Weight Cancer Research Results
Weight, Weight: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
OS↑, Results indicate that the AgNPs were efficient in prolongation of life span, reduction of tumor volume and body weight in tumor animals.
TumVol↓,
Weight↑,
AntiTum↑, AgNPs are potent in antitumor activity and the molecular mechanism is by the induction of apoptosis through the mitochondrial dependent and independent pathways.
Apoptosis↑,
mtDam↑,
TumVol↓, incidence and size of fibrosarcoma were reduced or delayed when murine fibrosarcoma groups were treated by AgNP-MSA
TNF-α↓, TNF-α, IL-6 and IL-1β these cytokines were found to be downregulated after treatment with AgNP-MSA
IL6↓,
IL1β↓,
*toxicity↝, liver sections were found to have normal architecture in all treated groups except those treated at the 9 and 10 mg/kg b.w. doses
TumCG↓, treatment with AgNPs, the logistic growth of the tumor incidence was significantly lower (
selectivity↑, MSA-AgNPs aggregated instantly in response to the acidic extracellular pH of solid tumors, leading to greatly enhanced uptake by cancer cells
selectivity↑, Because the particle size in the study was approximately 10 nm, any AgNP that escaped entry into the tumor microenvironment and entered the systemic circulation was effectively cleared from the body.
Weight↑, AgNP-MSA not only inhibited the tumor incidence but also helped to overcome the progressive body weight loss of tumor-bearing mice.
ROS↑, anticancer property demonstrated by AgNP can be attributed to this increase in oxidative stress in the tumor microenvironment.
NO↑, AgNPs significantly increased the oxygen free radical and NO levels in the tumor microenvironment, which oppose hypoxia.
OS↑, >9 years
Weight↑, up 30 lbs
TumVol↓, PET/CT scan
*cachexia↓, The results of this process favored L-carnitine supplementation in patients with cancer-related cachexia.
*Apoptosis↓, inhibiting apoptosis or reversing inflammatory processes.
*Inflam↓,
QoL↑, This treatment increased plasma-free carnitine concentrations and significantly improved fatigue, which was assessed using the functional assessment of cancer therapy, fatigue, and quality of life questionnaire, as well as quality-of-life measu
Dose↝, placebo-controlled trial, in which 2 g per day of LC was administrated orally for four weeks among eligible patients.
Weight↑, advanced pancreatic cancer received either LC (4 g/day orally) or a placebo for 12 weeks. The results showed that body mass index, nutritional status (body cell mass and body fat), and quality-of-life parameters increased
OS↝, There was an insignificant increase in overall survival, a decline in length of hospital stays, and decrease in fatigue among the LC-treated patients.
fatigue↓,
eff↝, some dietary factors, such as food intake restriction and intake of LC and certain micronutrients (vitamin C, vitamin B6, and iron, which are required as cofactors for endogenous LC biosynthesis) may have some effects on the efficacy of LC sup
Weight↑, During treatment body-mass-index increased by 3,4 ± 1,4% under L-Carnitine and decreased (−1,5 ± 1,4%) in controls
QoL↑, Moreover, nutritional status (body cell mass, body fat) and quality-of-life parameters improved under L-Carnitine.
OS↑, There was a trend towards an increased overall survival in the L-Carnitine group (median 519 ± 50 d versus 399 ± 43 d, not significant) and towards a reduced hospital-stay (36 ± 4d versus 41 ± 9d,n.s.).
Diar↓, Treatment with BJe decreased the appearance of diarrhea and body weight loss.
Weight↑,
NF-kB↓, BJe reduced nuclear NF-κB translocation, p-JNK activation, the pro-inflammatory cytokines release, the appearance of nitrotyrosine and PAR in the colon and reduced the up-regulation of ICAM-1 and P-selectin.
p‑JNK↓,
ICAM-1↓,
eff↝, beneficial effects of caffeic acid and ellagic acid were dependent upon the gut microbiota.
eff↑, caffeic acid, ferulic acid, and ellagic acid were also able to significantly ameliorate the severity of colitis, including reduced weight loss, decreased DAI score, relief of colon shortening and lower infiltration of inflammatory cell in the colonic
Weight↑,
*antiOx↑, Carnosic acid (CA) has been reported to possess antioxidative properties
*Weight↑, CA significantly prevented the loss of body weight and shortening of colon length in acute colitis induced by dextran sodium sulfate (DSS).
*p65↓, CA decreased the activation of p65 and c-Jun signalling.
*cJun↓,
*NLRP3↓, CA inhibited DSS-induced NLRP3 inflammasome activation by reducing caspase 1 activity.
*Casp1↓,
*NRF2↑, CA increased the level of Nrf2 and prevented the degradation of Nrf2 via ubiquitination by blocking the interaction between Cullin3 and Keap1,
*GSH↑, Finally, GSH levels and SOD activity were increased after CA treatment, while MDA and iNOS levels were significantly reduced.
