condition found tbRes List
CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown

Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓">NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
147- AG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑,
NF-kB↓,
PI3K/Akt↓,
STAT3↓,

465- CUR,    Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, HUH7 - vitro+vivo, Liver, MHCC-97H
TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

1505- CUR,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
TumCCA↑,
Apoptosis↑,
DNMTs↓, curcumin also inhibits DNMT activities and histone modification such as HDAC inhibition in tumorigenesis
HDAC↓,
HATs↓, inhibitory activity against HDACs and HATs in several in vitro cancer models
TumCP↓,
p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
HDAC1↓,
HDAC3↓,
HDAC8↓,
NF-kB↓, inhibition of nuclear translocation of the NF-κB/p65 subunit

1792- CUR,  LEC,    Chondroprotective effect of curcumin and lecithin complex in human chondrocytes stimulated by IL-1β via an anti-inflammatory mechanism
- in-vitro, Arthritis, RAW264.7 - NA, NA, HCC-38
*Inflam↓, curcumin is well known to regulate anti-inflammatory effects, primarily through the deactivation of NF-κB
*NF-kB↓,
*iNOS↓, 10 and 20 μM, complex also suppressed iNOS and COX-2 mRNA expression and inhibited NO and PGE2 production
*COX2↓,
*NO↓,
*PGE2↓,
*MMPs↑, 10 and 20 μM of the complex (Fig. 2A, B, and C). IL-1β noticeably upregulated the production of MMP-1, 2, 3, 9, and 13 and TIMP-1 compared to the control group
*TIMP1↑,
*BioEnh↑, In this study, the complex of curcumin and lecithin enhanced bioavailability of curcumin resulting in chondroprotective effect at relatively lower concentrations.

1809- CUR,  Oxy,    Long-term stabilisation of myeloma with curcumin
- Case Report, Melanoma, NA
*OS↑, plateaued and has remained stable for the last 5 years with good quality of life.
QoL↑, may help to improve quality of life,
Dose↑, few months later, she also embarked on a once-weekly course of hyperbaric oxygen therapy (90 min at 2 ATA) which she has maintained ever since.
Dose↑, oral curcumin complexed with bioperine (to aid absorption), as a single dose of 8 g each evening on an empty stomach.
IL6↓, curcumin prevents myeloma cell proliferation through inhibition of IL-6-induced STAT-3 phosphorylation
STAT3↓, curcumin downregulated the expression of NFkB, COX-2 and STAT3
NF-kB↓,
COX2↓,

2308- CUR,    Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
- in-vitro, Liver, HepG2
GlucoseCon↓, Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production
lactateProd↓,
ECAR↓,
NO↓,
ROS↑, Curcumin favors the ROS production in HepG2 cells in normal as well as hyperglycemic conditions. ROS production was detected in cancer cells treated with curcumin, or doxorubicin, or their combinations in NG or HG medium for 24 h
HK2↓, HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, tr
PFK1↓,
GAPDH↓,
PKM2↓,
LDHA↓,
FASN↓,
GLUT1↓, Curcumin treatment was able to significantly decrease the expression of GLUT1, HKII, and HIF-1α in HepG2 cells either incubated in NG or HG medium.
MCT1↓,
MCT4↓,
HCAR1↓,
SDH↑, Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition
ChemoSen↑, Curcumin Prevents High Glucose-Induced Chemoresistance
ROS↑, Treatment of cells with doxorubicin in presence of curcumin was found to cooperatively augment the ROS level in cells of both NG and HG groups.
BioAv↑, Curcumin Favors Drug Accumulation in Cancer Cells
P53↑, An increased expression of p53 in curcumin-treated cells can be suggestive of susceptibility towards cytotoxic action of anticancer drugs
NF-kB↓, curcumin has therapeutic benefits in hyperglycemia-associated pathological manifestations and through NF-κB inhibition
pH↑, Curcumin treatment was found to resist the lowering of pH of culture supernatant both in NG as well in HG medium.

