BUN Cancer Research Results
BUN, blood urea nitrogen: Click to Expand ⟱
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Blood urea nitrogen (BUN) is a measure of the amount of nitrogen in your blood that comes from the waste product urea. Urea is produced in the liver as a byproduct of protein metabolism and is normally excreted by the kidneys.
-BUN is commonly used as one indicator of kidney function. Elevated BUN levels may suggest that the kidneys are not effectively clearing urea from the blood.
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Scientific Papers found: Click to Expand⟱
*RenoP↑, We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled
*ROS↓, ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death.
*antiOx↑,
*Inflam↓,
*Sepsis↓, figure 1
*IronCh↑, ALA can also chelate metals such as zinc, iron, and copper and regenerate endogenous antioxidants—such as glutathione—and exogenous vitamin antioxidants—such as vitamins C and E—with minimal side effects
*BUN↓, ALA can decrease acute kidney injury by lowering serum blood urea nitrogen, creatinine levels, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), thereby decreasing endothelin-1 vasoconstriction, neutrophil dif
*creat↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓, pretreatment with ALA decreased MDA content and ameliorated renal oxidative stress
*NRF2↑, activate the Nrf2 signaling pathway, leading to upregulation of the second-phase cytoprotective proteins such as heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1)
*HO-1↑,
*NQO1↑,
*chemoP↑, ALA has also been shown to lower plasma creatinine levels and urine output, increase creatinine clearance and urine osmolality, and normalize sodium excretion in cisplatin kidney injury
*eff↑, ALA can also minimize renal toxicity induced by gold nanoparticles, which are often used as drug carriers
*NF-kB↓, Enhancing autophagy, inhibiting NF-KB, attenuating mitochondrial oxidative stress
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in-vitro, |
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NRK52E |
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in-vivo, |
NA, |
NA |
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*RenoP↑, WFA ameliorated renal damage, improved kidney function, and decreased levels of creatinine, BUN, UA, and XOD in PO-induced hyperuricemic mice.
*hepatoP↑,
*creat↓,
*BUN↓,
*uricA↓,
*Apoptosis↓, WFA markedly inhibited renal apoptosis, accompanied by changes of apoptosis-related proteins.
*α-SMA↓, Notably reduced α-SMA expression was observed after WFA administration, with WFA 10 mg/kg group presenting the most significant inhibitory effect.
*antiOx↑, Rats in Group 4 (cadmium-exposed and Rosmarinic acid-accessed) exhibited increased levels of total proteins, a significant increase in the levels of antioxidant markers including total thiols, glutathione, total antioxidant capacity (TAC),
*Thiols↑,
*GSH↑,
*TAC↑, decreased levels of total thiols, GSH, catalase, and TAC
*SOD↑, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase, and a significant decrease in the levels of blood cadmium, ALP, ALT, AST, creatinine, blood urea nitrogen (BUN), urea, bilirubin, and oxidation markers (H2O2, and MDA
*GPx↑,
*Catalase↑,
*ALP↓,
*ALAT↓,
*AST↓,
*creat↓,
*BUN↓,
*H2O2↓,
*MDA↓,
*ROS↓, significantly help attenuate the oxidative stress induced by cadmium
cardioP↑, benefits of RA are attributed to its anti-cancer, anti-depressive, antiallergic, anti-inflammatory, anti-angiogenic, cardioprotective, hepatoprotective, nephroprotective, neuroprotective, antimicrobial, hypoglycemic, and hypolipidemic bioactivities
hepatoP↑,
neuroP↑,
chemoP↑, Researchers at Roswell Park Comprehensive Cancer Center have demonstrated that selenium containing compounds are highly effective in preventing alopecia and severe bladder toxicity associated with cyclophosphamide as well as in preventing kidney toxi
creat↓, significant increase in creatinine and blood urea nitrogen (BUN) following treatment with cisplatin were restored to normal values in animals that were treated.
BUN↓,
*NRF2↑, silymarin activates the Nrf2/HO-1 pathway, thus providing cellular defense
*HO-1↑,
*creat↓, Silymarin diminished BPA-induced rise in serum urea, creatinine, BUN, and plasma kim-1 levels.
