ALP Cancer Research Results

ALP, Alkaline Phosphatase: Click to Expand ⟱

Source:

Type: enzyme

ALP (Alkaline Phosphatase) is an enzyme found in the body, and elevated levels of ALP in the blood can be associated with various conditions, including cancer.
Elevated ALP: Bone, Liver, pancreatic, breast, CRC, Prostate, thyroid, kidney, GI, Neuroblastoma

Used as a clinical biomarker for Liver function

Scientific Papers found: Click to Expand⟱

4390-

AgNPs,

Therapeutic Potential of Cucumis melo (L.) Fruit Extract and Its Silver Nanopartciles Against DEN-Induced Hepatocellular Cancer in Rats

in-vivo,

Liver,

 Wistar rats were divided into six groups and hepatic cancer was induced with 0.01% DEN (diethylnitrosamine) through drinking water for 16 weeks.

hepatoP↑, Treatment with crude extract and silver nanoparticles of Cucumis melo fruit indicates that Cucumis melo fruit could have exerted its protective effect.
AST↓, AST ALT, ALP, LDH, GGT
ALAT↓,
ALP↓,

3446-

ALA,

CUR,

The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression

in-vivo,

Nor,

Curc (200 mg/kg p. o.) and/or Lip acid (100 mg/kg i. p.)

rats

*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments

2677-

BBR,

Liposome-Encapsulated Berberine Alleviates Liver Injury in Type 2 Diabetes via Promoting AMPK/mTOR-Mediated Autophagy and Reducing ER Stress: Morphometric and Immunohistochemical Scoring

in-vivo,

Diabetic,

Rats

*hepatoP↑, berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM)
*LC3II↑, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats.
*Beclin-1↑,
*AMPK↑,
*mTOR↑,
*ER Stress↓, It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation.
*CHOP↓,
*JNK↓,
*ROS↓,
*Inflam↓,
*BG↓, Oral supplementation of diabetic rats either by Lip-BBR or Vild, 10 mg/kg of each, significantly (p < 0.001) lowered the blood glucose levels of tested diabetic rats compared to the diabetic group.
*SOD↑, when the diabetic rats received Lip-BBR, the decrements were less pronounced compared to the diabetic group by 1.16 fold, 2.52 fold, and 67.57% for SOD, GPX, and CAT, respectively.
*GPx↑,
*Catalase↑,
*IL10↑, Treatment of the diabetic rats with Lip-BBR significantly (p < 0.001) elevated serum IL-10 levels by 37.01% compared with diabetic rats.
*IL6↓, Oral supplementation of Lip-BBR could markedly (p < 0.0001) reduce the elevated serum levels of IL-6 and TNF-α when it is used as a single treatment by 55.83% and 49.54%,
*TNF-α↓,
*ALAT↓, ALT, AST, and ALP in the diabetic group were significantly higher (p < 0.0001) by 88.95%, 81.64%, and 1.8 fold, respectively, compared with those in the control group, but this was reversed by the treatment with Lip-BBR
*AST↓,
*ALP↓,

5633-

BCA,

Mechanisms Behind the Pharmacological Application of Biochanin-A: A review

Review,

Var,

Review,

AD,

*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.

3517-

Bor,

Se,

The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats

in-vivo,

Nor,

rats + Cyclophosphamide (CP) is an alkylating anticancer drug

*hepatoP↑, However, it was found that Se protects the liver slightly better against CP damage than B
*ALAT↓, statistically significant difference was observed in the serum levels of ALT, AST, ALP, TAS, TOS and OSI.
*AST↓,
*ALP↓,
*NF-kB↓, A statistically significant difference was observed in serum levels of NF-kB, TNF-α, IL -1β, IL -6 and IL -10 when the Se + CP and B + CP-treated groups were compared with the CP-treated group
*TNF-α↓, fig 9
*IL1β↓,
*IL6↓,
*IL10↑,
*SOD↑, A statistically remarkable change in serum levels of SOD, CAT, GPx, MDA and GSH was observed in the group receiving only CP compared to groups Se, B and the control.
*Catalase↑,
*MDA↓, Fig 10
*GSH↑,
*GPx↑,
*antiOx↑, suggests that B and Se increase intracellular antioxidant status.
*NRF2↑, Se and B treatment can protect rat liver tissue from CP-induced oxidative stress, inflammation, and apoptosis by regulating Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways.
*Keap1↓,

