Bacteria Cancer Research Results
Bacteria, Effect on Bacteria: Click to Expand ⟱
| Source: |
| Type: |
Effect on Bacteria
|
Scientific Papers found: Click to Expand⟱
AntiTum↑, Over the last twenty years, AF has also been repurposed as an antitumor, antiviral, and antibacterial drug.
Bacteria↓,
TrxR↓, ability to inhibit thioredoxin reductase (TrxR) and disrupt redox homeostasis, leading to selective cytotoxicity in cancer cells.
ChemoSen↑, synergistic effects observed when AF is combined with chemotherapeutics, targeted therapies, or immune modulators.
Dose↝, Patients received AF orally twice daily on days 1–28. atients received AF orally, 6 mg in the morning and 6 mg in the evening.
ROS↑, AF induces oxidative stress and apoptosis in cancer cells by disrupting redox homeostasis, while sirolimus inhibits mTOR signaling.
Apoptosis↑,
mTOR↓,
*Dose?, Subjects received orally 6 mg (p.o.) of auranofin daily, the recommended dose for rheumatoid arthritis, for 7 days and were followed for 126 days.
*Half-Life↝, The mean gold maximum concentration in plasma (Cmax) at day 7 was 0.312 μg/ml and the half-life (t1/2) 35 days, so steady-state blood levels would not be reached in short-term therapy.
*Dose↑, The highest concentration of gold, 13 μM (auranofin equivalent), or more than 25× the 50% inhibitory concentration (IC50) for E. histolytica and 4× that for Giardia, was in feces at 7 days.
*toxicity↝, Long-term (months to years) auranofin therapy was linked to side effects, including diarrhea (40% of subjects), skin rashes (2% to 5%), hematologic abnormalities (rare), and proteinuria (5%)
*Bacteria↓, Higher doses of auranofin will clearly be required for some infections.
*Dose↑, The FDA has approved clinical trials using auranofin at up to 21 mg/day for treatment of relapsed chronic lymphocytic leukemia after daily doses of 9 and 12 mg for at least 28 days were well tolerated
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
BPH, |
NA |
|
|
|
ROS↑, capacity of these nanostructures to release silver ions (Ag+) and enhance the production of reactive oxygen species (ROS) has been explored in combination with light to treat several diseases.
EPR↓, Furthermore, the use of NPs in biomedical applications takes advantage of the enhanced permeability and retention (EPR) effect, a phenomenon that enables greater penetration and longer retention times in cancer cells compared to normal cells
eff↑, When the AgNPs are exposed to an electromagnetic field, the electrons in the metals’ conduction band oscillate collectively and in resonance with the light frequency, generating the LSPR at the AgNPs’ surface.
Bacteria↓, NPs have already been approved by the Food and Drug Administration (FDA) as antibacterial agents for clinical use [
eff↑, Smaller AgNPs have been appointed as having greater reactivity compared to larger ones, due to their higher surface area-to-volume ratio and enhanced cellular uptake.
eff↑, TSC-coated AgNPs exhibited stronger binding affinity to Gram-positive bacteria, while the positively charged AgNPs-TMA were more efficiently internalized by Gram-negative bacteria.
TumVol↓, After PTT treatment with a AgNPs-PVP dose of 50 mg.kg−1 for 5 min, the prostate size of the BPH-bearing animals was reduced compared with non-treated rats, showing that AgNPs could prevent the progression of BHP.
*Bacteria↓, strong antibacterial, anticancer, anti-inflammatory, and wound-healing properties.
AntiCan↑,
*Inflam↓,
*Wound Healing↑,
eff↑, Cytotoxic effects of anticancer drugs such as verapamil, cisplatin, carmustine, and methotrexate are improved by citrate-coated silver oxide NP
ChemoSen↑,
EGFR↓, silver (AgNPs), gold (AuNPs), and superparamagnetic iron oxide nanoparticles (SPIONPs) have shown the
ability to interfere with EGFR
ROS↑, In MCF-7 breast cancer cells, AgNP induced ROS activated proteins, such as p53, Bax, and caspase-3, cause programmed cell death
P53↑,
BAX↑,
Casp3↑,
toxicity↝, AgNPs produce ionic silver and ROS that have
antibacterial properties, but their non-specific absorption
can harm healthy cells.
