toxicity Cancer Research Results
toxicity, toxicity: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*BBB↑, A growing body of evidence confirms that the ‘orifice-opening’ effect of borneol is principally derived from opening the BBB. Borneol is therefore believed to be an effective adjuvant that can improve drug delivery to the brain
*other↑, Borneol also protects the structural integrity of the BBB against pathological damage.
*P-gp↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*toxicity⇅, Natural borneol has been extensively used in aromatherapy and in natural and cosmetic products because of its low toxicity compared to synthetic borneol, which toxicity is relatively high as it degrades slowly during storage, and noxious camphor
*BioAv⇅, In mice, a single oral dose of borneol accumulates in organs in the order of liver > brain > kidney > heart > spleen > muscle > lung, which confirms its considerably higher bioavailability in the brain than in most other organs
*Dose↑, Intranasal drug delivery can avoid gastrointestinal destruction and hepatic first-pass metabolism, resulting in rapid onset of effect and high brain bioavailability.
*ABC↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*MRP1↓, including multidrug resistance protein 1 (Mrp1), 1a (Mdr1a) and 1 b (Mdr1b),
*5HT↑, systemic borneol was found to increase the levels of histamine and serotonin in the hypothalamus
*GABA↑, and levels of l-aspartic acid, glutamate, glycine and γ-aminobutyric acid (GABA) in the corpus striatum of rats (Zhang et al., 2012).
*eff↑, Co-incubation with borneol increased the uptake of Huperzine A loaded aprotinin-modified nanoparticles by capillary endothelial cells
toxicity⇅, Due to unfavorable toxicity profile and undefined mechanism, Celastrol's application in clinical cancer therapy remains limited.
toxicity↓, Celastrol has no obvious toxic effect at 1.5 mg/kg/day in a 15 days' administration
TumCG↓, Celastrol inhibits tumor growth and increases ROS in a STAT3 dependent manner in gastric and ovarian cancer celllines.
ROS↑,
IL6↓, downregulates IL-6 level and inhibits the JAK2/STAT3 signaling pathway by suppressing STAT3' activation
JAK2↓,
STAT3↓,
BioAv↓, application prospect of celastrol is largely limited by its low bioavailability, poor water solubility, and undesired off-target cytotoxicity
toxicity⇅,
BioAv↑, Covalently attaching groups directly to celastrol allows precise control over physicochemical properties like solubility and stability. This can more reliably improve bioavailability.
AntiCan↑, Camptothecin has been widely investigated over the past decades as an anti-cancer agent.
BioAv↓, However, its applications have been limited by poor water solubility, low stability, and substantial toxicity.
toxicity⇅,
TOP1↓, Camptothecin and its derivatives (CPTs) are potent antineoplastic agents that exert their effects by inhibiting DNA topoisomerase I, leading to apoptosis during cell proliferation.
Apoptosis↑,
TumCP↓,
other↝, Despite extensive research, only two CPTs, irinotecan and topotecan, have received health authority approval.
BioAv↑, CPT-11 (Figure 3A), was the first clinically evaluated water-soluble CPT derivative
other↝, The metabolism of CPT-11 involves its conversion to SN-38 primarily by the enzyme carboxylesterase (Figure 4), found in the liver and intestines
eff↑, CPT-11 remains one of the most important chemotherapeutic agents in oncology treatment. It has been moved to the first-line therapy in combination with 5-fluorouracil and leucovorin for patients with metastatic colon cancer
*AntiDiabetic↑, Metformin is a drug commonly prescribed to treat patients with type 2 diabetes.
*AntiAge↑, Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice
*toxicity⇅, while a higher dose (1% w/w) was toxic.
*CRM↑, The effects of metformin resembled to some extent the effects of caloric restriction, even though food intake was increased.
*Strength↑, Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels without a decrease in caloric intake
*LDL↓,
*AMPK↑, metformin increases AMP-activated protein kinase activity and increases antioxidant protection, resulting in reductions in both oxidative damage accumulation and chronic inflammation
*TAC↑,
*ROS↓, consistent with decreased oxidative stress damage in the liver of metformin-treated mice
*Inflam↓, Metformin inhibits chronic inflammation
Risk↓, metformin treatment has been associated with reduced risk of cancer4 and cardiovascular disease
*cardioP↑,
*ALAT↓, Ala aminotransferase (U/L) 90 ± 58 64 ± 29
*NRF2↑, The increase in Nrf2/ARE reporter activity occurred with an ED50 of ~1.5 mM metformin without reduction in cell survival
*SOD2↑, 0.1% metformin contributed to an increase in the level of antioxidant and stress response proteins, including SOD2, TrxR1, NQO1 and NQO2
*TrxR1↑,
*NQO1↑,
*NQO2↑,
Apoptosis↑, Salinomycin (SAL) shows high potential to induce apoptosis in human cancer cells.
CSCs↓, SAL is effective for cancer cells characterized by MDR and for cancer stem cells.
ChemoSen↑, Combined therapy with SAL and other chemotherapeutics or radiotherapy.
RadioS↑,
selectivity↑, Significant selectivity of action of SAL is proved.
Wnt↓, SAL treatment inhibits Wnt signaling pathway involved in tumorigenesis and embryogenesis through more than one mechanism
toxicity⇅, Like any other bioactive substance, SAL used in the amount above a certain dose also induces toxic effects.
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 1,
Cell Death ⓘ
Apoptosis↑, 2,
Transcription & Epigenetics ⓘ
other↝, 2,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, STAT3↓, 1, TOP1↓, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
TumCP↓, 1,
Immune & Inflammatory Signaling ⓘ
IL6↓, 1, JAK2↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 2, ChemoSen↑, 1, eff↑, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, Risk↓, 1, toxicity↓, 1, toxicity⇅, 4,
Total Targets: 22
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
NQO1↑, 1, NRF2↑, 1, ROS↓, 1, SOD2↑, 1, TAC↑, 1, TrxR1↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 1, CRM↑, 1, LDL↓, 1,
Transcription & Epigenetics ⓘ
other↑, 1,
Protein Folding & ER Stress ⓘ
NQO2↑, 1,
Barriers & Transport ⓘ
BBB↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↑, 1, GABA↑, 1,
Drug Metabolism & Resistance ⓘ
ABC↓, 1, BioAv⇅, 1, Dose↑, 1, eff↑, 1, MRP1↓, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, cardioP↑, 1, Strength↑, 1, toxicity⇅, 2,
Total Targets: 28
Scientific Paper Hit Count for: toxicity, toxicity
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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