3510-

Bor,

Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks

in-vivo,

Nor,

ostrich chicks

*RenoP↑, Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney
*ROS↓, The low doses regulate the oxidative and enzyme activity in the kidney.
*antiOx↑, boron at low doses upregulated the expression of genes involved in the antioxidant pathway
*Apoptosis↓, low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick's kidney
*NRF2↑, maximum localization of Nrf2 in 80 mg/L BA dose group
*HO-1↑, As the boron concentration increased, the expression of Nrf2, GCLc, and HO-1 genes upregulated
*MDA↓, In comparison to those of the group 1, MDA content (lipid peroxidation marker) was significantly decreased by 26.02 and 48.12% in the 40 and 80 mg/L BA groups
*lipid-P↓,
*GPx↓, GSH-PX activity of ostrich chick kidney tissue was slightly increased in the 40 and 80 mg/L BA groups,
*Catalase↑, supplementation of low doses of boron in the ostrich drinking water has resulted in stimulation of antioxidant capacity of GR, CAT, and SOD significantly.
*SOD↑,
*ALAT↓, boron supply in low doses (especially 80 mg/L BA) showed decrease levels in the activity of ALT, AST, and ALP.
*AST↓,
*ALP↓,

5887-

CAR,

TV,

Antitumor Effects of Carvacrol and Thymol: A Systematic Review

Review,

Var,

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

5909-

CAR,

Potential preventive effect of carvacrol against diethylnitrosamine-induced hepatocellular carcinoma in rats

*AST↓, Carvacrol supplementation (15 mg/kg body weight) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑,
*Catalase↑,
*GSH↑,
*GPx↑,
*GSR↑,
*hepatoP↑, These findings suggest that carvacrol prevents lipid peroxidation, hepatic cell damage, and protects the antioxidant system in DEN-induced hepatocellular carcinogenesis.
*lipid-P↓,

5894-

CAR,

Targeting Gastrointestinal Cancers with Carvacrol: Mechanistic Insights and Therapeutic Potential

Review,

Var,

AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.

2785-

CHr,

Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin

Review,

Var,

*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,

1607-

EA,

Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions

Review,

GC,

STAT3↓, EA inhibits STAT3 signaling
TumCP↓, EA inhibits cell proliferation, induces apoptosis
Apoptosis↑,
NF-kB↓, inhibiting nuclear factor-kappa B
EMT↓, suppressing epithelial–mesenchymal transition
RadioS↑, In liver cancer, EA exhibits radio-sensitizing effects
antiOx↑, As a potential antioxidant agent,
COX1↓, EA suppresses the expression of several factors, including COX1, COX2, c-myc, snail, and twist1
COX2↓,
cMyc↓,
Snail↓,
Twist↓,
MMP2↓, significantly decreased MMP-2 and MMP-9 expression and activity.
P90RSK↓,
CDK8↓, downregulate CDK8 expression and activity
PI3K↓, inactivating PI3K/Akt signaling
Akt↓,
TumCCA↑, promote cell cycle arrest
Casp8↑, ctivating caspase-8, and lowering proliferating cell nuclear antigen (PCNA) expression,
PCNA↓,
TGF-β↓,
Shh↓, suppression of the Akt, Shh, and Notch pathways, EA can prevent the growth, angiogenesis, and metastasis of pancreatic cancer
NOTCH↓,
IL6↓,
ALAT↓, decreasing liver injury biomarkers such as alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST)
ALP↓,
AST↓,
VEGF↓,
P21↑,
*toxicity∅, no toxicity was found for a 50% effective dose by the intraperitoneal route inferior to 1 mg/kg/day
*Inflam↓, ncluding anti-inflammatory [10], anti-oxidant [11], anti-allergic [12], and anti-mutagenic [13] properties, as well as potential health advantages like gastroprotective [14], cardioprotective [15], neuroprotective [16, 17], and hepatoprotective [18,
*cardioP↑,
*neuroP↑,
*hepatoP↑,
ROS↑, Exposure to EAs induced apoptosis, accelerated cell cycle arrest, and elevated the generation of reactive oxygen intermediates [59].
*NRF2↓, As a potential antioxidant agent, it scavenges reactive oxygen species (ROS), and by upregulating of Nrf2,
*GSH↑, Moreover, EA increases reduced glutathione (GSH), which is critical for cellular defense against oxidative stress and liver damage,

