Inflam Cancer Research Results
Inflam, inflammation: Click to Expand ⟱
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Cancer and inflammation are closely linked, with chronic inflammation contributing to the development and progression of cancer. Various inflammatory mediators and cells are involved in this process.
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Scientific Papers found: Click to Expand⟱
*Inflam?, NSAID diclofenac, 2-[2-(2,6-dichloroanilino)phenyl]acetic acid, which is conventionally used in clinical practice as a potent anti-inflammatory drug, owing to its proven safety records is also being tested for its antineoplastic potential
*COX1↓, anti-inflammatory action of diclofenac has been mainly attributed to its ability to inhibit prostaglandin-endoperoxide synthase-1 and 2 (PGES), commonly known as Cyclooxygenase-1 and 2
*COX2↓,
GLUT1↓, our results of docking analysis indicated optimum binding strength of diclofenac with targets in following order GLUT1, MCT4, LDH A, COX1, BCRP/ABCG2, HDM2/MDM2, COX2, MRP1, MnSOD/SOD2, Myc, β-Catenin, VEGF, IκB, c-Jun and E2F1.
MCT4↓,
LDHA↓,
ABCG2↓,
MDM2↓,
MRP1/ABCC1↓,
SOD2↓,
Myc↓,
β-catenin/ZEB1↓,
VEGF↓,
IKKα↓,
cJun↓,
E2Fs↓,
*Inflam?, Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties.
*antiOx↑,
*tau↓, While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects.
*Aβ↓,
*neuroP↑, In recent years, several studies have advocated for a robust neuroprotective function of emodin
*ROS↓,
*memory↑, Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature
*cognitive↑,
*other↝, Well-known sources of emodin include Rheum palmatum,10Polygonum cuspidatum,11Aloe vera,12Polygonum multifarum,13 and Casia obtusofolia.
*AChE↓, potent in vitro inhibition of AChE (IC50 of 21.8 μM), in addition to amelioration of H2O2-induced oxidative damage in PC12 cells
*BACE↓, potent inhibition of the activities of BACE-1 (IC50 of 4.5 μM) and AChE (IC50 of 9.7 μM); and strong and mixed-type inhibition for BACE-1 (Ki of 20 μM) in kinetic studies
*LC3II↓, Inhibition of autophagic (LC3-II and beclin-1)
*Beclin-1↓,
*p‑tau↓, 80 mg/kg/day for 2 weeks (intragastric administration) repression of the levels of BACE-1, Aβ species and phosphorylated-tau, stimulation of CREB signaling
*CREB↑,
*HNE↓, downregulation of Aβ and phosphorylated-tau levels, reduced oxidative damage and 4-HNE levels
*BioAv↓, Bioavailability of exogenously administered emodin suffers from some issues, including its weak intestinal absorption, high rate of elimination, and first-pass metabolism
*BioAv↝, bioavailability of orally supplemented emodin may show appreciable dependence on gender, given that there are four times higher plasma levels of emodin in male rats, compared to females after a single oral dosing of emodin at 8 mg/kg body weight.
*BioAv↑, pretreatment with stilbene glucosides from Radix Polygoni Multiflori prevents glucuronidation of emodin, and increases its plasma concentration upon oral administration
*BioAv↑, cotreatment with piperine was also found to inhibit glucuronide formation of orally administered emodin, while increasing the bioavailability of its free form
*BioAv↑, Nanoemulsification may also decreses the clearance of orally administered emodin, while increasing its brain distribution and bioavailability.
*BioAv↑, Lastly, treatment of emodin with sodium hydroxide to form its sodium salt may represent another strategy for improving the solubility and bioavailability of emodin
BioAv↑, ultrasound-sensitive emodin-containing lecithin-based nanoformulations squamous cell carcinoma FaDu and CAL-27 cells neck squamous cell carcinoma sonodynamic therapy-based beneficial actions
*HO-1↑, figure 3, neuroproctive
*PKCδ↑,
*Akt↑,
*NLRP3↓,
*NF-kB↓,
*TLR3↓,
*ALAT↓, shikonin was found to mitigate the rise in ALT and AST levels triggered by LPS/GalN
*AST↓,
*Inflam?, demonstrated the anti-inflammatory properties of shikonin within two traditional mouse models frequently employed in pharmacological research to assess anti-inflammatory activities
*EMT↑, Shikonin stimulates EMT by weakening the nuclear translocation of NF-κB p65
ROS?, naphthoquinone framework possesses the capacity to produce ROS, which in turn modulate cellular oxidative stress levels
TrxR1↓, Duan and colleagues demonstrated that shikonin specifically inhibits the physiological function of TrxR1 by targeting its Sec residue
PERK↑, In vivo Western blot of HCT-15(colon cancer) xenografts showed shikonin upregulated PERK/eIF2α/ATF4/CHOP and IRE1α/JNK pathways.
eIF2α↑,
ATF4↑,
CHOP↑,
IRE1↑,
JNK↑,
eff↝, oral shikonin did not demonstrate anti-tumor effects in the colorectal cancer model, intraperitoneal injection significantly inhibited tumor growth.
DR5↑, upregulation of Death Receptor 5 (DR5) in cholangiocarcinoma cells through ROS-induced activation of the JNK signaling cascade.
Glycolysis↓, inhibited glycolysis in HepG2 cells by suppressing the activity of PKM2, a critical enzyme within the glycolytic pathway
PKM2↓,
ChemoSen↑, The combination of shikonin with drugs can reverse drug resistance and enhance therapeutic efficacy
GPx4↓, shikonin conjunction with cisplatin overcame drug resistance in cancer cells, downregulated GPX4, and upregulated haemoglobin oxygenase 1 (HMOX1) inducing iron death in cells.
HO-1↑,
Showing Research Papers: 1 to 3 of 3
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
GPx4↓, 1, HO-1↑, 1, ROS?, 1, SOD2↓, 1, TrxR1↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1, LDHA↓, 1, MCT4↓, 1, PKM2↓, 1,
Cell Death(tgid=5) ⓘ
DR5↑, 1, JNK↑, 1, MDM2↓, 1, Myc↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
cJun↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↑, 1, eIF2α↑, 1, IRE1↑, 1, PERK↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
E2Fs↓, 1,
Migration(tgid=13) ⓘ
β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↑, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IKKα↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ABCG2↓, 1, BioAv↑, 1, ChemoSen↑, 1, eff↝, 1, MRP1/ABCC1↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
Myc↓, 1,
Total Targets: 30
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, HNE↓, 1, HO-1↑, 1, ROS↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, CREB↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1, LC3II↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↑, 1,
Migration(tgid=13) ⓘ
PKCδ↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↓, 1, COX2↓, 1, Inflam?, 3, NF-kB↓, 1, TLR3↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1, tau↓, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1,
Functional Outcomes(tgid=23) ⓘ
cognitive↑, 1, memory↑, 1, neuroP↑, 1,
Total Targets: 31
Scientific Paper Hit Count for: Inflam, inflammation
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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