*SOD↑,
*MDA↓,
*iNOS↓,
other↝, Moreover, many compounds from natural products, such as ellagic acid, gallic acid and quercetin, have been shown to prevent IBD through their antioxidative properties
Apoptosis↑, It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity,
TumCCA↑, accumulation of cells in the G1 phase, together with a reduction of cells in the S phase, slowing cell cycle/mitosis and provoking cell death.
TumMeta↓,
TumCP↓, antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
eff↑, carvacrol appears to be more potent than thymol
*Inflam↓, these compounds present anti-inflammatory (Li et al., 2018; Chamanara et al., 2019) and antioxidant
*antiOx↑,
AXL↓, These effects occurred mainly through the inhibition of tyrosine kinase receptor (AXL) expression and an increase in malondialdehyde (MDA
MDA↑,
Casp3↑, caspase-3 activation and Bcl-2 inhibition
Bcl-2↓,
MMP2↓, promoted a decrease in Bcl-2, metalloproteinase-2 and -9 (MMP-2 and MMP-9), p-ERK, p-Akt, cyclin B1 levels and an increase in p-JNK, Bax levels, resulting in cell cycle arrest at the G2/M phase
MMP9↓,
p‑JNK↑,
BAX↑,
MDA↓, In respect of breast cancer, treatment with carvacrol decreases MDA-MB231 (Jamali et al., 2018; Li et al., 2021) and MCF-7 cells line viability
TRPM7↓, TRPM7 pathway is one of the suggested pharmacological mechanisms of action
MMP↓, decreased mitochondrial membrane potential, cytochrome C release, caspase activation, PARP cleavage
Cyt‑c↑,
Casp↑,
cl‑PARP↑,
ROS↑, Carvacrol also induced cytotoxicity and apoptosis (via caspase-3 and reactive oxygen species—ROS) of human oral squamous cell carcinoma (OC2 cell line)
CDK4↓, In tongue cancer (Tca-8113, SCC-25 cell lines), Dai et al. (2016) reported that carvacrol effectively inhibited cell proliferation through the negative regulation of CCND1 and CDK4 expression, and the positive regulation of p21 expression,
P21↑,
F-actin↓, A blockade of TRPM7 channels, reduced expression of MMP-2 and F-actin, was also observed, together with the inhibition of PI3K/Akt and MAPK
GSH↓, by increasing ROS, Bax, Caspase-3, -9 levels and reducing Bcl-2 and GSH levels.
*SOD↑, Moreover, carvacrol was able to increase the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH), along with a reduction of lipid peroxides and the enzymes AST, ALT, AL
*Catalase↑,
*GPx↑,
*GSR↑,
*GSH↑,
*lipid-P↓,
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
DNAdam↑, hepatocellular carcinoma induced by diethylnitrosamine (DEN), carvacrol treatment promoted DNA fragmentation
AFP↓, carvacrol showed a reduction in serum levels of alpha-fetoprotein (AFP), alpha l-fucosidase (AFU), vascular endothelial growth factor (VEGF
VEGF↓,
Weight↑, Carvacrol supplementation significantly improved the weight gain and growth rate of animals with colon cancer
*chemoP↑, reduction in oxidative stress damage (higher levels of GSH, GPx, GR, SOD and CAT), suggesting that carvacrol presents chemopreventive effects
ROS↑, In vitro, carvacrol and thymol increased the generation of reactive oxygen species in 24.63% (n = 17) of the studies, a fact that is also observed in chemotherapeutics
| - |
vitro+vivo, |
Lung, |
A549 |
|
|
|
- |
in-vitro, |
Nor, |
BEAS-2B |
|
|
|
- |
in-vitro, |
Lung, |
PC9 |
|
|
|
Dose↝, prepare a carvacrol nanoemulsion (CANE) using an ultrasonication technique and further evaluation of its anticancer potential against human lung adenocarcinoma A549 cells. (160nm)
mt-ROS↑, The CANE induced reactive oxygen species (ROS) production in A549 cells,
p‑JNK↑, leading to activation of key regulators of apoptosis such as p-JNK, Bax and Bcl2 as well as release of cytochrome C, and activation of the caspase cascade.
BAX↑,
Cyt‑c↑,
Casp↑,
AntiTum↑, CANE displayed a strong antitumor potential in vivo using an athymic nude mice model.