1606-

EA,

Ellagic acid inhibits proliferation and induced apoptosis via the Akt signaling pathway in HCT-15 colon adenocarcinoma cells

in-vitro,

Colon,

HCT15

20-120 uM

TumCP↓,
cycD1/CCND1↓,
Apoptosis↑,
PI3K↓, strong inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt pathway by EA
Akt↓,
ROS↑, production of reactive oxygen intermediates, which were examined by 2,7-dichlorodihydrofluorescein diacetate (H2DCF-DA), increased with time, after treatment with EA
Casp3↑, EA promoted the expression of Bax, caspase-3, and cytochrome c, and suppression of Bcl-2 activity in HCT-15 cells
Cyt‑c↑,
Bcl-2↓,
TumCCA↑, induces G2/M phase cell cycle arrest in HCT-15 cells
Dose∅, since 60 lM of the drug concentration could cause attentional loss of cells (60 and 45 % were viable in 12 and 24 h treatment, respectively) for crucial experiments, we used this dosage to assess the effect of EA in killing HCT-15 cells
ALP↓, significant decrease in the activity of ALP at 60 lM concentration of EA for the 12 h treatment
LDH↓, decrease in the activity of LDH in cells was proportional to increase in the incubation time with EA.
PCNA↓, EA down-regulated the expressions of PCNA and cyclin D1
P53↑, EA promoted p53 gene expression
Bax:Bcl2↑, increase in the Bcl-2/Bax ratio

4022-

FulvicA,

Chemo,

Shilajit potentiates the effect of chemotherapeutic drugs and mitigates metastasis induced liver and kidney damages in osteosarcoma rats

in-vivo,

OS,

AST↓, Co-treatment of shilajit and drug cocktails also markedly alleviated histopathological changes in liver and kidney tissues.
ALAT↓, (AST)* and alanine aminotransferase (ALT), alkaline phosphatase (ALP), total proteins, albumin, bilirubin, creatinine, urea, and uric acid.
ALP↓,
Bil↝,
creat↓,
uricA↓,
ChemoSen↑, shilajit may potentiate the effects of chemotherapy drugs and mitigate the metastasis-induced liver and kidney damage in osteosarcoma.
chemoP↑,

2868-

HNK,

Honokiol: A review of its pharmacological potential and therapeutic insights

Review,

Var,

Review,

Sepsis,

*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2Î±, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786â0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice

3842-

Moringa,

Bioactive Components in Moringa Oleifera Leaves Protect against Chronic Disease

Review,

Var,

Review,

AD,

*antiOx↑, rich in antioxidants
*ROS↓, MO leaves also protect against oxidative stress [14], inflammation [15], hepatic fibrosis [16], liver damage [17], hypercholesterolemia [18,19], bacterial activity [20], cancer [14] and liver injury [21].
*hepatoP↑, methanol extract of MO leaves has a hepatoprotective effect, which might be due to the presence of quercetin
*lipid-P↓, reductions in lipids and lipid peroxidation levels in the liver of rats
*ALAT↓, MO leaves have been shown to reduce plasma ALT, AST, ALP and creatinine [82,83] and to ameliorate hepatic and kidney damage induced by drugs.
*AST↓,
*ALP↓,
*creat↓,
*RenoP↑,
NF-kB↓, MO was shown to contain the growth of pancreatic cancer cells, by inhibiting NF-ĸB signaling as well as increasing the efficacy of chemotherapy, by enhancing the effect of the drug in these cells
ChemoSen↑,
*memory?, MO, have been demonstrated to enhance memory by nootropics activity and protect against the oxidative stress present in AD