| - |
in-vitro, |
CRC, |
HCT116 |
|
|
|
- |
in-vitro, |
Melanoma, |
A2780S |
|
|
|
Bacteria↓, The antioxidant activity of the synthesized AgNPs was assessed using the DPPH method, which confirmed their significant antioxidant properties alongside their antibacterial activity.
antiOx↑, AgNPs but also exhibits substantial antioxidant properties
AntiCan↑, anticancer activities
eff↑, The combination of Asplenium dalhousiae leaf methanolic extracts and synthesized silver nanoparticles (AgNPs: aqueous, n-hexane, and CHCl3 fractions) exhibits varied apoptotic activity against ovarian and colorectal cancer cells.
| - |
in-vitro, |
Lung, |
A549 |
|
|
|
- |
in-vitro, |
PC, |
MIA PaCa-2 |
|
|
|
- |
in-vitro, |
Pca, |
PC3 |
|
|
|
- |
in-vitro, |
Nor, |
HEK293 |
|
|
|
AntiCan↑, (AgNPs) have emerged as promising multifunctional agents in biomedical applications due to their notable antimicrobial and anticancer properties.
selectivity↑, demonstrated significant cytotoxic effects on cancer cells while sparing normal cells
Apoptosis↑, Apoptosis induction, cell cycle arrest, and gene expression analyses further validated their anticancer efficacy.
TumCCA↑,
Bacteria↓, Figure 6a,b show the inhibition zones of 10 µg ampicillin and 10, 50, 100, and 150 μg/mL AgNPs against bacteria on agar for two repeated tests.
tumCV↓, AgNPs at concentrations of 6.3, 6.8, 7.5, 8.3, 9.4, 10.7 and 12.5 µg/mL for 24 h. After treatment, a significant decrease in cell viability was observed in different cancer cell types,
selectivity↑, The toxic effect was weaker in healthy cells than in cancer cells
Apoptosis↑, Fig. 8a–c, a significant increase (p < 0.01; p < 0.001) in the rate of early and late apoptotic cells was observed in A549, MIA PaCa-2 and PC-3 cells.
TumCCA↑, accompanied by arrest in the S phase and, particularly, the G2/M phase.
*Bacteria↓, broad-spectrum antimicrobial efficacy, silver nanoparticles have opened new horizons towards novel approaches in the control of infections in wound healing.
*eff↑, It is accepted that Ag nanoparticles with small diameter have a superior antimicrobial effect than those with a larger diameter, and their antibacterial activity is higher than their bulk equivalents
*other↝, Today, due to their broad-spectrum antibacterial capability, silver-based creams and ointments, as well as AgNPs-based biomedical products, such as wound dressings, are commercially available for different medical applications
*toxicity↓, In low concentrations, silver has been indicated as non-toxic material to humans, and it has been assessed as a promising material in pharmaceutical and biomedical fields
| - |
in-vitro, |
Colon, |
HCT116 |
|
|
|
- |
in-vitro, |
Nor, |
NCM460 |
|
|
|
*Bacteria↓, Nano Ag has excellent antibacterial properties and is widely used in various antibacterial materials, such as antibacterial medicine and medical devices, food packaging materials and antibacterial textiles
ROS↑, intracellular reactive oxygen species (ROS) increased
p‑p38↑, Ag NPs can promote the increase in P38 protein phosphorylation levels in two colon cells and promote the expression of P53 and Bax.
BAX↑,
Bcl-2↓, Ag NPs can promote the down-regulation of Bcl-2, leading to an increased Bax/Bcl-2 ratio and activation of P21, further accelerating cell death
BAX↑,
P21↑,
TumCD↑,
toxicity↝, low concentration of nano Ag has no obvious toxic effect on colon cells, while nano Ag with concentrations higher than 15 μg/mL will cause oxidative damage to colon cells.
eff↑, uptake of silver nanoparticles in cells of the human intestinal LoVo cell line was dependent on size.
TumCD↑, Silver nanoparticles in sizes of 10–100 nm induced cytotoxicity in a size- and dose-dependent manner via ROS generation.