ER Stress↑, Abnormally high ROS levels create ER stress with the involvement of three major signaling proteins IRE1-α, PERK and ATF-6
LDH↑, higher LDH activity, which is a well-established biomarker released by damaged cells, was observed in CANE-treated cells
selectivity↑, CANE displayed no cytotoxicity up to 100 µg/ml against normal bronchial epithelium cells (BEAS-2B)
Apoptosis↑, Induction of apoptosis and ROS production in the presence of CANE
DNAdam↑, potential role on DNA damage and chromatin condensation
IRE1↑, We observed a higher expression of IRE1-α in CANE treated cells
XBP-1↑, similar expression pattern for XBP-1
CHOP↓, down-regulation of CHOP, p-eIF2α, and GRP78 was observed in CANE-treated cells
p‑eIF2α↓,
GRP78/BiP↓,
Ca+2↑, increase of Ca+2 levels in CANE-treated cells. A 2.5 fold higher Ca+2 was observed at 100 μg/ml CANE treated cells
MMP↓, CANE severely altered mitochondrial membrane potential (Δψm) in a dose-dependent manner.
Bcl-2↓, up- and down-regulation of pro-apoptotic (Bax) and anti-apoptotic (Bcl2) proteins
Casp3↑, higher levels of cleaved caspase-9 and caspase-3 in cells treated with CANE in a dose-dependent manner
Casp9↑,
eff↓, To confirm this, A549 cells were first treated with N-acetyl-L-cysteine NAC (5 mM), a strong scavenger of ROS, prior to CANE (100 µg/ml) treatment and observed a marked reduction in ROS generation
TumW↓, A significant (p < 0.05) 34.2 and 62.1% reduction in tumor weight was observed in the mice treated with 50 and 100 mg/Kg CANE, orally three times in a week
Weight↑, body weights of 100 mg/kg CANE treated mice remained static up to the second week and increased further up to 4 weeks
eff↑, ultrasonication consider as simple, cost-effective, clean and prompt aseptic technique16, wherein large droplets ruptured into small droplets by ultrasound leading to the formation of nano-scale droplets
eff↑, We selected polysorbate 80 as a surfactant (HLB, 15), which is regarded as safe for using in pharmaceutical and food industries1
Dose∅, 10 grams with each meal, every eight hours, and omeprazole 40 mg every 12 hours
Weight↑,
OS↑,
| - |
Case Report, |
Thyroid, |
NA |
|
|
|
OS↑,
Weight↑, increasing health
Dose∅, 1-1.5g for 20kg boy
eff↑, when his treatment formally began; he also received omeprazol, 20 mg and sucralfate, 500 mg a day.
Weight↑, alleviated loss of body weight
Th17↓,
STAT3↓, potential of magnolol for treating MS as novel STAT3 inhibitor.
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the
same RMF can also selectively kill cultured human glioblastoma and
non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the
growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were
activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of
Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly
associated with increased calcium tunnel activity and intracellular Ca2+
level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the
damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF
delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the
health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,
| - |
in-vivo, |
GC, |
HL-60 |
|
|
|
- |
in-vivo, |
GC, |
SK-HEP-1 |
|
|
|
OS↑, 8months compared to 3-5 normally
Pain↓, low-frequency rotary MFs improved abdominal pain in 9/21 (42.9%), nausea/vomiting in 4/21 (19.0%), weight loss in 11/21 (52.4%), ongoing blood loss in 2/21 (9.5%), physical strength in 5/21 (23.8%), and sleep quality in 4/21 (19.0%) patients.
ChemoSideEff↓,
Weight↑,
Strength↑,
Sleep↑,
QoL↑, higher proportion of participants with improved HRQOL, stable disease, and increased serum p53 levels
P53↑,
OS↑, The PFS time in the study group was significantly longer than that of the control group (p < 0.05).
Cyt‑c↝, Serum cytochrome c levels were non-significantly decreased in the study group
other↝, β-phenylethyl isothiocyanate (PEITC) is a phytochemical naturally present in cruciferous vegetables such as watercress, broccoli, wasabi, and cabbage
ROS↑, PEITC was selectively toxic to numerous types of cancer cells via reactive oxygen species, (ROS)-mediated mechanisms
selectivity↑,
P21↑, PEITC led to increased oxidative stress, nuclear translocation of p53 and p21, and cell cycle arrest in TP53-mutated oral cancer cells
TumCCA↑,
Dose↝, PEITC at 5 or 10 mg per kg body weight can slow down tumor growth and prolong the survival of cancer-bearing mice along with increased p53 expression
BioAv↑, Nutri-PEITC Jelly containing 40 mg of PEITC per day can be absorbed rapidly within a few hours and eliminated completely within 24 h
Weight↑, the Nutri-PEITC Jelly group had a significantly higher proportion of participants with improved BMI than that of the placebo control group (40% vs. 20%, p < 0.05)
chemoP↑, Therefore, Nutri-PEITC Jelly at the dose of 20 mg/day of PEITC did not inhibit the disease progression and the clinical application of this product is rather a functional food for tertiary chemoprevention than a therapy.
*SIRT1↑, Here we show that resveratrol, the activator of Sirt1, could alleviate the bowel inflammation induced by irradiation and the expression of Sirt1 is consistent with the inflammation level.
