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, |
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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↑, Several studies demonstrated the antioxidant, anti-inflammatory, and antiapoptotic effects of dandelion leaf extract (DLE);
*Inflam↓,
*Apoptosis↓,
*NF-kB↓, DLE reduced nuclear factor-κB and cytochrome c expression, and DNA fragmentation
*Cyt‑c↓,
*DNAdam↓,
*GSH↑, also maintained levels of reduced glutathione, superoxide dismutase, and serum albumin.
*SOD↑,
*Albumin↝,
*creat↓, Treatment with DLE + CP maintained the levels of creatinine at all different DLE doses.
*BUN↓, Treatment with DLE + CP significantly ameliorated the elevated levels of creatinine and BUN.
*RenoP↑, These results demonstrate that DLE administration protected the kidney from renal injury that could occur by CP injection.
*lipid-P↓, The DLE pretreated rats showed a significant decline in LPO levels compared to that observed with CP treatment alone
*TNF-α↓, DLE alone decreased the levels of TNF-α by 15% of control levels. Rats treated with DLE prior to CP exhibited a significant (P < .001) suppression in the levels of TNF-α compared to CP-treated rats.
*Casp3↓, animals treated with DLE prior to CP administration showed significant decrease in caspase-9 and caspase-3 to levels comparable to the control and compared to rats treated with CP alone
*Casp9↓,
*chemoP↑, nephroprotective activity of DLE against CP-induced nephrotoxicity.
RenoP↑, H2 inhalation significantly attenuated cisplatin-induced kidney injury by reducing inflammation and apoptosis in renal tissue.
BHB↑, H2 upregulated the ketone body metabolic pathway, particularly enhancing β-hydroxybutyrate (β-HOB) synthesis via increased expression of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2).
HMGCS2↑,
chemoP↑, Molecular hydrogen confers protection against cisplatin-induced nephrotoxicity by modulating β-HOB metabolism through upregulation of HMGCS2, thereby suppressing renal inflammation and apoptosis.
*IL2↓, IL-1β, IL-6, MCP-1, and TNF-α in kidney tissue. Levels of these proinflammatory mediators were significantly elevated following cisplatin treatment. H2 inhalation significantly suppressed these cytokines,
*IL6↓,
*MCP1/CCL2↓,
*TNF-α↓,
*KeyT↝, H2 upregulated HMGCS2 to enhance ketone body metabolism
*Inflam↓, H2 has been demonstrated protective effects in various inflammatory and oxidative stress-related conditions
*ROS↓,
*MMP↑, Several studies have shown that H2 can preserve mitochondrial membrane potential, boost ATP generation, and improve mitochondrial dynamics and biogenesis by activating pathways such as mitofusin-2 (Mfn2) and PGC-1α
*ATP↑,
*MFN2↑,
*PGC-1α↑,
*BUN↓, Our work confirmed that H2 inhalation significantly ameliorated cisplatin-induced histological damage, elevated BUN and creatinine levels, renal inflammation, and tubular apoptosis.
*creat↓,
*ROS↓, reduces reactive oxygen species, which have very strong oxidative capacity, and indirectly exerts antioxidant, anti-inflammatory
*antiOx↑,
*Inflam↓,
*chemoP↑, Our comprehensive literature review revealed that H2 protects against tissue injuries induced by cisplatin, oxaliplatin, doxorubicin, bleomycin, and gefitinib.
AntiCan↑, Animal and clinical studies showed that H2 itself exhibits anticancer activity, and its combination with anticancer drugs achieved excellent anticancer activity
ChemoSen↑,
chemoP↑, Our literature review revealed that H2 reduced the side effects of CIS-induced nephrotoxicity, ototoxicity, and ovarian injury, CIS- or OXA-induced peripheral neuropathy, DXR-induced cardiotoxicity and hepatotoxicity, and BLM- or GEF-induced lung inj
*BUN↓, CIS Nephrotoxicity BUN ↓, Creatinine ↓, TUNEL ↓
*creat↓,
*TUNEL↓,
*MDA↓, CIS Ototoxicity MDA ↓, 8-iso-PGF2α ↓
*SOD↑, CIS Ovarian injury SOD ↑, CAT ↑, MDA ↓, Nrf2 ↑
*Catalase↑,
*NRF2↑,
*BNP↓, DXR Cardiotoxicity and hepatotoxicity BNP ↓, AST ↓, ALT ↓, ROS ↓, MDA ↓, TNF-α ↓, IL-1β ↓, IL-6 ↓, TUNEL ↓, Bax/Bcl-2 ↓, Caspase-3 ↓, Caspase-8 ↓
*AST↓,
*ALAT↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*Casp3↓,
*Casp9↓,
*GPx↑, BLM Lung injury ROS ↓, MDA ↓ TGF-β1 ↓,TNF-α ↓, GSH-PX ↑, E-cadherin ↑, Vimentin ↓, α-SMA ↓, Collagen I ↓
*E-cadherin↑,
*Vim↓,
*α-SMA↓,
*COL1↓,
*cardioP↑, H2 ameliorated DXR-induced cardiotoxicity and hepatotoxicity by attenuating inflammation and apoptosis.