ROS↑,
Bacteria↓, antimicrobial properties of silver nanoparticles (AgNPs)
ROS↑, the most remarkable mechanistic mode of AgNP-based antimicrobial effects is represented by their adhesion to microbial cells, ROS and free-radical generation, microbial wall piercing and penetration inside cells, and modulation and modification of mi
*toxicity↓, high intrinsic antimicrobial efficiency and non-toxic nature
*Bacteria↓,
*Inf↓, silver-based compounds and materials were used for the unconventional and effective control of distinctive infections
*Diff↑, Previous studies reported that AgNPs naturally improve the differentiation process of MC3T3-1 pre-osteoblast cells and subsequent bone-like tissue mineralization,
*eff↑, studies showed that AgNP-implanted titanium displayed improved antibacterial ability,
RadioS↑, making them suitable candidates for detection and dose-enhancement purposes in X-ray irradiation applications
selectivity↑, selective uptake into cancerous cells, AgNP-derived scattered light can be used for imaging purposes, whereas absorbed light can be used for selective hyperthermia
| - |
in-vitro, |
Liver, |
HepG2 |
|
|
|
- |
in-vitro, |
Diabetic, |
NA |
|
|
|
AntiCan↑, The PGE-AgNPs showed a dose-dependent response against human liver cancer cells (HepG2) (IC50; 70 μg/mL) indicating its greater efficacy in killing cancer cells.
Dose↝, surface charge of synthesized AgNPs was highly negative (−26.6 mV) and particle size distribution was ranging from ∼35 to 60 nm and the average particle size was about 48 nm determined by dynamic light scattering (DLS)
*antiOx↑, literature suggests that AgNPs display considerable antioxidant activity in vitro
*AntiDiabetic↑, Antidiabetic potential of biosynthesized AgNPs
*Bacteria↓, Synergistic antibacterial potential of AgNPs with standard antibiotics
| - |
in-vitro, |
Melanoma, |
A431 |
|
|
|
MMP↓, The depolarization of mitochondrial membrane potential ΔΨm through excess ROS production was deduced to be the triggering force behind the apoptotic cell death mechanism of the skin carcinoma
ROS↑,
*toxicity↓, AgNPs provides an economic, nontoxic, specific approach for targeting skin carcinoma with additional benefits of antibacterial activities.
Bacteria↓,
| - |
in-vitro, |
Lung, |
A549 |
|
|
|
- |
in-vitro, |
Liver, |
HepG2 |
|
|
|
*Bacteria↓, silver nanoparticles synthesized from Dendropanax morbifera Léveille leaves (D-AgNPs) exhibit antimicrobial activity and reduce the viability of cancer cells without affecting the viability of RAW 264.7 macrophage-like cells
tumCV↓,
selectivity↑,
ROS↑, enhanced the production of ROS in both cell lines.
Apoptosis↑, An increase in cell apoptosis and a reduction in cell migration in A549 cells were also observed after D-AgNP treatment.
TumCMig↓,
AntiCan↑, potential of D-AgNPs as a possible anticancer agent, particularly for the treatment of non-small cell lung carcinoma.
*Bacteria↓, Although the positively charged nanoparticles showed the highest level of effectiveness against the organisms tested, the neutrally charged particles were also potent against most bacterial species.
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Diabetic, |
NA |
|
|
|
ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
*Bacteria↓, lity. The antimicrobial properties of Ag NPs are finding their application in
enhancing the activity of drugs (like Amphotericin B, Nystatin, Fluconazole) and composite scaffolds for controlled release of
drugs and targeted delivery of drugs due to t
*eff↑, 2]. However, mild reducing agents like ascorbic acid leads to the controlled growth of the Ag NP : ascorbic acid was added to reduce the remaining Ag + ions
*Bacteria↓, The green-synthesized AgNPs displayed potent antibacterial efficacy,
AntiCan↑, cytotoxicity against human colon carcinoma (HT-29) cells. The MTT assay confirmed their anticancer potential, with an IC50 value of 150.8 μg/mL.
DNAdam↑, Ag-NPs, accumulating in the nucleus, may cause genotoxicity, DNA damage, and chromosomal aberrations
ATP↓, Ag-NP exposure disrupts calcium homeostasis, leading to mitochondrial dysfunction, ATP depletion, and apoptosis.