3844-

Moringa,

Review of the Safety and Efficacy of Moringa oleifera

Review,

NA,

*antiOx↑, biological activities including antioxidant, tissue protective (liver, kidneys, heart, testes, and lungs), analgesic, antiulcer, antihypertensive, radioprotective, and immunomodulatory actions.
*RenoP↑,
*hepatoP↑,
*radioP↑, Two studies have shown that extracts of M. oleifera can provide radioprotection in mice.
*eff↑, leaves are widely used as a basic food because of their high nutrition content
*toxicity↓, authors concluded that consumption of M. oleifera leaves at doses of up to 2000 mg/kg were safe.
*ROS↓, Chumark et al. (2008) demonstrated the free radical scavenging ability of an aqueous extract of M. oleifera leaves in several in vitro systems, and also showed that the extract inhibited lipid peroxidation in both in vitro and ex vivo systems.
*lipid-P↓,
*DNAdam↓, inhibit oxidative damage to DNA
*Catalase↑, increased the antioxidant enzymes catalase and superoxide dismutase while decreasing lipid peroxidases
*SOD↑,
*GPx↑, increases in the antioxidant enzymes glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase, and glutathione S‐transferase (Sreelatha and Padma, 2010).
*GSR↑,
*GSTs↑,
*AST↓, M. oleifera leaves protects against liver damage as demonstrated by reductions in tissue histopathology and serum activities of marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP)
*ALAT↓,
*ALP↓,
*Bil↓, extract decreased drug‐induced levels of AST, ALT, ALP, and bilirubin

1660-

PBG,

Emerging Adjuvant Therapy for Cancer: Propolis and its Constituents

Review,

Var,

MMPs↓, inhibition of matrix metalloproteinases, anti-angiogenesis
angioG↓,
TumMeta↓, prevention of metastasis, cell-cycle arrest
TumCCA↑,
Apoptosis↑,
ChemoSideEff↓, moderation of the chemotherapy-induced deleterious side effects
eff∅, components conferring antitumor potentials have been identified as caffeic acid phenethyl ester, chrysin, artepillin C, nemorosone, galangin, cardanol, etc
HDAC↓, Taiwanese green propolis extract was used to develop an anticancer agent NBM-HD-3, a histone deacetylase inhibitor (HDACis).
PTEN↑, found to increase phosphatase and tensin homolog (PTEN) and protein kinase B (Akt) protein levelssignificantly, while decreasing phospho-PTEN and phospho-Akt levels markedly
p‑PTEN↓,
p‑Akt↓,
Casp3↑, Propolis induced apoptosis and caspase 3 cleavage, increased phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2), protein kinase B/Akt1 and focal adhesion kinase (FAK).
p‑ERK↑,
p‑FAK↑,
Dose?, When administered orally for 20 weeks at a dose of 100-300 mg/kg, the protective role against the lingual carcinogenesis was observed
Akt↓, treatment reduced the protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3Î², FOXO1, FOXO3a, phospho-FOXO1
GSK‐3β↓,
FOXO3↓,
eff↑, Co-treatment with CAPE and 5-fluorouracil exhibited additive anti-proliferation of TW2.6 cells.
IL2↑, Propolis administration stimulated IL-2 and IL-10 production
IL10↑,
NF-kB↓, reduces the expression of growth and transcription factors, including NF-ÎºB.
VEGF↓, CAPE dose-dependently suppresses vascular endothelial growth factor (VEGF) formation by MDA-231 cells,
mtDam↑, Brazilian red propolis significantly reduced the cancer cell viability through the induction of mitochondrial dysfunction, caspase-3 activity and DNA fragmentation.
ER Stress↑, the action was believed to be due to endoplasmic reticulum stress-related signalling induction of CCAAT/enhancer-binding protein homologous protein (CHOP)
AST↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALAT↓, Rats,(250 mg/kg) thrice a week for 3 weeks
ALP↓, Rats,(250 mg/kg) thrice a week for 3 weeks
COX2↓, Rats,(250 mg/kg) thrice a week for 3 weeks, Expression of COX-2 and NF-kB p65 was significantly lowered
eff↑, co-treatment of cancer cells with 100 ng/mL TRAIL and 50 Î¼g/mL propolis extract increased the percentage of apoptotic cells to about 66% and caused a significant disruption of membrane potential in LNCaP cells (
Bax:Bcl2↑, decreased Bcl-2/Bax ratio