*hepatoP↑,
*p‑mTOR↓, decreased the phosphorylated mammalian target of rapamycin (p-mTOR) to mTOR
*EMT↓, H2 gas also inhibited BLM-mediated epithelial-to-mesenchymal transition by increasing the expression level of the epithelial cell marker E-cadherin and decreasing that of the mesenchymal cell marker vimentin [
eff∅, On the other hand, H2 did not impair the anticancer effects of GEF in in vitro experiments on lung cancer cell lines or in in vivo experiments on carcinoma-bearing mice
*LPS↓, figure 2
*TLR4↓,
radioP↑, radioprotective effects of H2 have also been reported in many in vitro and in vivo studies, and clinical trials recently showed that the inhalation of H2 gas mitigated decreases in quality of life and bone marrow damage associated with radiation [
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection
RenoP↑, renoprotective effects and mechanism of isovitexin, a glycosylflavonoid isolated from rice hulls of Oryza sativa, against cisplatin-induced kidney injury in mice.
*BUN↓, isovitexin inhibited CP-induced increases in serum BUN and creatinine.
*creat↓,
*TNF-α↓, Isovitexin inhibited CP-induced inflammation by inhibiting TNF-α, IL-1ß and IL-6 production in kidney tissues.
*IL1β↓,
*IL6↓,
*MDA↓, isovitexin inhibited CP-induced oxidative stress by inhibiting MDA and ROS production.
*ROS↓,
*NF-kB↓, isovitexin was found to inhibit CP-induced NF-κB activation and increase Nrf2 and HO-1 expression.
*NRF2↑,
*HO-1↑,
TumVol?, LCA alone significantly inhibited the size of the solid tumours in CT-26 cell-inoculated Balb/c mice, without any detectable induction of nephrotoxicity, hepatotoxicity and oxidative stress.
TumCP↓, LCA also suppressed cell proliferation by reducing DNA synthesis of CT-26 murine colon cancer cells in a dose-dependent manner.
*RenoP↑, Furthermore, LCA inhibited the cisplatin-induced kidney damage characterized by increases in the serum creatinine and blood urea nitrogen,
*creat↓,
BUN↓,
hepatoP↑, as well as the cisplatin-induced liver damage characterized by increases in the serum alanine aminotransferase and aspartate aminotransferase.
*ALAT↓,
*AST↓,
*NO↓, repeated oral administration of LCA prior to cisplatin treatment exerted a preventive effect on the cisplatin-mediated increases in the serum nitric oxide and the tissue lipid peroxidation levels, and recovered the depleted reduced glutathione levels
*lipid-P↓,
*GSH↑,
chemoP↑, LCA may be beneficial in counteracting the side effects of cisplatin therapy in cancer patients.
Dose↝, LCA (1 mg/kg body weight, per orally)
*RenoP↑, Lico A treatment significantly ameliorated CP-induced AKI, accompanied by reduced serum levels of urea nitrogen and creatinine, downregulated expression of kidney injury molecule-1 and neutrophil-gelatinase-associated lipocalin, and attenuated renal
*Urea↓,
*BUN↓,
*creat↓,
*Apoptosis↓, Lico A reduced CP-triggered renal apoptosis and the expression of apoptosis-related proteins.
*Ferroptosis↓, Lico A mitigated ferroptosis by suppressing iron overload, oxidative stress, lipid peroxidation and mitochondrial dysfunction.
*Iron↓,
*ROS↓,
*lipid-P↓,
*mtDam↓,
*NRF2↑, Lico A also markedly activated nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) signaling
Dose↝, Test group (15 patients) received oral bLF 250 mg/day beside chemotherapy for three months. Control group (15 patients) received chemotherapy only.
toxicity↓, 3 months after treatment indicates that no significant difference in mean values of serum creatinine, AST, ALT, serum LF, serum GST enzyme, INF-γ, WBCs count, platelet count, CEA, RBCs count, neutrophil count, and Hb level of patients
INF-γ↝, Mean percent of change of main parameters (serum LF, serum GST enzyme, and INF-γ) after than before treatment among the studied patients indicate significant improvement in patients who received oral bLF 3 months
other↑, The results of this trial indicate that oral bLF made a significant increase in serum LF levels of patients in the test group 3 months after treatment compared to patients in the control group (P ≤ 0.05).
*ROS↓, Iron is essential as a catalyst for the production of reactive oxygen species. Therefore, lactoferrin can diminish the harmful influence of reactive oxygen species produced by leukocytes at the sites of inflammation
Imm↑, This result indicates that oral bLF enhances the immune system of colorectal cancer patients.