Apoptosis↑,
ROS↓, induce cytotoxicity through numerous mechanisms viz., oxidative stress, mitochondrial dysfunction, DNA damage, cell cycle arrest, and subsequent apoptosis.
TumCCA↑,
*Bacteria↓, effectiveness as an antibacterial agent.
*BMD↑, Bone Repair Applications
*Bacteria↓, AgNPs showed antibacterial activity against Gram-positive and Gram-negative strains.
*selectivity↑, AgNPs did not show cytotoxicity on VERO cells ranging from 0.5 to 150 μg mL−1 with a good gemoprotection.
*Bacteria↓, Ch-AgNPs (8–48 nm) exhibited significant antibacterial and antibiofilm activity.
*Wound Healing↑, Ch-AgNPs promoted wound healing activity at 75 and 100 μg mL−1 after 24 h.
TumCG↓, Ch-AgNPs effective inhibited the MCF-7 human breast cancer cells at 100 μg mL−1 after 24 h.
*Bacteria↓, antibacterial activity of chitosan conjugated silver nanoparticles against broad-spectrum Gram-negative and Gram-positive microbial pathogens
*Bacteria↓, Further, the silver chitosan nanoparticles showed antibacterial activity against two important clinical pathogens, S. aureus and E. coli.
*Wound Healing↑, Chitosan and silver each address infection and wound healing through distinct mechanisms.
*Bacteria↓, Overall, these results highlight Ag-Chi-NPs as sustainable bio-nanocomposites that combine antioxidant, antibacterial, and cytocompatibility properties, making them promising candidates for wound healing materials, antimicrobial coatings
*Wound Healing↑,
*Bacteria↓, The reduction of silver ion by chitosan slurry leads to the green synthesis of well-characterized silver nanoparticles (10 nm) stabilized within the chitosan–silver nanocomposite film with enhanced antibacterial activities.
*Bacteria↓, Notably, incorporating α-aminophosphonate and Ag0NPs into chitosan-backbone markedly enhanced its antimicrobial efficacy against bacterial and fungal biofilms.
*Bacteria↓, Chi/Ag-NPs showed promising antifungal features against Candida albicans, Aspergillus fumigatus, Aspergillus terreus, and Aspergillus niger, where inhibition zones were 22, 29, 20, and 17 mm, respectively.
*Wound Healing↑, Wound healing results illustrated that fibroblasts advanced toward the opening to close the scratch wound by roughly 50.5% after a 24-h exposure to Chi/Ag-NPs, greatly accelerating the wound healing process.
*Bacteria↓, SPE@Ag-NPs showed antibacterial, anticoagulant and antiplatelet activity.
*AntiAg↑,
*toxicity↓, SPE@Ag-NPs did not induce edema and hemorrhage in the experimental mice and also did not hydrolyze RBC cells suggesting its nontoxic property.
*AntiAg↑, n the present study we show that nanosilver has an innate antiplatelet property and effectively prevents integrin-mediated platelet responses, both in vivo and in vitro, in a concentration-dependent manner
*Bacteria↓, We have recently reported synthesis of highly stable, uniformly sized silver nanoparticles endowed with enhanced antibacterial properties.
*Dose↝, Nanoparticles were spherical in shape, 10-15nm in diameter and monodispersed
*Dose↝, The extent of inhibition was the same irrespective of whether platelets were aspirinized or not. More than 80% (n $ 10) inhibition in amplitude was recorded at a nanoparticle concentration of 50 uM, which also reduced the slope of agregation/min
*Dose↝, (2!8 mg/kg body weight) in two different mice strains led to significant inhibition of platelet aggregation in mouse whole blood (studied by electronic impedance) in a dose-dependent manner
*toxicity↝, a dose of nanosilver up to 300 mg/kg was nontoxic to rodents.
*AntiAg↑, Together with its inherent antiplatelet and antibacterial properties,
*Bacteria↓,
| - |
in-vitro, |
Var, |
MCF-7 |
|
|
|
- |
NA, |
NA, |
HEK293 |
|
|
|
toxicity↓, Using 20% (v/v) KQE, highly stable, spherical KQ-AgNPs (12.3 ± 3.0 nm) were synthesized via in-situ generation of free radicals, such as ortho-quinones, which reduced Ag+ ions.