2466- CUR,    Regulatory Effects of Curcumin on Platelets: An Update and Future Directions
- Review, Nor, NA
*AntiAg↑, Several studies have proved the beneficial role of curcumin on platelets . in-vivo study exhibited that curcumin inhibited platelet aggregation in monkeys
*antiOx↑, Curcumin exhibits promising antioxidant activity
*Inflam↓,
*12LOX↑, increased the production of 12-LOX
COX1↓, Curcuminoids have been demonstrated to inhibit cyclo-oxygenase and 12-lipoxygenase activities in human platelets, thus showing antioxidant activity
COX2↓, Its effectiveness in cancer is mediated by inhibition of COX-2, MMP-9, and NF-kB
MMP9↓,
NF-kB↓,

484- CUR,  PDT,    Low concentrations of curcumin induce growth arrest and apoptosis in skin keratinocytes only in combination with UVA or visible light
- in-vitro, Melanoma, NA
Cyt‑c↑, release of cytochrome c from mitochondria
Casp9↑,
Casp8↑,
NF-kB↓,
EGFR↓,

485- CUR,  PDT,    Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin
- in-vitro, Melanoma, NA
NF-kB↓,
Casp8↑,
Casp9↑,
p‑Akt↓,
p‑ERK↓,

1411- CUR,  Cisplatin,    Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects
- Review, Var, NA
ChemoSen↑, decreasing CP's adverse impacts and improving its antitumor
*ROS↓, Curcumin administration reduces ROS levels to prevent apoptosis in normal cells.
*NF-kB↓, curcumin can inhibit inflammation via down-regulation of NF-κB to maintain the normal function of organs.
TumCCA↑,

1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, Curcumin downregulates the cyclooxygenase-2 (COX-2) pathway, reducing the production of prostaglandins associated with inflammation
*Inflam↓,
*5LO↓, directly inhibits lipoxygenase (LOX)
*NO↓,
*NF-kB↓,
*TNF-α↓,
*IL1↓,
*IL2↑,
*IL6↓,
*IL8↓,
*IL12↓,
*MCP1↓,
*PGE2↓,
*MMP2↓,
*MMP3↓,
*MMP9↓,
*NLRP3↓,
*ROS↓, arthritis(basically normal cell)

1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,

136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
BAX↑,
BID↑,
PARP↑,
NF-kB↓,
CDK1↓,
COX2↓,
RTK-RAS↓,
PI3K/Akt↓,
EGFR↓,
HER2/EBBR2↓,
P53↑,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓,
Shh↓,
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓,
survivin↓,

13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
NF-kB↝,
Akt↝,
AR↝,
Apoptosis↝,
Bcl-2↝,
Casp3↝,
BAX↝,
P21↝,
ROS↝,
Apoptosis↝,
Bcl-xL↝,
JNK↝,
MMP2↝,
P53↝,
PSA↝,
VEGF↝,
COX2↝,
cycD1↝,
EGFR↝,
IL6↝,
β-catenin/ZEB1↝,
mTOR↝,
NRF2↝,
p‑Akt↝,
AP-1↝,
Cyt‑c↝,
PI3K↝,
PTEN↝,
Cyc↝,
TNF-α↝,

123- CUR,    Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells
- in-vitro, Colon, LoVo - in-vitro, Colon, COLO205 - in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1
NF-kB↓, curcumin analog

124- CUR,    Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TGF-β↓,
Wnt↓,
PI3k/Akt/mTOR↓,
NF-kB↓,
PTEN↑,
Apoptosis↑,

160- CUR,    Curcumin inhibits prostate cancer metastasis in vivo by targeting the inflammatory cytokines CXCL1 and -2
CXCc↓, CXCL1,2
IκB↓,
NF-kB↓,
COX2↓,
SPARC↓,
EFEMP↓,

424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓,
p‑STAT1↓, pSTAT-1
p‑Akt↓,
p‑p44↓, p-p44
p‑p42↓, p-p42
RAS↓,
Raf↓, c-RAF
Vim↓,
β-catenin/ZEB1↓,
P53↓,
Bcl-2↓,
Mcl-1↓,
PIAS-3↑,
SOCS-3↑,
SOCS1↑,
ROS↑,
NF-kB↓, NF-kB inactivation, ROS generation and PA depletion in MCF-7, MDA-MB-453 and MDA-MB-231 breast can- cer cells
PAO↑,
SSAT↑,
P21↑,
Bak↑,

