AntiFungal Cancer Research Results
AntiFungal, AntiFungal: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
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*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.
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*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation
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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
*Inflam↓, It has anti-inflammatory, rheumatological, ulcer inhibiting, anticholinergic, analgesic, antimicrobial, antistress, antidiabetes, anticancer, liver protection, anthelmintics, antioxidants, antifungal, and wound healing propertie
*AntiBio↑,
*AntiDiabetic↑,
*hepatoP↑,
*antiOx↑,
*AntiFungal↑,
*Wound Healing↑,
*other↑, Garlic has a higher concentration of sulfur compounds (allicin, diallyl disulfide, S-allylcysteine, and diallyl trisulfide), which are responsible for its therapeutic properties.
*BP↓, Garlic consumption lowers blood pressure, inhibits atherosclerosis, decreases serum cholesterol and triglycerides, suppresses platelet aggregation, and increases fibrinolytic activity, among other things
*LDL↓,
*AntiAg↑,
*cognitive↑, Garlic can also aid in preventing cognitive decline by shielding neurons from neurotoxicity and apoptosis, which helps to prevent ischemia, obsessive-compulsive disorder (OCD), and neuronal death while also boosting learning and memory retention
*memory↑,
Risk↑, People who consumed more garlic had a 54% decreased risk of pancreatic cancer than those who consumed fewer amounts of garlic
*COX1↓, Garlic supplements have been demonstrated to reduce cyclooxygenase activity and thromboxane A2 production, resulting in antiplatelet action
*TXA2↓,
*Bacteria↓, PA-AgNPs was active against Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus, with 100% inhibition.
*AntiFungal↑, The PA-AgNPs also displayed good antifungal properties, as the concentrations of 100 and 150 µg/mL had 100% inhibition toward Aspergillus fumigatus and Aspergillus flavus.
*AntiAg↑, PA-AgNPs also prevented the coagulation of human blood
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AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,
*neuroP↑, According to the literature survey, C. asiatica (gotu kola) has been reported to have a comprehensive neuroprotection by different modes of action such as enzyme inhibition, prevention of amyloid plaque formation in Alzheimer's disease, dopamine neur
*Aβ↓,
*ROS↓, dopamine neurotoxicity in Parkinson's disease, and decreasing oxidative stress.
*Wound Healing↑, Monographs of the plant describing mainly its wound healing and memory enhancement effects exist in the European Pharmacopeia
*memory↑,
*Inflam↓, anti-inflammatory [8, 9], antipsoriatic [10], antiulcer [11, 12], hepatoprotective
*hepatoP↑,
*Imm↑, anticonvulsant [14], sedative [15], immunostimulant [16], cardioprotective [17, 18], antidiabetic [19], cytotoxic and antitumor [20, 21], antiviral [22], antibacterial [23], insecticidal [24], antifungal [25], antioxidant
*cardioP↑,
*AntiDiabetic↑,
*AntiFungal↑,
*antiOx↑,
*Dose↝, Presence of several flavonoid derivatives such as quercetin, kaempferol, patuletin, rutin, apigenin, castilliferol (Figure 3), castillicetin, and myricetin has been reported in C. asiatica [35, 39, 42], while isolation of polysaccharides (e.g., cente
*AChE↓, The extract was found to inhibit AChE with 50% of inhibition rate at 150 μg/mL concentration . only the standardized extract was found to inhibit AChE
*BChE↓, ethanol extracts of the plant samples from Turkey and India exerted 46.95 ± 0.94% and 70.30 ± 3.77% against BChE, respectively, and a notable inhibition against TYRO
*Tyro3↓,
*lipid-P↓, showing a neuroprotective effect in old rats by way of bringing about a significant decrease in PCO contents and lipid peroxidation.
*Bacteria↓, multiple pharmacological properties such as antibacterial, antifungal, antiparasitic, antineuraminidase, antioxidant, anti-inflammatory, and anticancer activities.