WBC↑, As a result of this increase in WBCs and neutrophil count patients disease state may be improved, because the body immune system can fight the disease more efficiently compatible with some previous studies
Neut↑,
T-Cell↑, These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status
*antiOx↑, The effect of antioxidants such as LF increase intracellular glutathione (GSH) levels in vascular endothelial cells by modulation of the GSH redox
*GSH↑,
*chemoP↑, On the other hand, oral bLF administration decreased chemotherapy related side effects as it enhances both renal and hepatic function tests.
*RenoP↑, Also, LF decreased chemotherapy related side effects by protecting liver and kidney from toxicity and improving their function test values
*hepatoP↑, Oral lactoferrin may increase liver functions and protect it from damage by reactive oxygen species since LF can function as an antioxidant, reducing intracellular levels of ROS
BUN↓, mean serum BUN decreased from 16.23 mg/dL before treatment to 11.43 mg/dL after 3 months of treatment in patients in the test group
creat↓, This decrease in BUN and serum creatinine may be due to the antioxidant effect of LF as mentioned in a former preclinical study on rat model of ferric nitrilotriacetate- (Fe-NTA-) induced renal tubular oxidative injury.
ALAT↓, Also, there was a significant decrease in serum ALT and AST in patients in test group 3 months after treatment compared to patients in the control group
AST↓,
RBC↑, Oral bLF administration enhanced anemia which is a very common chemotherapy related side effect; as results have shown, there were significant increases in RBCs count and serum Hb in patients in test group 3 months after treatment compared to patient
PC↑, There was a significant increase in platelets count in patients in test group after 3 months compared to control group
Mucositis↓, Patients in test group had less severed mucositis than patients in control group after every chemotherapy cycle;
*AntiBio↑, As mentioned before, lactoferrin has protective effects that range from direct antimicrobial activities against a large panel of microorganisms, including bacteria, viruses, fungi, and parasites, to anti-inflammatory and anticancer activities [
*AntiViral↑,
*AntiFungal↑,
*Inflam↓,
*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 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:
NA, unassigned(tgid=0) ⓘ
BHB↑, 1, HMGCS2↑, 1, MTA1↓, 1, Mucositis↓, 1, PC↑, 1, RBC↑, 1, WBC↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↓, 1, GSH↓, 1, ROS↓, 1, SOD↓, 1, TAC↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, BUN↓, 3,
Cell Death(tgid=5) ⓘ
Akt↓, 1, BAD↑, 1, Bak↑, 1, BAX↑, 1, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 1, Casp8↑, 1, Cyt‑c↑, 1, Fas↑, 1, p27/CDKN1B↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTOR↓, 1, P70S6K↓, 1,
Migration(tgid=13) ⓘ
LRP1↓, 1, MMP2↓, 1, TIMP2↓, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 1, IL6↓, 1, IL8↓, 1, Imm↑, 1, INF-γ↝, 1, Neut↑, 1, NF-kB↓, 1, PD-L1↓, 1, T-Cell↑, 1, TLR4↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↝, 2, eff∅, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, creat↓, 2, IL6↓, 1, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, cardioP↑, 1, chemoP↑, 4, hepatoP↑, 2, neuroP↑, 1, radioP↑, 1, RenoP↑, 2, toxicity↓, 1, TumVol?, 1,
Total Targets: 68
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 1, antiD↓, 1, Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 6, Catalase↑, 3, Ferroptosis↓, 2, GPx↑, 3, GPx1↑, 1, GPx4↑, 1, GSH↑, 5, GSR↓, 1, GSR↑, 1, GSTs↓, 1, H2O2↓, 1, HO-1↑, 4, Iron↓, 1, lipid-P↓, 5, MDA↓, 6, MFN2↑, 1, NQO1↑, 1, NRF2↑, 6, ROS↓, 8, selenoP↑, 1, SOD↑, 4, TAC↑, 2, Thiols↑, 1, uricA↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1, mtDam↓, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 4, BUN↓, 12, KeyT↝, 1, LDH↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 3, Casp3↓, 3, Casp9↓, 2, Cyt‑c↓, 2, Ferroptosis↓, 2, MAPK↓, 1, p38↓, 1, TUNEL↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 2,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, p‑mTOR↓, 1,
Migration(tgid=13) ⓘ
COL1↓, 1, E-cadherin↑, 1, PAI-1/SERPINE1↓, 1, Vim↓, 1, α-SMA↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 5, IL2↓, 1, IL6↓, 4, Inflam↓, 6, LPS↓, 1, MCP1/CCL2↓, 1, NF-kB↓, 4, TLR4↓, 1, TNF-α↓, 6,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
BNP↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
eff↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 4, Albumin↝, 1, ALP↓, 1, AST↓, 4, creat↓, 10, IL6↓, 4, LDH↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, cardioP↑, 2, chemoP↑, 4, hepatoP↑, 4, neuroP?, 1, radioP↑, 1, RenoP↑, 9,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 2, Bacteria↓, 1, Sepsis↓, 2,
Total Targets: 85
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1338 State#:% Dir#:1
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