Bacteria↓, KQ-AgNPs exhibit superior antibacterial activity against both gram-positive and gram-negative bacteria compared to chemically synthesized AgNPs (AgNPs-Chem) and KQE alone
selectivity↑, (MCF-7) with an IC50 of 21.25 ± 1.14 µg/mL, significantly lower than AgNPs-Chem (33.05 ± 3.13 µg/mL), while maintaining high biocompatibility with normal cells (HEK-293) with a greater IC50 of 169.96 ± 2.3 µg/mL.
| - |
in-vitro, |
BC, |
MCF-7 |
|
|
|
- |
in-vitro, |
BC, |
T47D |
|
|
|
Bacteria↓, Nowadays, silver nanoparticles (AgNP) are widely used in the medical field mainly for their antibacterial properties
Apoptosis↑, AgNP of 2 (AgNP2) and 15 nm (AgNP15) induce apoptosis in human MCF-7 and T-47D breast cancer cells.
ER Stress↑, Treatment with AgNP2 and AgNP15 led to accumulation and aggregation of misfolded proteins causing an endoplasmic reticulum (ER) stress and activating the unfolded protein response (UPR).
UPR↑,
PERK↑, The three main ER sensors, PERK, IRE-1α and ATF-6, were rapidly activated in response to AgNP2 and AgNP15
IRE1↑,
ATF6↑,
ATF4↑, AgNP2 and AgNP15 induced upregulation of the transcription factors ATF-4 and GADD153/CHOP
CHOP↑,
Casp9↑, Moreover, the initiating caspase-9 and the effector caspase-7 were activated in response to these NPs.
Casp7↑,
Mcl-1↓, In contrast, a downregulation of Mcl-1 and xIAP protein expression as well as a processing of PARP were observed.
XIAP↓,
PARP↝,
selectivity↑, Of note, the non-cancerous MCF-10A cells were more resistant to both AgNP2 and AgNP15 when compared to MCF-7 and T-47D cell lines.
Bacteria↓, fabrication of immobilized Ag-NPs on
device such as catheters
Bacteria↓, effective, but not against the predominat E. coli
Bacteria↓, AuNP/AgNPs were known to have antimicrobial effects.
eff↑, Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin.
AntiThr↑, ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities.
Bacteria↓,
LDH↓,
TumCP↓, Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1
TumCCA↑, Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
Bcl-2↓, The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3.
Cyt‑c↑,
Casp3↑,
*cardioP↑, Allicin has many health-promoting properties, such as cardioprotective, antimicrobic, cholesterol-lowering, anti-inflammatory, and antitumor.
*Bacteria↓,
*Inflam↓,
AntiTum↑,
*DNAdam↓, DNA damage protection, induction of cell death, inhibition of cell proliferation, and block of angiogenesis and metastasis formation.
TumCP↓,
angioG↓,
TumMeta↓,
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,
Apoptosis↑, Astaxanthin causes apoptosis in
several in vitro studies, including both oral and liver cancer cells
EMT↓, AXT inhibits the EMT pathway in colon cancer cells and can reduce breast cancer cells' proliferation and growth
AntiCan↑, Astaxanthin can address human health problems, including cancer, cardiovascular, and neurodegenerative diseases.
*cardioP↑,
*neuroP↑,
TumCG↓, 100 mg/kg Astaxanthin strongly inhibited tumor growth relative to the TC group, with an inhibitory rate of 41.7%.
*antiOx↑, .ASX is often referred to as the "super antioxidant" since it has the strongest antioxidant activity of current carotenoids.
*Bacteria↓, Studies have demonstrated antioxidant and antimicrobial, immunomodulatory, hepatoprotective, anticancer, and antidiabetic effects of ASX.
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
ROS↓, Astaxanthin and carbendazim function in conjunction to inhibit cell proliferation while reducing ROS production in
breast cancer cells.
*chemoPv↑, Chemopreventive and therapeutic efficacy of astaxanthin against cancer
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.