*AntiFungal↑,
*antiOx↑,
*Inflam↓,
AntiCan↑,
*AntiDiabetic↑, also demonstrated an antidiabetic effect, through its role in the prevention of obesity and metabolic problems associated with high-fat diets
*Obesity↓,
TumCCA↑, Anticancer mechanisms of carvone are due to its different actions against checkpoints of cancer cells such as inducing apoptosis and cell cycle arrest
*AntiArt↑, figure 2
Imm↑,
*P450↓, decreased levels of phase I enzymes (cytochrome P450 and cytochrome b5) with increased levels of phase II enzymes (GR, GST, and GSH) and increased expression of Bax, caspase-3, and caspase-9 with decreased expression of mutated p53 and Bcl-2 in anima
*GSR↑,
GSTs↑,
GSH↑,
BAX↑,
Casp3↑,
TumCP↓, Results showed that L-carvone exhibited a strong antiproliferative effect against MCF7 (IC50 = 1.2 mM) and MDA MB 231 cells (IC50 = 1.0 mM), inhibited the migration of breast cancer cell lines, and induced apoptosis.
TumCMig↓,
Apoptosis↑,
*antiOx↑, antioxidant and anti-inflammatory activities
*Inflam↓,
*AntiBio↑, Eugenol has also shown excellent antimicrobial activity in studies, being active against fungi and a wide range of gram-negative and gram-positive bacteria.
*Bacteria↓,
*AntiFungal↑,
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ROS↑, However, being a quinone molecule, juglone could also act as a redox cycling agent and produce reactive oxygen species.
Pin1↓, Notably, juglone is an inhibitor of Pin1 (peptidyl-prolyl cis/trans isomerase) that could regulate phosphorylation of Tau, implicating potential effects of juglone in Alzheimer’s disease.
antiOx⇅, Juglone may have either pro- or antioxidant characteristics depending on the concentrations
*ROS↓, A recent study in a transgenic mouse model of Alzheimer’s disease demonstrated that the walnut supplementation can reduce oxidative damage
SMAD2↓, juglone reduces oxidative stress by inhibiting the phosphorylation of Smad2 in the kidney
GSH↓, cytotoxicity of juglone is due to two different mechanisms, namely, redox cycling and the reaction with glutathione (GSH) . toxicity of juglone is the formation of adducts, which also causes the glutathione depletion.
lipid-P↑, Juglone enhances lipid peroxidation predominantly through redox cycling
TumCCA↓, Figure3
BAX↑,
Bcl-2↓,
Casp3↑,
Casp9↑,
Ca+2↑,
Cyt‑c↑,
AntiFungal↑, Juglone may be as effective as commercially available antifungal agents including zinc undecylenate and selenium sulfide
Bacteria↓, Juglone has been shown to possess antibacterial activities
Akt↓, juglone has been shown to suppress the Akt pathway
*antiOx↑, its role as health-promoting effect is attributed because it is rich source of antioxidant.
P53↑, anticancer management through the modulation of various molecular pathways including p53, pTEN, NF-κB, PI3K/Akt, Bcl-2, and VEGF
PTEN↑, figure 2
NF-kB↓,
PI3K↓,
Akt↓,
Bcl-2↓,
VEGF↓,
*Inflam↓, Neem also plays role as anti-inflammatory via regulation of proinflammatory enzyme activities including cyclooxygenase (COX), and lipoxygenase (LOX) enzyme.
*COX2↓,
*5LO↝,
*Wound Healing↑, figure 1
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
*AntiViral↑,
*Bacteria↑,
*AntiBio↑,
*AntiFungal↑,
cMyc↓, figure 2
BAX↓,
IAP1↓, Nimbolide downregulated cell survival proteins, including I-FLICE, cIAP-1, cIAP-2, Bcl-2, Bcl-xL, survivin, and X-linked inhibitor of apoptosis protein, and upregulated the proapoptotic proteins p53 and Bax
IAP2↓,
Bcl-xL↓,
survivin↓,
XIAP↓,
angioG↓, ethanolic fraction of neem leaf (EFNL) treatment effectively inhibited the expression of proangiogenic genes,
*Inflam↓, anti-inflammatory, anti-microbial, and anti-proliferative agent.
*eff↑, shown promise in clinical trials for treatment of acne, psoriasis, eczema, common warts, and molluscum contagiosum.
*5LO↓, The oil inhibits the oxidative enzyme 5-lipoxygenase and has DPPH radical scavenging activity and,
*DPPH↓,
*hepatoP↑, in vivo, SAO was able to protect mouse livers from damage resulting from oxidative stress and the formation of reactive oxygen species.