164- CUR,    Anti-tumor activity of curcumin against androgen-independent prostate cancer cells via inhibition of NF-κB and AP-1 pathway in vitro
- in-vitro, Pca, PC3
NF-kB↓,
AP-1↓,

170- CUR,    Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis
- vitro+vivo, Pca, PC3
TRAILR↑,
BAX↑,
P21↑,
p27↑,
NF-kB↓,
cycD1↓,
VEGF↓,
uPA↓,
MMP2↓,
MMP9↓,
Bcl-2↓,
Bcl-xL↓,

183- CUR,    Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
AR↓,
AP-1↓,
NF-kB↓, The results obtained here demonstrate that curcumin has a potential therapeutic effect on prostate cancer cells through down-regulation of AR and AR-related cofactors (AP-1, NF-kappaB and CBP).
CBP↓,

2980- CUR,    Inhibition of NF B and Pancreatic Cancer Cell and Tumor Growth by Curcumin Is Dependent on Specificity Protein Down-regulation
- in-vivo, PC, NA
TumCG↓, curcumin inhibits Panc28 and L3.6pL pancreatic cancer cell and tumor growth in nude mice bearing L3.6pL cells as xenografts
p50↓, curcumin decreased expression of p50 and p65 proteins and NFkappaB-dependent transactivation and also decreased Sp1, Sp3, and Sp4 transcription factor
p65↓,
NF-kB↓,
Sp1/3/4↓,
MMP↓, Curcumin also decreased mitochondrial membrane potential and induced reactive oxygen species in pancreatic cancer cell
ROS↑,

3574- CUR,    The effect of curcumin (turmeric) on Alzheimer's disease: An overview
- Review, AD, NA
*antiOx↑, Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD
*Inflam↓,
*lipid-P↓,
*cognitive↑,
*memory↑, overall memory in patients with AD has improved.
*Aβ↓, curcumin may help the macrophages to clear the amyloid plaques found in Alzheimer's disease.
*COX2↓, Curcumin is found to inhibit cyclooxygenase (COX-2),
*ROS↓, The reduction of the release of ROS by stimulated neutrophils, inhibition of AP-1 and NF-Kappa B inhibit the activation of the pro-inflammatory cytokines TNF (tumor necrosis factor)-alpha and IL (interleukin)-1 beta
*AP-1↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*SOD↑, It also increased the activity of superoxide dismutase, sodium-potassium ATPase that normally decreased with aging.
*GSH↑, followed by a significant elevation in oxidized glutathione content.
*HO-1↑, curcumin induces hemoxygenase activity.
*IronCh↑, curcumin effectively binds to copper, zinc and iron.
*BioAv↓, Curcumin has poor bioavailability. Because curcumin readily conjugated in the intestine and liver to form curcumin glucuronides.
*Half-Life↝, , serum curcumin concentrations peaked one to two hours after an oral dose
*Dose↝, Peak serum concentrations were 0.5, 0.6 and 1.8 micromoles/L at doses of 4, 6 and 8 g/day respectively.
*BBB↑, Curcumin crosses the blood brain barrier and is detected in CSF
*BioAv↑, Absorption appears to be better with food.
*toxicity∅, A phase 1 human trial with 25 subjects using up to 8000 mg of curcumin per day for three months found no toxicity from curcumin.
*eff↑, Co-supplementation with 20 mg of piperine (extracted from black pepper) significantly increase the bioavailablity of curcumin by 2000%