*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*eff↑, borneol has shown superior ability for anti-inflammatory and analgesic activities when coupled with other active ingredients from ancient times.
BBB↑, Given its ability to enhance cross-barrier permeation
ChemoSen↑, interest in borneol, for various purposes, including anti-inflammatory, analgesic, neuronal protection, permeability promotion, chemotherapy sensitization and borneol-modified nano-drug delivery system
*Inflam↓, borneol and its synthetic counterpart exhibit noteworthy anti-inflammatory properties by reducing inflammatory factors, namely NO, TNF-α, and IL-6
*NO↓,
*TNF-α↓,
*IL6↓,
*Bacteria↓, Borneol has shown exceptional anti-bacterial effect activity and has been coupled in TCM formulas for external use against bacteria growth
*eff↑, Studies indicated that the combined administration of edaravone and borneol (i.e. Edaravone Dexborneol) exhibited synergistic effects in the treatment of ischemic stroke
*Aβ↓, efficient prohibition of the accumulation of Aβ in the brain
*SOD↑, Borneol has been reported to exhibit exceptional potential in the augmentation of superoxide dismutase (SOD) activity
*neuroP↑, Both naturally occurring and artificially synthesized borneol exhibited neuroprotective properties
*EPR↑, The permeation-enhancing effects of natural borneol and synthetic borneol on various drug properties have been observed,
toxicity↓, Borneol is an ideal absorption enhancer with low toxicity, little stimulation to gastrointestinal mucosa and strong permeability
P-gp↓, The inhibition of P-gp expression has been observed as a potential mechanism for reversing multidrug resistance, with borneol implicated in this process
eff↑, Research findings indicated that natural borneol can substantially enhance the anticancer properties of paclitaxel and curcumin.
other↝, specifically, the incorporation of borneol has been associated with improvements in drug solubility, enhanced cellular uptake, reduced organ toxicity, and mitigation of multiple drug resistances.
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
*eff↑, L-borneol has better potential in cerebrovascular diseases.
*eff↑, D-borneol exhibits better antitumour sensitizing effects than L-borneol.
*toxicity↝, Synthetic borneol is less safe. Synthetic borneol is widely used because of its advantages of low cost and easy availability.
*Inflam↓, It has anti-inflammatory, analgesic, antipyretic, antibacterial, neuroprotective, and permeation-promoting effects.
*Bacteria↓,
*neuroP↑,
*Half-Life↝, oral administration. It reaches its highest concentration in 30 min, and its half-life is 18 h
*BBB↑, and can easily pass through the BBB and blood–ocular barrier (BOB).
*BioEnh↑, Borneol can promote the absorption and affect the distribution of other drugs, which is beneficial for reducing the dosage, prolonging the action time, and improving the curative effects of these drugs
*P-gp↓, inhibitory activity against P-gp is as follows: L-borneol > D-borneol ≈ synthetic borneol.
*CYP3A4↓, inhibition of intestinal CYP3A4 would improve the bioavailability of drugs.
*ROS↓, and reduce the rate of cerebral oedema and the volume of infarcts by inhibiting oxidative stress
*neuroP↑, neuroprotective effects of the three kinds of borneol are as follows: L-borneol > synthetic borneol > D-borneol
*antiOx↑, Bergamot whole-fruit showed a high in vitro and ex vivo antioxidant activity.
*Bacteria↓, Bergamot extract exerted antibacterial activity against pathogenic bacteria.
*GutMicro↑, Bergamot extract slightly stimulated gut-beneficial bacteria.
*Imm↑, CA enhances immune responses, reduces inflammation, exerts antimicrobial effects, and improves overall fish health.
*Inflam↓,
*Bacteria↓,
*eff↑, sustainable functional-feed strategies that diminish antibiotic reliance in aquaculture.