3587-

PI,

Piperine: A review of its biological effects

Review,

Park,

Review,

AD,

*hepatoP↑, piperine has also been documented for its hepatoprotective, anti-allergic, anti-inflammatory, and neuroprotective properties
*Inflam↓,
*neuroP↑,
*antiOx↑, antiangiogenesis, antioxidant, antidiabetic, antiobesity, cardioprotective,
*angioG↑,
*cardioP↑,
*BioAv↑, nano-encapsulation and resulting piperine-loaded nanoparticles enhance the bioavailability of piperine via oral administration
*P450↓, piperine inactivates cytochrome P450 (CYP) 3A (CYP3A), which plays a critical role in drug metabolism
*eff↑, enhances the anti-inflammatory effects when combined with resvera- trol
*BioAv↑, piperine increases the bioavailability of various compounds such as ciprofloxacin, norfloxacin, metronidazole, oxytetracycline, nimesulide, pentobarbitone, phenytoin, resveratrol, beta-carotene, curcumin, gallic acid, tiferron, nevirapine, and sparte
E-cadherin↓, Downregulates the E-cadherin (E-cad), estrogen receptor (ER), matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP- 9), vascular endothelial growth factor (VEGF) levels, and c-Myc.
ER(estro)↓,
MMP2↓,
MMP9↓,
VEGF↓,
cMyc↓,
BAX↑, Increases the expressions of Bax and p53.
P53↑,
TumCG↓, Lowers the tumor growth and elevates survival time
OS↑,
*cognitive↑, piperine ameliorated the neuro-chemical, neuroinflammatory, and cognitive alterations caused by chronic exposure to galactose
*GSK‐3β↓, piperine reversed D-Gal-induced GSK-3Î² activation through modulating PKC and PI3K/AKT pathways, s
*GSH↑, Piperine stimulates glutathione levels in rats' striatum, reduced caspase-3 and 9 activation, and diminished release of cytochrome-c from mitochondria along with a reduction in lipid peroxidation
*Casp3↓,
*Casp9↓,
*Cyt‑c↓,
*lipid-P↓,
*motorD↑, piperine also caused improvement in motor coordination and balance behavior along with reduction in contralateral rotations.
*AChE↓, significantly amended impaired memory and hippo-campus neurodegeneration and lowered lipid peroxidation and acetylcholinesterase enzyme
*memory↑,
*cardioP↑,
*ROS↓, fig 6
*PPARγ↑,
*ALAT↓, piperine lowers alanine aminotransferase (ALT), AST, and ALP levels in sera of cholesterol-fed albino mice
*AST↓,
*ALP↓,
*AMPK↑, reversed the downregulation of AMPK signaling molecules, which are responsible for fatty acid oxidation, insulin signaling, and lipogenesis in mouse liver.
*5HT↑, t causes a significant decrease in serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) contents in the hippocampus and frontal cortex.
*SIRT1↑, , it may enhance the SIRT1 expression in cells and SIRT1 activity enhancing its potential to prevent SIRT1-mediated disease
*eff↑, combination ther- apy of resveratrol and piperine as an approach to enhance the biologi- cal effects with respect to cerebral blood flow and improved cognitive functions

