 1,   P70S6K↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiCG↑, 1,   CYP2D6↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 2,   GSH↑, 2,   lipid-P↓, 1,   MDA↓, 2,   NRF2↑, 1,   ROS↓, 2,   SOD?, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

H2S↑, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   Casp3↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,  

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

PDGFRB↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

PDGFR-BB↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL10↓, 1,   IL1β↓, 2,   IL6↓, 1,   IL6↑, 1,   IL8↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BDNF↑, 2,   NGF↑, 1,   TrkB↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   IL6↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   Diar↓, 1,  
Total Targets: 39

Scientific Paper Hit Count for: SOD, superoxide dismutase
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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