*ROS↓, Reduced MDA levels and ROS accumulation
*MDA↓,
*Catalase↑, Increased CAT, GSH, and T-AOC activities
*GSH↑,
*TAC↑,
*NF-kB↓, Suppressed the activation of the NF-κB signaling pathway and the NLRP3 inflammasome pathway in the gills
*NLRP3↓,
*eff↑, In rainbow trout (Oncorhynchus mykiss), co-supplementation with 1–3 g RA/kg and Lactobacillus rhamnosus yielded synergistic improvements in growth, antioxidant capacity, and stress tolerance
*AST↓, In rainbow trout, CinA (0.25–1.5 g/kg) lowered intestinal pH, serum triglycerides, and hepatic enzyme levels (AST and ALT), while upregulating hepatic antioxidant genes (SOD and GST) [49]
*ALAT↓,
*SOD↑,
*GSTA1↑,
*Bacteria↓, properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities.
*AntiCan↑,
*Imm↑,
*Wound Healing↑,
*NF-kB↓, including inhibition of the transcription factors NF-κB
*5LO↓, use of CAPE in diabetes therapy have shown that caffeic acid phenethyl ester inhibits the enzyme 5-lipoxygenase
*AntiDiabetic↑, Antidiabetic Properties
ChemoSen↑, CAPE treatment enhances the antitumor effect of cytostatic drugs, such as vinblastine, paclitacol, estramustine and docetaxel, used in the chemotherapy of prostate cancer [76,81,82].
selectivity↑, CAPE acts selectively on diseased cells, without adversely affecting normal cells [88]
chemoPv↑, CAPE may be useful as support for cancer therapy in terms of chemoprevention of non-cancerous cells
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
Diabetic, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,
TumCG↓, In this study, we showed that carvacrol inhibited HepG2 cell growth by inducing apoptosis
Apoptosis↓,
Casp3↓, activation of caspase-3, cleavage of PARP and decreased Bcl-2 gene expression
cl‑PARP↑,
Bcl-2↓,
p‑ERK↓, decreasing phosphorylation of ERK1/2 significantly in a dose-dependent manner, and activated phosphorylation of p38
p‑p38↑,
*Bacteria↓, carvacrol has been shown to exhibit anti-microbial, anti-mutagenic, anti-platelet, analgesic, anti-inflammatory, anti-angiogenic, anti-oxidant, anti-elastase, insecticidal, anti-parasitic,cell-protective, AChE inhibitor and anti-tumor activity
*AntiAg↑,
*Inflam↓,
*antiOx↑,
*AChE↓,
AntiTum↑,
MMP↓, classical apoptosis response, including decrease in mitochondrial membrane potential and increase in cytochrome c release from mitochondria, decrease in Bcl-2/Bax ratio, increase in caspase activity and cleavage of PARP and fragmentation of DNA,
Cyt‑c↑,
Bax:Bcl2↑,
Casp↑,
DNAdam↑,
selectivity↑, we found that carvacrol induced stronger effects on hepatocellular carcinoma cells compared to normal human fetal liver cells.
BioAv↑, hybrid compounds containing their pharmacophores to enhance their therapeutic efficacy and improve their bioavailability.
AntiCan↑, figure 2
*antiOx↑,
*Inflam↑,
*Bacteria↓,
ROS↑, they produce more reactive oxygen species (ROS), which interrupt the DNA of cancer cells
DNAdam↑,
*Bacteria↓, oil-derived compounds against a broad spectrum of Gram-positive and Gram-negative bacteria, including multidrug-resistant (MDR) strains
*Inflam↓, anti-inflammatory activity of these compounds is also highlighted, with emphasis on their modulation of key signaling pathways such as nuclear factor-kappa B (NF-κB)
*cardioP↑, figure 1
*neuroP↑,
*NADPH↓, thymol has been shown to inhibit NADPH production at a concentration of 200 µg/mL
*NRF2↑, thymol has been shown to activate the nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway
*HO-1↑,
*IL1β↓, carvacrol has also shown anti-inflammatory properties [107,108], being able to inhibit pro-inflammatory mediators as IL-1β and TNF-α