*BUN↓,
*RenoP↑, improved renal histoarchitecture in BPA-exposed rats.
*MDA↓, suppression of BPA-induced rise in renal iron, MDA, TNF-α, IL-1β, and cytochrome c levels, and myeloperoxidase and caspase 3 activities by silymarin therapy.
*TNF-α↓,
*IL1β↓,
*Cyt‑c↓,
*Casp3↓,
*GSTs↓, silymarin attenuated BPA-induced downregulation of Nrf2 and GSH levels, and HO-1, GPX4, SOD, catalase, GST, and GR activities.
*GSH↑,
*GPx4↑,
*SOD↑,
*GSR↓,
*Ferroptosis↓, silymarin mitigated post-weaning BPA-induced renal toxicity by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 modulation.
*radioP↑, Ebselen, and sodium selenite, emerges as a promising radioprotective agent with demonstrated efficacy across diverse radiation-injured organs, highlighting its significance as an effective and potent antioxidant that affordable for most patients.
*antiOx↑,
*Inflam↓, In short, the antioxidation, anti-inflammatory effect and DNA stabilizing formed the protective effects of selenium against DNA damage induced by radiation
*DNAdam↓,
*lipid-P↓, Se-Met could efficiently inhibit the formation of lipid peroxy radicals, preventing lipid peroxidation
*selenoP↑, primarily enhance the expression of selenoproteins, thus sodium selenite may not be inherently antioxidant until incorporated into selenoproteins with oxidoreductase functions
*GPx1↑, sodium selenite could increase GPx-1 activity in a dose- and time-dependent manner
*BUN↓, 100 µg/day of selenium in the form of sodium selenite or Se-L-Met, blood urea nitrogen (BUN) level of rats significantly decreased.
*RenoP↑, Pre-, post-, and cotreatment with TQ alleviated kidney injury
*TAC↑, by replenishing antioxidant reserves, reducing serum toxicity, decreasing ROS generation and lipid peroxidation, downregulating p38 MAPK/NF-κB axis/pathway proteins, and upregulating Nrf2 and HO-1,
*ROS↓, high-dose TQ alleviated ROS and H2O2 levels in groups III and IV
*lipid-P↓,
*p38↓,
*MAPK↓,
*NF-kB↓,
*NRF2↑,
*HO-1↑,
*MDA↓, TQ diminishes MDA levels
*GPx↑, GPx, GR, and CAT : restoration of GSH reserves and the abovementioned antioxidant enzymes
*GSR↑,
*Catalase↑,
*BUN↓, noticeable inhibition was observed in BUN, Cr, LDH, and KIM-1 at both doses
*LDH↓,
*IL1β↓, downregulation of IL-1β, diminishing inflammation
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Core Metabolism/Glycolysis ⓘ
BUN↓, 1,
Clinical Biomarkers ⓘ
creat↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, chemoP↑, 1, hepatoP↑, 1, neuroP↑, 1,
Total Targets: 6
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↑, 2, Ferroptosis↓, 1, GPx↑, 2, GPx1↑, 1, GPx4↑, 1, GSH↑, 2, GSR↓, 1, GSR↑, 1, GSTs↓, 1, H2O2↓, 1, HO-1↑, 3, lipid-P↓, 2, MDA↓, 4, NQO1↑, 1, NRF2↑, 3, ROS↓, 3, selenoP↑, 1, SOD↑, 2, TAC↑, 2, Thiols↑, 1, uricA↓, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, BUN↓, 6, LDH↓, 1,
Cell Death ⓘ
Apoptosis↓, 1, Casp3↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 1, MAPK↓, 1, p38↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Migration ⓘ
α-SMA↓, 1,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 3, IL6↓, 1, Inflam↓, 2, NF-kB↓, 2, TNF-α↓, 2,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, creat↓, 4, IL6↓, 1, LDH↓, 1,
Functional Outcomes ⓘ
chemoP↑, 1, hepatoP↑, 1, radioP↑, 1, RenoP↑, 4,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 51
Scientific Paper Hit Count for: BUN, blood urea nitrogen
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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