3014-

RosA,

Rosmarinic Acid Supplementation Acts as an Effective Antioxidant for Restoring the Antioxidation/Oxidation Balance in Wistar Rats with Cadmium-Induced Toxicity

in-vivo,

Nor,

rats

*antiOx↑, Rats in Group 4 (cadmium-exposed and Rosmarinic acid-accessed) exhibited increased levels of total proteins, a significant increase in the levels of antioxidant markers including total thiols, glutathione, total antioxidant capacity (TAC),
*Thiols↑,
*GSH↑,
*TAC↑, decreased levels of total thiols, GSH, catalase, and TAC
*SOD↑, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase, and a significant decrease in the levels of blood cadmium, ALP, ALT, AST, creatinine, blood urea nitrogen (BUN), urea, bilirubin, and oxidation markers (H2O2, and MDA
*GPx↑,
*Catalase↑,
*ALP↓,
*ALAT↓,
*AST↓,
*creat↓,
*BUN↓,
*H2O2↓,
*MDA↓,
*ROS↓, significantly help attenuate the oxidative stress induced by cadmium
cardioP↑, benefits of RA are attributed to its anti-cancer, anti-depressive, antiallergic, anti-inflammatory, anti-angiogenic, cardioprotective, hepatoprotective, nephroprotective, neuroprotective, antimicrobial, hypoglycemic, and hypolipidemic bioactivities
hepatoP↑,
neuroP↑,

4757-

Se,

Chemo,

The protective role of selenium on the toxicity of cisplatin-contained chemotherapy regimen in cancer patients

Trial,

NA,

400 μg per day of Se as Seleno-Kappacarrageenan

20 patients with Se administration

Dose↝, The 400 μg per day of Se as Seleno-Kappacarrageenan were administered from 4 before to 4 d after chemotherapy for study cases.
*ALP↓, The urine enzymes NAG, GGT, AAP, and ALP after chemotherapy for cases were significantly lower than the controls.
chemoP↑, No toxicity of Seleno-Kappacarrageenan was noted. The above results suggest that the Se can be used as an agent for reducing the nephrotoxicity and bone marrow suppression induced by cisplatin.

4488-

Se,

Chit,

PEG,

Anticancer effect of selenium/chitosan/polyethylene glycol/allyl isothiocyanate nanocomposites against diethylnitrosamine-induced liver cancer in rats

in-vivo,

Liver,

HepG2

 size ranging from 390 to 450 nm

diethylnitrosamine (DEN)-induced liver cancer in rats

in-vivo,

Nor,

HL7702

tumCV↓, The SCPg-AI-NCs effectively decreased the cell viability and induced apoptosis in the HepG2 cells.
Apoptosis↑,
*GSH↑, The SCPg-AI-NCs treatment effectively decreased the TBARS and improved the GSH, vitamin-C & -E contents in the DEN-induced rats
*VitC↑,
*VitE↑,
*SOD↑, The activities of SOD, GPx, and GR were also improved by the SCPg-AI-NCs treatment in the DEN-induced rats.
*GPx↑,
*GR↑,
ALAT↓, The activities of ALT, ALP, AST, LDH, and GGT was remarkably decreased by the SCPg-AI-NCs treatment in the DEN-provoked liver cancer rats.
ALP↓,
AST↓,
LDH↓,
selectivity↑, same doses of SCPg-AI-NCs did not showed the cytotoxicity to the normal liver HL7702 cells
eff↑, The utilization of nanocomposites as drug delivery systems has a efficacy to solve the several side effects triggered by chemotherapeutic drugs to normal cells

4446-

SeNPs,

Antioxidant and Hepatoprotective Effects of Moringa oleifera-mediated Selenium Nanoparticles in Diabetic Rats.