*TNF-α↓,
Showing Research Papers: 1 to 50 of 89
Page 1 of 2
Next
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 89
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Catalase↓, 1, GSH↓, 2, HO-1↓, 1, lipid-P↓, 1, lipid-P↑, 1, MDA↓, 1, NRF2↑, 1, RNS↓, 1, ROS↓, 2, ROS↑, 15, SOD↑, 1, TrxR↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 2, MMP↓, 4, XIAP↓, 2,
Core Metabolism/Glycolysis ⓘ
ACSL4↑, 1, ALAT↓, 1, LDH↓, 1, LDL↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↓, 2, Apoptosis↑, 9, BAX↑, 3, Bax:Bcl2↑, 1, Bcl-2↓, 3, Bcl-2↑, 1, Casp↑, 1, Casp1↑, 1, Casp3↓, 2, Casp3↑, 3, Casp7↑, 1, Casp9↑, 2, Cyt‑c↓, 1, Cyt‑c↑, 3, iNOS↓, 1, JNK↓, 1, MAPK↓, 1, Mcl-1↓, 1, p‑p38↑, 2, TumCD↑, 2,
Transcription & Epigenetics ⓘ
AntiThr↑, 1, other↓, 1, other↝, 2, tumCV↓, 3,
Protein Folding & ER Stress ⓘ
ATF6↑, 1, CHOP↑, 1, ER Stress↑, 1, HSP27↓, 1, IRE1↑, 1, PERK↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3I↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 5, P53↑, 2, P53↝, 1, PARP↝, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, P21↑, 2, TumCCA↑, 7,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, EMT↓, 1, ERK↓, 2, p‑ERK↓, 1, GSK‐3β↓, 1, mTOR↓, 2, NOTCH↓, 1, PI3K↓, 3, TumCG↓, 3,
Migration ⓘ
E-cadherin↓, 1, MMP2↓, 2, MMP9↓, 2, MMPs↓, 2, TumCMig↓, 1, TumCP↓, 3, TumMeta↓, 3, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, ATF4↑, 1, EGFR↓, 2, EPR↓, 1, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 1, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IFN-γ↓, 1, IL2↓, 1, IL4↓, 1, IL6↓, 1, Imm↑, 1, NF-kB↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, BioAv↝, 1, ChemoSen↑, 6, Dose↝, 3, eff↑, 14, RadioS↑, 3, selectivity↑, 8,
Clinical Biomarkers ⓘ
ALAT↓, 1, BP↓, 1, EGFR↓, 2, IL6↓, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 8, AntiTum↑, 3, chemoP↑, 1, chemoPv↑, 1, cognitive↑, 1, memory↑, 1, toxicity↓, 2, toxicity↝, 2, TumVol↓, 1,
Infection & Microbiome ⓘ
Bacteria↓, 13,
Total Targets: 122
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 7, Catalase↑, 3, GPx↑, 3, GSH↑, 1, GSR↑, 1, GSTA1↑, 1, HO-1↑, 1, lipid-P↓, 2, MDA↓, 3, NRF2↑, 2, ROS↓, 4, SOD↑, 5, TAC↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, CYP3A4↓, 1, glucose↓, 1, LDH↓, 1, NADPH↓, 1,
Cell Death ⓘ
necrosis↓, 1,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
Diff↑, 1, TRPM7↓, 1,
Migration ⓘ
5LO↓, 1, AntiAg↑, 6,
Angiogenesis & Vasculature ⓘ
EPR↑, 1, NO↓, 1,
Barriers & Transport ⓘ
BBB↑, 2, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL1β↓, 1, IL6↓, 1, Imm↑, 4, Inflam↓, 11, Inflam↑, 1, NF-kB↓, 4, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 2,
Protein Aggregation ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 1,
Hormonal & Nuclear Receptors ⓘ
CYP19↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioEnh↑, 1, Dose?, 1, Dose↑, 2, Dose↝, 4, eff↑, 10, Half-Life↝, 2, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 3, BMD↑, 1, GutMicro↑, 1, IL6↓, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, AntiDiabetic↑, 7, Bone Healing↑, 1, cardioP↑, 6, chemoPv↑, 1, hepatoP↑, 4, memory↑, 1, motorD↑, 1, neuroP↑, 9, Obesity↓, 3, OS↑, 1, Pain↓, 3, RenoP↑, 1, toxicity↓, 6, toxicity↝, 3, Wound Healing↑, 8,
Infection & Microbiome ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 37, Diar↓, 1, Inf↓, 1,
Total Targets: 79
Scientific Paper Hit Count for: Bacteria, Effect on Bacteria
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#:591 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page