*radioP↑,
*NLRP3↓, against radiation-induced inflammatory bowel disease via NLRP-3 inflammasome repression in mice and supports Sirt1 as a potential biomarker
*Weight↑, The weight of C57BL / 6 mice in each group treated with resveratrol gradually increased from the 6th day after irradiation, while the weight of C57BL/6 mice in the irradiation group still showed a downward trend.
*IL1β↓, Resveratrol Inhibited the Expression of IL-1β and NLRP-3 in Spleen and Thymus
| - |
in-vitro, |
BC, |
4T1 |
|
|
|
- |
in-vivo, |
BC, |
4T1 |
|
|
|
*antiOx↑, Silymarin (SLM) has been extensively investigated due to its potent antioxidant properties and demonstrated efficacy against cancer cells.
ROS↑, we hypothesized that the simultaneous administration of iron (Fe) could alter the antioxidant characteristic of SLM nanoliposomes (SLM Lip) to a prooxidant state
OS↑,
Weight↑,
TumVol↓,
eff↑, In the current study, silymarin nanoliposomes showed higher toxicity on 4 T1 cells when combined with iron sucrose.
Fenton↑, By exchanging iron species during the Fenton reaction (Fe3+ ↔ Fe2+), the ROS levels could increase
TumVol↓, tumors were reduced over 25% in diameter
Remission↑, The effective rate was 63.3%, remission rate 36.9%, survival rate of one year 47.3%.
OS↑,
QoL↑, After treatment the life quality of patients were greatly improved
Weight↑, The patients got better appetite and their body weights were increased
*toxicity∅, It had no harmful effects on peripheral blood picture, heart, kidney and liver. Shikonin mixture is safe and effective for later-stage cancer
Showing Research Papers: 1 to 19 of 19
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Fenton↑, 1, GSH↓, 1, MDA↓, 1, MDA↑, 1, ROS↑, 6, mt-ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, MMP↓, 3, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
LDH↑, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 3, BAX↑, 2, Bcl-2↓, 2, Casp↑, 2, Casp3↑, 3, Casp9↑, 1, Cyt‑c↑, 2, Cyt‑c↝, 1, p‑JNK↓, 1, p‑JNK↑, 2, MAPK↓, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
BowelM↑, 1, ChrMod↑, 1, other↝, 2,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, p‑eIF2α↓, 1, ER Stress↑, 1, GRP78/BiP↓, 1, IRE1↑, 1, XBP-1↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, P21↑, 2, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
mTOR↓, 1, PI3K↓, 1, STAT3↓, 1, TRPM7↓, 1, TumCG↓, 2,
Migration ⓘ
AXL↓, 1, Ca+2↑, 2, F-actin↓, 1, MMP2↓, 1, MMP9↓, 1, TumCP↓, 1, TumMeta↓, 3,
Angiogenesis & Vasculature ⓘ
NO↑, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 1, DCells↑, 1, ICAM-1↓, 1, IL1β↓, 1, IL6↓, 2, Imm↑, 1, NF-kB↓, 1, Th17↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, Dose↝, 3, Dose∅, 2, eff↓, 1, eff↑, 6, eff↝, 2, selectivity↑, 5,
Clinical Biomarkers ⓘ
AFP↓, 1, IL6↓, 2, LDH↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiTum↑, 2, Appetite↑, 1, breath↑, 1, chemoP↑, 2, ChemoSideEff↓, 1, fatigue↓, 1, hepatoP↑, 1, OS↑, 9, OS⇅, 1, OS↝, 1, Pain↓, 3, QoL↑, 5, radioP↑, 1, Remission↑, 1, Sleep↑, 2, Strength↑, 3, toxicity↓, 1, TumVol↓, 5, TumW↓, 1, Weight↑, 17,
Infection & Microbiome ⓘ
CD8+↑, 1, Diar↓, 1,
Total Targets: 94
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↑, 1, GPx↑, 1, GSH↑, 2, GSR↑, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, SOD↑, 2,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 1, LDH↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 1, Casp1↓, 1, iNOS↓, 1,
Transcription & Epigenetics ⓘ
cJun↓, 1,
DNA Damage & Repair ⓘ
P53↓, 1,
Cell Cycle & Senescence ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State ⓘ
mTOR↓, 1,
Migration ⓘ
β-Endo↑, 1,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 1, Inflam↓, 2, p65↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↓, 1,
Protein Aggregation ⓘ
NLRP3↓, 2,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, BMD↑, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, cachexia↓, 1, chemoP↑, 1, OS↑, 1, radioP↑, 1, toxicity↝, 1, toxicity∅, 1, Weight↑, 2,
Total Targets: 39
Scientific Paper Hit Count for: Weight, Weight
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#:603 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
Home Page