in-vivo,

Diabetic,

0.25 mg/kg BW of MO-SeNPs

Rats

*glucose↓, MO-SeNPs treatment significantly reduced blood glucose levels (p < 0.05) and restored insulin resistance, with lower dose demonstrating better glycaemic control than larger dose.
*antiOx↑, MO-SeNPs also increased hepatic antioxidant enzyme activity, including GSH-Px, CAT, and T-SOD, which neutralise oxidative stress
*GPx↑,
*Catalase↑,
*SOD↑,
*ROS↓,
*cardioP↑, MO-SeNPs also improves cardiovascular health by raising HDL and lowering LDL.
*HDL↑,
*LDL↓,
*hepatoP↑, MO-SeNPs showed hepatoprotective benefits by lowering inflammatory markers such TNF-α, IL-6, IL-1β, iNOS, and AGEs, and reduced lipid peroxidation.
*TNF-α↓,
*IL6↓,
*IL1β↓,
*lipid-P↓,
*Inflam↓, The reduction in these indicators shows MO-SeNPs reduce liver inflammation and protect the liver.
*ALAT↓, The normalisation of liver enzyme levels (ALT, AST, ALP) showed improved liver function.
*AST↓,
*ALP↓,
*Dose↝, For the aqueous extract, 20 g of powdered leaves were homogenized in 800 mL of boiling distilled water, shaken at 150 rpm for 4 hours, centrifuged at 4000 rpm for 20 minutes, and filtered using Whatman filter paper No. 1 (Cat No. 1001 125) from GE H
*Dose↝, Selenium nanoparticles (MO-SeNPs) were synthesized by adding 5 mL of a 50 mM sodium selenite solution dropwise to 20 mL of Moringa oleifera extract under magnetic stirring, followed by incubation at 37 °C for 48 hours at pH 8 to facilitate the green

4453-

SeNPs,

Selenium Nanoparticles: Green Synthesis and Biomedical Application

Review,

NA,

*toxicity↓, “Green” synthesis has special advantages due to the growing necessity for environmentally friendly, non-toxic, and low-cost methods.
*Bacteria↓, SeNPs are active against both Gram-positive and Gram-negative microorganisms
ROS↑, The cancer cells exhibit an acidic pH and an imbalanced redox state. These conditions in cancer cells initiate the pro-oxidant conversion of SeNPs and trigger the development of free radicals in malignant cells
MMP↓, mitochondrial membrane destruction
ER Stress↑, on the other hand, to stress in the endoplasmic reticulum (ER)
P53↑, Selenium nanoparticles can stimulate p53 expression in cancer cells, leading to caspase-9 activation, mitochondrial membrane potential depletion, and the induction of apoptosis.
Apoptosis↑,
Casp9↑,
DNAdam↑, In addition, in cellular processes, DNA structure is damaged, causing the cell cycle to stop and, ultimately, cell death.
TumCCA↑,
eff↑, positively charged SeNPs may have a strong affinity for breast cancer cells, causing the enhanced anticancer efficacy of SeNPs
Catalase↓, was accompanied by a decrease in antioxidant marker levels (CAT, SOD, GPx activity and GSH levels) in MCF-7 cells exposed to green SeNPs
SOD↓,
GSH↓,
selectivity↓, in contrast to control cells
selectivity↑, SeNPs selectively affect LDH leakage and membrane disruption in cancer cells because the SeNP concentration required to influence LDH leakage in normal cells is much higher compared to that in cancer cells
PCNA↓, SeNPs reduced the PCNA expression level in MCF-7 cells, showing their role in suppressing oncogenesis and proliferation in breast cancer by inhibiting PCNA gene expression
eff↑, Nanoparticle capping can enhance their absorption via accumulation by endocytosis in cancer cells, which can therefore lead to ROS generation induction
*ALAT↓, SeNPs could significantly decrease hepatic (serum ALT, AST, and ALP) and renal (serum uric acid, urea, and creatinine) function markers, total lipid, total cholesterol, triglyceride and low-density lipoprotein cholesterol levels, and glucose-6-phosph
*AST↓,
*ALP↓,
*creat↓,
*Inflam↓, selenium nanoparticles appear to be a possible anti-inflammatory agent.
*toxicity↓, Most studies confirm that SeNPs are less toxic than sodium selenite
selectivity↑, despite affecting cancer cells and causing their death, SeNPs do not harm normal cells,