3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓, treatment with CUR enhances pro-oxidant levels, antioxidant enzymes activities and anti-inflammatory cytokine production and decreases apoptotic cells in AlCl3-exposed hippocampus rats.
*BBB↑, CUR is able to cross the blood–brain barrier
*NRF2↑, CUR was shown to provide neuroprotection by inducing the upregulation of the transcription of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and by suppression of NF-κB activation
*NF-kB↓,
*cognitive↑, CUR Protects against AlCl3-Induced Cognitive Impairment
*ROS↓, Co-treatment with CUR significantly attenuated oxidative stress in the hippocampus by decreasing levels of MDA and enhancing SOD and catalase activities, when compared to AlCl3-treated animals.
*MDA↓,
*SOD↑,
*Catalase↑,
*INF-γ↓, CUR significantly reduced INF-γ concentration,
*IL4↓, our results showed that co- and post-treatments of CUR reduce IL-4 concentration.
*memory↑, CUR treatments protect rats against deterioration of spatial memory and
*TNF-α↓, CUR modulated the inflammatory status by the (i) inhibition of TNF-α and IL-1β production in the rat brain
*IL1β↓,

3583- CUR,    Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers
- Review, Arthritis, NA
*TNF-α↓, Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-α action and production in in vitro models, in animal models and in humans
*IL1β↓, curcumin has been found to down-regulate the expression of TNF-α and IL-1β in ankle joints and decrease NF-κB activity, PGE2 production, COX-2 expression and MMP secretion in synoviocytes.
*NF-kB↓,
*PGE2↓,
*COX2↓,
*MMPs↓,
*eff↑, curcumin has been shown to have a synergistic effect with methotrexate in decreasing adjuvant-induced arthritis in mice

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↓,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

2814- CUR,    Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management
- Review, Var, NA
*BioAv↓, curcumin’s practical application in medicine is hindered by its limited bioavailability. low solubility in water and rapid breakdown in the body
*Inflam↓, anti-inflammatory, antioxidant, and potential anticancer abilities
*antiOx↑,
AntiCan↑,
CK2↓, Curcumin exhibited an IC50 of 2.38 ± 0.15 μM against CK2α
GSK‐3β↓, roles of GSK3β and how they are suppressed by curcumin
EGFR↓, roles of EGFR and how it is inhibited by the curcumin analog, 3a
TOP1↓, unwinding of DNA supercoils by Topo I and Topo II and their inhibition by cyclocurcumin
TOP2↓,
NF-kB↓, The activation of NF-kB signaling and the inhibition of NF-kB’s activity are portrayed in Figure 5.
COX2↓, curcumin itself interacts with COX-2 and potentially inhibits its function
CRP↓, ole of CRP in inducing inflammation and its inhibition by curcumin are depicted in Figure 6.

2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, Curcumin has an outstanding safety profile and a number of pleiotropic actions with potential for neuroprotective efficacy, including anti-inflammatory, antioxidant, and anti-protein-aggregate activities.
*Inflam↓,
*antiOx↑,
*BioAv↓, despite concerns about poor oral bioavailability, curcumin has at least 10 known neuroprotective action
*AP-1↓, Curcumin inhibition of AP-1 and NF-κB-mediated transcription occurs at relatively low (<100 nM) doses and might be due to inhibition of histone acetylase (HAT) or activation of histone deacetylase (HDAC) activity
*NF-kB↓,
*HATs↓,
*HDAC↑,
Dose↑, At high doses (>3 µM) that are relevant to colon cancer but unlikely achievable with oral delivery in plasma and tissues outside of the gut, curcumin can act as an alkylating agent,10 a phase II enzyme inducer,11 and stimulate antioxidant response el
*ROS↓, We also found that curcmin reduced oxidative damage, inflammation, and cognitive deficits in rats receiving CNS infusions of toxic Aβ
*cognitive↑,
*Aβ↓, dose-dependently blocked Aβ aggregation at submicromolar concentrations

2976- CUR,    Curcumin suppresses the proliferation of oral squamous cell carcinoma through a specificity protein 1/nuclear factor‑κB‑dependent pathway
- in-vitro, Oral, HSC3 - in-vitro, HNSCC, CAL33
tumCV↓, Cur significantly inhibited the viability and colony formation ability of HSC3 and CAL33 cells.
Sp1/3/4↓, Cur decreased the expression of Sp1, p65 and HSF1 by suppressing their transcription levels.
p65↓,
HSF1↓,
NF-kB↓, Cur decreased NF‑κB activity in OSCC cells, and Sp1 downregulation enhanced the effect of Cur.