*ROS↓,
*PGE2↓, Production of PGE2 was also suppressed, suggesting that SAO might be acting, at least in part, through inhibition of cyclooxygenase
*IL1β↓, The oil also suppressed the expression of the pro-inflammatory cytokine, IL-1b, in keratinocytes and reduced irritant dermatitis in mouse skin stimulated with haptens.
*IL17↓, reduce levels of IL-17 and the activity of PDE4.
*PDE4↓,
*tyrosinase↓, Alpha-santalol was found to be an inhibitor of tyrosinase, a key enzyme in the biosynthetic pathway for the skin pigment melanin.
*AntiFungal↑, SAO has demonstrated potent activity against many fungal dermatophytes and yeasts including Trichophyton, Microsporum and Candida
angioG↓, alpha-santalol, the primary component of SAO, is anti-angiogenic and inhibits the growth of hepatocellular carcinoma and prostate tumors in vitro and in vivo.
TumCG↓,
DNAdam↑, MCF-7) and non-tumorigenic epithelial breast cells (MCF-10A).42 The authors demonstrated that the oil induced deoxyribonucleic acid (DNA) strand breaks in both cell lines.
*Snail↑, SAO enhanced expression of transcription factors (snail, twist) and mesenchymal factor (vimentin), all of which are related to the epithelial-mesenchymal transition (EMT).
*Twist↑,
*Vim↑,
*EMT↓,
*toxicity↓, other species of sandalwood, such as Western Australian (Santalum spicatum) or Hawaiian sandalwood (Santalum paniculatum), contain significant percentages of farnesol, an irritant, that is not found in oil from S. album.
*AntiBio↑, antimicrobial and anti-inflammatory activities of the oil
*other↝, Terpinen-4-ol ≥30c 40.1%
*AntiFungal↑, TTO vapors have also been demonstrated to inhibit fungal growth
*Inflam↓, Numerous recent studies now support the anecdotal evidence attributing anti-inflammatory activity to TTO.
*ROS⇅, TTO decreases the production of reactive oxygen species by both stimulated neutrophils and monocytes and that it also stimulates the production of reactive oxygen species by nonprimed neutrophils and monocytes
*toxicity↑, TTO can be toxic if ingested, as evidenced by studies with animals and from cases of human poisoning.
*AntiBio↑, TQ, have a broad antimicrobial spectrum including Gram-negative, Gram-positive bacteria, viruses, parasites, schistosoma and fungi.
*AntiViral↑,
*AntiFungal↑,
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*Dose↝, Turmeric rhizome oil (TO) : Ar-turmerone, α-turmerone, and β-turmerone are the principal bisabolane sesquiterpenes
*BioEnh↑, the role of TO as a bioavailability enhancer is of current interest
*BBB↑, The high brain bioavailability of TO is relevant not only for its role as an enhancer but also for its intrinsic therapeutic properties.
*ROS↓, The radical scavenging assay and the ferric reducing antioxidant power test displayed significant antioxidant activity for TO
*GSH↑, oral administration of TO for 30 days prompted a relevant increase in glutathione and antioxidant enzyme concentrations of superoxide dismutase and glutathione reductase in plasma
*SOD↑,
*GSR↑,
*NO↓, TO decreased nitric oxide (NO) synthase expression and displayed immune-modulatory properties since it restricted neutrophil infiltration in the ischemic area of a murine cerebral focal ischemia model.
*P450↓, TO significantly hindered cytochrome p450 enzymes
OS↑, hepatic arterial infusion with TO promoted a longer survival time in liver cancer patients
TumCG↓, TO inhibited in vitro growth of two human colon cancer cells (HT-29 and HCT-116).
*GutMicro↑, oral administration of TO and curcumin in mice also shifted the fecal microbial composition. The Bacteroidaceae, Ruminococcaceae, Clostridiales, Firmicutes, and Parabacteroids families were markedly reduced, and the concentration of anti-inflammatory
*Pain↓, TO was capable of substantially increasing the pain threshold
*neuroP↑, TO exerts its neuroprotective activity by reducing NOS expression, NO-mediated peroxynitrite synthesis, oxidative stress, and neuronal apoptosis.