3572-

TQ,

Enhanced oral bioavailability and hepatoprotective activity of thymoquinone in the form of phospholipidic nano-constructs

in-vivo,

Nor,

TQ, phospholipid nanoconstructs (PNCs)

*BioAv↑, After oral administration of a single dose of PNC, it showed a relative bioavailability of 386.03% vis-à-vis plain TQ suspension
*hepatoP↑, TQ-loaded PNC demonstrated significant enhanced hepato-protective effect vis-à-vis pure TQ suspension and silymarin, as evidenced by reduction in the ALP, ALT, AST, bilirubin, and albumin level and ratified by histopathological analysis.
*ALAT↓,
*ALP↓,
*AST↓,

616-

VitC,

Suppression of alkaline phosphatase in prostate cancer patients by high dose intravenous Vitamin C Treatment: Three cases

Case Report,

NA,

PSA↓,
ALP↓,

Showing Research Papers: 1 to 25 of 25

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 9, Bil↓, 1, Catalase↑, 10, GPx↓, 1, GPx↑, 10, GSH↑, 9, GSR↑, 4, GSTs↑, 1, H2O2↓, 1, HDL↑, 1, HO-1↑, 2, Keap1↓, 1, lipid-P↓, 9, MDA↓, 4, NRF2↓, 1, NRF2↑, 4, ROS↓, 11, SOD↑, 11, TAC↑, 1, Thiols↑, 1, VitC↑, 1, VitE↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 15, AMPK↑, 2, BUN↓, 1, glucose↓, 1, LDH↓, 3, LDL↓, 1, NADPH↓, 1, PPARγ↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Apoptosis↓, 1, Casp3↓, 2, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 1, JNK↓, 1,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, ER Stress↓, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1, LC3II↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1, mTOR↑, 1,

Migration ⓘ

COL3A1↓, 1, p‑Rac1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 1,

Barriers & Transport ⓘ

P-gp↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 2, IKKα↑, 1, IL10↓, 1, IL10↑, 2, IL1β↓, 2, IL6↓, 4, Inflam↓, 8, NF-kB↓, 4, PGE2↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 2,

Protein Aggregation ⓘ

BACE↓, 1,

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1, GR↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 3, Dose↝, 2, eff↑, 3, P450↓, 1,

Clinical Biomarkers ⓘ

ALAT↓, 15, ALP↓, 17, AST↓, 17, BG↓, 1, Bil↓, 1, creat↓, 3, IL6↓, 4, LDH↓, 3,

Functional Outcomes ⓘ

AntiDiabetic↑, 1, cardioP↑, 6, chemoP↑, 1, cognitive↑, 1, hepatoP↑, 12, memory?, 1, memory↑, 2, motorD↑, 1, neuroP↑, 5, Obesity↓, 1, radioP↑, 1, RenoP↑, 4, toxicity↓, 4, toxicity∅, 1,

Infection & Microbiome ⓘ

Bacteria↓, 2,
Total Targets: 92

Scientific Paper Hit Count for: ALP, Alkaline Phosphatase

3 Selenium
3 Carvacrol
2 Boron
2 Ellagic acid
2 Chemotherapy
2 Moringa oleifera
2 Selenium NanoParticles
1 Silver-NanoParticles
1 Alpha-Lipoic-Acid
1 Curcumin
1 Berberine
1 Biochanin A
1 Thymol-Thymus vulgaris
1 Chrysin
1 Shilajit/Fulvic Acid
1 Honokiol
1 Propolis -bee glue
1 Piperine
1 Rosmarinic acid
1 chitosan
1 polyethylene glycol
1 Thymoquinone
1 Vitamin C (Ascorbic Acid)

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#:689  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

ALP Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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