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, Several studies have shown that curcumin could prevent and/or palliate chemotherapy-induced liver injury
*Inflam↓, mainly due to its anti-inflammatory, antioxidant, antifibrotic and hypolipidemic properties.
*antiOx↓,
*lipid-P↓, Curcumin can lower lipid peroxidation by increasing the content of GSH, a major endogenous antioxidant,
*GSH↑,
*SOD↑, as well as by enhancing the activity of endogenous antioxidant enzymes, such as SOD, CAT, GPx and GST
*Catalase↑,
*GPx↑,
*GSTs↑,
*ROS↓, elimination of ROS
*ALAT↓, attenuated the increase in serum levels of TNF-α as well as several liver enzymes, including ALT, AST, alkaline phosphatase and MDA which are markers of liver damage caused by MTX or cisplatin.
*AST↓,
*MDA↓,
*NRF2↑, Curcumin also attenuated DILI through activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway
*COX2↑, Curcumin can also inhibit the expression of cyclooxygenase-2 (COX-2)
*NF-kB↓, NF-κB inhibition, which decreased the downstream induction of COX-2, ICAM-1 and MCP-1 pro-inflammatory regulators
*ICAM-1↓,
*MCP1↓,
*HO-1↑, increase in HO-1 and NQO1 expression
CXCc↓, Downregulation of pro-inflammatory chemokines, (CXCL1, CXCL2, and MCP-1)

2974- CUR,    Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition, and E-Cadherin Upregulation in Colorectal Cancer
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, CRC, HCT15 - in-vitro, CRC, COLO205 - in-vitro, CRC, SW-620 - in-vivo, NA, NA
TumCMig↓, Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo.
TumCI↓,
TumCG↓,
TumMeta↓,
Sp1/3/4↓, curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells.
HDAC4↓,
FAK↓, Curcumin inhibits focal adhesion kinase (FAK) phosphorylation
CD24↓, Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells
E-cadherin↑, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT.
EMT↓,
TumCP↓,
NF-kB↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
AP-1↝,
STAT3↓, downregulation of CD24 reduces STAT and FAK activity, decreases cell proliferation, metastasis in human tumor
P53?,
β-catenin/ZEB1↓, CUR could activate protein kinase D1 (PKD1) suggesting that suppressing of β-catenin transcriptional activity prevents growth of prostate cancer
NOTCH1↝,
Hif1a↝,
PPARα↝,
Rho↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
MMP2↓,
MMP9↓,

649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, increase EGCG bioavailability is using other natural products such as curcumin and piperine
EGFR↓,
HER2/EBBR2↓,
IGF-1↓,
MAPK↓,
ERK↓, reduction in ERK1/2 phosphorylation
RAS↓,
Raf↓, Raf-1
NF-kB↓, Numerous investigations have proven that EGCG has an inhibitory effect on NF-κB
p‑pRB↓, EGCG were displayed to reduce the phosphorylation of Rb, and as a result, cells were arrested in G1 phase
TumCCA↑, arrested in G1 phase
Glycolysis↓, EGCG has been found to inhibit key enzymes involved in glycolysis, such as hexokinase and pyruvate kinase, thereby disrupting the Warburg effect and inhibiting tumor cell growth
Warburg↓,
HK2↓,
Pyruv↓,

139- Tomatine,  CUR,    Combination of α-Tomatine and Curcumin Inhibits Growth and Induces Apoptosis in Human Prostate Cancer Cells
- in-vitro, Pca, PC3
NF-kB↓,
Bcl-2↓,
p‑Akt↓,
p‑ERK↓, ERK1/2

2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. Tq + Cur treatment significantly improved these conditions.
*TNF-α↓,
*IL6↓,
*MRP↓,
*GFR↑,
*mt-ATPase↑, antioxidant enzyme levels and mitochondrial ATPases were restored upon treatment,
*p‑Akt↑, Tq + Cur treatment increased the expressions of phosphorylated Akt, Nrf2 and HO-1 proteins while decreasing the levels of cleaved caspase 3 and NFκB in kidney homogenates.
*NRF2↑,
*HO-1↑,
*Casp3↓,
*NF-kB↓,
*RenoP↑, In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 37