*AChE↓, the oil inhibited the activity of acetylcholinesterase (p < 0.01) and adenosine deaminase
*BDNF↑, upregulation of brain-derived neurotrophic factor (BDNF),
*Bacteria↓, Antibacterial: TO inhibited Porphyromonas gingivalis, a pathogen responsible for periodontitis
*AntiFungal↑, TO showed in vitro antifungal activity against Candida tropicalis, Penicillium notatum, Aspergillus fumigatus, A. niger, A. flavus, Trichophyton rubrum, T. violceum, T. mentagrophytes, Epidermophyton floccosum, Microsporum gypseum, and Sporothrix sch
*toxicity↓, Nevertheless, no toxicity warning has been reported for any of the components of the oil extracted from turmeric. Methyl eugenol, a genotoxic carcinogen, is the sole constituent of turmeric leaf oil (~3%). It is not present in turmeric rhizome oil
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:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx⇅, 1, GSH↓, 1, GSH↑, 1, GSTs↑, 1, lipid-P↑, 2, MFN2↑, 1, ROS↑, 3,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
cMyc↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 5, Apoptosis↑, 3, Bak↓, 1, BAX↓, 1, BAX↑, 4, Bcl-2↓, 3, Bcl-xL↓, 1, BID↑, 1, Casp3↑, 3, cl‑Casp3⇅, 1, Casp8↑, 1, Casp9↑, 3, Cyt‑c↑, 4, Fas↑, 1, IAP1↓, 1, IAP2↓, 1, JNK↓, 1, MAPK↝, 1, p38↑, 1, survivin↓, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1, tumCV↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 3, P53↑, 3, P53↝, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
FGF↓, 1, GSK‐3β↑, 1, mTOR↝, 1, PI3K↓, 2, PTEN↑, 1, TumCG↓, 2, Wnt↓, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 1, CEA↓, 1, fascin↓, 1, MMP9↓, 1, MMPs↓, 1, SMAD2↓, 1, TGF-β↓, 1, TIMP2↑, 1, TumCMig↓, 1, TumCP↓, 2, TumMeta↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↑, 1, EPR↑, 1, HIF-1↓, 1, VEGF↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 2, Imm↑, 1, NF-kB↓, 1, NF-kB↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↝, 1, eff↑, 7, RadioS↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
CEA↓, 1, EGFR↑, 1, HER2/EBBR2↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, OS↑, 1, Pin1↓, 1, Risk↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, Bacteria↓, 1,
Total Targets: 80
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 8, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 7, Catalase↑, 3, DPPH↓, 1, GPx↑, 1, GSH↑, 3, GSR↑, 2, HO-1↑, 1, Keap1↑, 1, lipid-P↓, 4, MDA↓, 2, NRF2↑, 1, ROS↓, 6, ROS⇅, 1, SOD↑, 4, TAC↑, 1, TBARS↓, 1, uricA↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
glucose↓, 1, LDL↓, 1, NADPH↑, 1, PPARγ↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Cyt‑c↓, 1, iNOS↓, 2, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1, other↝, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↓, 1, GSK‐3β↓, 2, tyrosinase↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, 5LO↝, 1, AntiAg↑, 2, MMP13↓, 1, Snail↑, 1, Twist↑, 1, Tyro3↓, 1, VCAM-1↓, 1, Vim↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 2, TXA2↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 5, GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX1↓, 1, COX2↓, 3, ICAM-1↓, 1, IL17↓, 1, IL1β↓, 4, IL4↓, 1, IL6↓, 3, IL6↑, 1, Imm↑, 3, Inflam↓, 11, MUC2↓, 1, NF-kB↓, 2, PGE2↓, 3, TNF-α↓, 3,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 3, BChE↓, 2, BDNF↑, 1, tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 3, BACE↓, 2, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 5, BioEnh↑, 1, Dose↝, 2, eff↑, 4, Half-Life↝, 1, P450↓, 2,
Clinical Biomarkers(tgid=22) ⓘ
BP↓, 1, creat↓, 1, GutMicro↑, 1, IL6↓, 3, IL6↑, 1, MUC19↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 5, Bone Healing↑, 1, cardioP↑, 4, cognitive↑, 1, hepatoP↑, 4, memory↑, 2, motorD↑, 1, neuroP↑, 6, Obesity↓, 1, Pain↓, 2, PDE4↓, 1, RenoP↑, 1, toxicity↓, 4, toxicity↑, 1, Wound Healing↑, 4,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 14, AntiViral↑, 5, Bacteria↓, 6, Bacteria↑, 1, CD8+↑, 1,
Total Targets: 107
Scientific Paper Hit Count for: AntiFungal, AntiFungal
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#:1382 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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