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   Akt↑,1,   Akt↝,1,   p‑Akt↓,3,   p‑Akt↝,1,   angioG↓,1,   AntiCan↑,1,   AP-1↓,2,   AP-1↝,2,   Apoptosis↑,3,   Apoptosis↝,2,   AR↓,1,   AR↝,1,   ATPase↓,1,   Bak↑,1,   BAX↑,2,   BAX↝,1,   Bax:Bcl2↑,1,   Bcl-2↓,6,   Bcl-2↝,1,   Bcl-xL↓,2,   Bcl-xL↝,1,   BID↑,1,   BioAv↓,1,   BioAv↑,2,   Casp3↑,1,   Casp3↝,1,   Casp8↑,2,   Casp9↑,2,   CBP↓,1,   CD24↓,1,   CD31↓,1,   CDK1↓,1,   chemoP↑,1,   ChemoSen↑,5,   CK2↓,1,   cMyc↓,1,   COX1↓,1,   COX2↓,7,   COX2↝,1,   CRP↓,1,   CSCs↓,1,   CXCc↓,2,   CXCL12↓,1,   Cyc↝,1,   cycD1↓,3,   cycD1↝,1,   Cyt‑c↑,1,   Cyt‑c↝,1,   DNAdam↑,1,   DNMT1↓,1,   DNMTs↓,1,   Dose↑,3,   DR5↑,1,   E-cadherin↑,1,   ECAR↓,1,   EFEMP↓,1,   eff↑,1,   EGFR↓,5,   EGFR↝,1,   EMT↓,2,   ER(estro)↓,1,   ERK↓,1,   p‑ERK↓,2,   EZH2↓,1,   FAK↓,1,   Fas↑,1,   FASN↓,1,   FGF↓,1,   GAPDH↓,1,   Gli1↓,1,   GlucoseCon↓,1,   GLUT1↓,1,   Glycolysis↓,1,   GM-CSF↓,2,   GSK‐3β↓,1,   HATs↓,1,   HCAR1↓,1,   HDAC↓,1,   HDAC1↓,1,   HDAC3↓,1,   HDAC4↓,1,   HDAC8↓,1,   HER2/EBBR2↓,3,   HH↓,1,   Hif1a↓,1,   Hif1a↝,1,   HK2↓,2,   HO-1↑,1,   HSF1↓,1,   IGF-1↓,1,   p‑IKKα↓,1,   IL1↓,2,   IL12↓,1,   IL18↓,1,   IL2↓,1,   IL5↓,1,   IL6↓,4,   IL6↝,1,   IL8↓,1,   IR↓,1,   IκB↓,1,   JAK↓,1,   JAK2↓,1,   JNK↑,1,   JNK↝,1,   lactateProd↓,1,   LAMs↓,1,   LC3II↓,1,   LDHA↓,1,   MAPK↓,2,   Mcl-1↓,2,   MCT1↓,1,   MCT4↓,1,   MDSCs↓,1,   miR-21↓,1,   miR-27a-3p↓,1,   MMP↓,1,   MMP2↓,3,   MMP2↝,1,   MMP9↓,4,   MMPs↓,1,   mTOR↝,1,   MyD88↓,1,   n-MYC↓,1,   Nanog↓,1,   NF-kB↓,27,   NF-kB↝,1,   NO↓,1,   NOTCH1↓,2,   NOTCH1↝,1,   NQO1↑,1,   NRF2↑,1,   NRF2↝,1,   OCT4↓,1,   other↑,1,   p16↑,1,   P21↑,2,   P21↝,1,   p27↑,1,   p300↓,1,   p‑p42↓,1,   p‑p44↓,1,   p50↓,1,   P53?,1,   P53↓,1,   P53↑,3,   P53↝,1,   p65↓,2,   PAK↓,1,   PAO↑,1,   PARP↑,1,   PDGF↓,1,   PFK1↓,1,   PGE2↓,1,   pH↑,1,   PI3K↝,1,   PI3K/Akt↓,2,   PI3k/Akt/mTOR↓,1,   PIAS-3↑,1,   PKM2↓,1,   PPARα↝,1,   PPARγ↑,1,   p‑pRB↓,1,   PSA↝,1,   PTCH1↓,1,   PTEN↑,2,   PTEN↝,1,   Pyruv↓,1,   QoL↑,1,   radioP↑,1,   RadioS↑,1,   Raf↓,2,   RAS↓,2,   Rho↓,1,   ROS↑,5,   ROS↝,1,   RTK-RAS↓,1,   SDH↑,1,   Shh↓,1,   SOCS-3↑,1,   SOCS1↑,1,   SOX2↓,1,   SOX9?,1,   Sp1/3/4↓,4,   SPARC↓,1,   Src↓,1,   SSAT↑,1,   STAT1↓,1,   p‑STAT1↓,1,   STAT3↓,5,   STAT4↓,1,   STAT5↓,1,   survivin↓,1,   TGF-β↓,3,   TLR4↓,1,   TNF-α↝,1,   TOP1↓,1,   TOP2↓,1,   TP53↑,1,   TRAILR↑,1,   TumCCA↑,3,   TumCG↓,3,   TumCI↓,1,   TumCMig↓,1,   TumCP↓,2,   tumCV↓,1,   TumMeta↓,1,   uPA↓,1,   VEGF↓,4,   VEGF↝,1,   Vim↓,1,   Warburg↓,1,   Wnt↓,1,   XIAP↓,1,   ZBTB10↑,1,   α-SMA↓,2,   β-catenin/ZEB1↓,3,   β-catenin/ZEB1↝,1,  
Total Targets: 219

Results for Effect on Normal Cells:
12LOX↑,1,   5LO↓,1,   AIF↓,1,   Akt↓,1,   p‑Akt↑,1,   ALAT↓,1,   AntiAg↑,1,   antiOx↓,2,   antiOx↑,5,   AP-1↓,2,   Apoptosis↓,1,   AST↓,1,   ATP↑,1,   mt-ATPase↑,1,   Aβ↓,2,   BBB↑,2,   BioAv↓,3,   BioAv↑,1,   BioEnh↑,2,   cardioP↑,1,   Casp3↓,2,   Casp9↓,1,   Catalase↑,3,   cognitive↑,5,   COX2↓,6,   COX2↑,1,   creat↓,1,   Dose↝,1,   eff↑,2,   GFR↑,1,   GPx↑,3,   GSH↑,4,   GSK‐3β↓,1,   GSR↓,1,   GSTs↑,1,   H2O2↓,1,   Half-Life↝,1,   HATs↓,1,   HDAC↑,1,   hepatoP↑,1,   HO-1↑,4,   ICAM-1↓,1,   IL1↓,1,   IL12↓,1,   IL1β↓,4,   IL2↓,1,   IL2↑,1,   IL4↓,2,   IL6↓,3,   IL8↓,1,   INF-γ↓,2,   Inflam↓,10,   iNOS↓,2,   IronCh↑,1,   LDH↓,1,   lipid-P↓,3,   MCP1↓,2,   MDA↓,4,   memory↑,3,   MMP2↓,1,   MMP3↓,1,   MMP9↓,1,   MMPs↓,1,   MMPs↑,1,   MRP↓,1,   NADPH↑,1,   neuroP↑,2,   NF-kB↓,9,   NLRP3↓,1,   NO↓,3,   NO↑,1,   NRF2↑,5,   OS↑,1,   p300↓,1,   PGE2↓,4,   RenoP↑,1,   ROS↓,10,   SOD↑,5,   STAT↓,1,   STAT3↓,1,   TIMP1↑,1,   TNF-α↓,6,   toxicity∅,1,  
Total Targets: 83

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
37 Curcumin
2 EGCG (Epigallocatechin Gallate)
2 Photodynamic Therapy
2 Cisplatin
2 Chemotherapy
1 Arctigenin
1 Lecithin
1 Oxygen, Hyperbaric
1 Radiotherapy/Radiation
1 Docetaxel
1 Ursolic acid
1 Piperine
1 Tomatine
1 Thymoquinone
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:214  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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