IL10 Cancer Research Results

IL10, Interleukin-10: Click to Expand ⟱

Source:

Type:

IL-10 is a multifaceted immune-suppressive cytokine and possesses immune-regulatory and angiogenic functions.
It primarily acts as an anti-inflammatory cytokine, protecting the body from an uncontrolled immune response, mostly through the Jak1/Tyk2 and STAT3 signaling pathway. On the other hand, IL-10 can also have immunostimulating functions under certain conditions.
The role of IL-10 in tumor pathogenesis is currently highly controversial, with some findings showing that IL-10 promotes tumor development and angiogenesis, while others supporting that it inhibits tumor growth and metastasis.

IL-10 is often expressed in various cancers, including breast cancer, colorectal cancer, melanoma, and lymphoma. Its expression can vary significantly depending on the tumor type and the immune context.
Elevated levels of IL-10 are frequently associated with the presence of tumor-infiltrating immune cells, particularly Tregs and M2 macrophages.

Scientific Papers found: Click to Expand⟱

4447-

AgNPs,

Anti-inflammatory action of silver nanoparticles in vivo: systematic review and meta-analysis

Review,

Nor,

*Inflam↓, Qualitative analysis showed a reduction in pro-inflammatory proteins and in the COX-2 pathway.
*COX2↓,
*ROS↓, Its in vitro mechanism of action shows potential to eliminate free radicals
*Dose↝, The method of synthesizing nanoparticles (NPs) influences parameters such as size, shape, topography, stability, concentration, purity and release of Ag + ions, which in turn influences their anti-inflammatory activity
*eff↑, In vitro studies have compared the ingestion of AgNPs at low concentrations (0.012 % per kg) with gold standard drugs (glucocorticoids; 0.1 % per kg) and observed higher efficacy of NPs in promoting therapeutic effect
*toxicity↓, another study has shown that chronic in vivo application of AgNPs at the minimum concentration necessary to promote therapeutic effect does not cause toxic effects
*IL4↑, AgNPs and mitoxantrone increased levels of anti-inflammatory cytokines (IL4, IL5, IL10, IL13, and IFNα) and decreased pro-inflammatory cytokines (IL1, IL6, IL12, IL18, IFNY and TNFα).
*IL5↑,
*IL10↑,
*IL1↓,
*IL6↓,
*TNF-α↓,
*NF-kB↓, AgNPs selectively inhibit COX-2 and the NF-kB pathway.
*MDA↓, AgNPs reduce biomarkers of oxidative stress [55], such as malondialdehyde (MDA) and cell membrane peroxidation [19,31] and increase intracellular GSH
*GSH↑,

5365-

AV,

Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications

Review,

Nor,

Review,

IBD,

Review,

Diabetic,

*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

2605-

Ba,

BA,

Potential therapeutic effects of baicalin and baicalein

Review,

Var,

Review,

Stroke,

Review,

IBD,

Review,

Arthritis,

Review,

AD,

Review,

Park,

cardioP↑, cardioprotective activities.
Inflam↓, Decreasing the accumulation of inflammatory mediators and improving cognitive function
cognitive↑,
*hepatoP↑, Decreasing inflammation, reducing oxidative stress, regulating the metabolism of lipids, and decreasing fibrosis, apoptosis, and steatosis are their main hepatoprotective mechanisms
*ROS?, Reducing oxidative stress and protecting the mitochondria to inhibit apoptosis are proposed as hepatoprotective mechanisms of baicalin in NAFLD
*SOD↑, Baicalin could reduce the levels of ROS and fatty acid-induced MDA, and increase superoxide dismutase (SOD) and glutathione amounts compared to the control.
*GSH↑,
*MMP↑, Moreover, baicalin could partially restore mitochondrial morphology and increase ATP5A expression and mitochondrial membrane potential (Gao et al., 2022).
*GutMicro↑, After baicalein treatment, a remodelling in the overall structure of the gut microbiota was observed
ChemoSen↑, Besides, a combination of baicalin and doxorubicin could elevate the chemosensitivity of MCF-7 and MDA-MB-231 breast cancer cells
*TNF-α↓, Baicalin can protect cardiomyocytes from hypoxia/reoxygenation injury by elevating the SOD activity and anti-inflammatory responses through reducing TNF-α, enhancing IL-10 levels, decreasing IL-6, and inhibiting the translocation of NF-κB to the nucl
*IL10↑,
*IL6↓,
*eff↑, Studies show that baicalin and baicalein may be effective against IBD by suppressing oxidative stress and inflammation, and regulating the immune system.
*ROS↓,
*COX2↓, baicalein can improve the symptoms of ulcerative colitis by lowering the expression of pregnane X receptor (PXR), (iNOS), (COX-2), and caudal-type homeobox 2 (Cdx2), as well as the NF-κβ and STAT3
*NF-kB↓,
*STAT3↓,
*PGE2↓, Administration of baicalin (30-90 mg/kg) could decrease the levels of prostaglandin E2 (PEG2), myeloperoxidase (MPO), IL-1β, TNF-α, and the apoptosis-related genes including Bcl-2 and caspase-9
*MPO↓,
*IL1β↓,
*MMP2↓, Rheumatoid arthritis RA mouse model by supressing relevant proinflammatory cytokines such as IL-1b, IL-6, MMP-2, MMP-9, TNF-α, iNOS, and COX-2)
*MMP9↓,
*β-Amyloid↓, Alzheimer’s disease (AD) : reduce β-amyloid and trigger non-amyloidogenic amyloid precursor proteins.
*neuroP↑, For instance, administration of baicalin orally for 14 days (100 mg/kg body weight) exhibited neuroprotective effects on pathological changes and behavioral deficits of Aβ 1–42 protein-induced AD in vivo.
*Dose↝, administration of baicalin (500 mg/day, orally for 12 weeks) could improve the levels of total cholesterol, TGs, LDLC and apolipoproteins (APOs), and high-sensitivity C-reactive protein (hs-CRP) in patients with rheumatoid arthritis and coronary arte
*BioAv↝, the total absorption of baicalin depends on the activity of intestinal bacteria to convert baicalin to baicalein as the first step.
*BioAv↝, Kidneys, liver, and lungs are the main organs in which baicalin accumulates the most.
*BBB↑, Baicalin and baicalein can pass through the blood brain barrier (BBB)
*BDNF↑, mechanism of action for baicalein is illustrated in Figure 3. Activation of the BDNF/TrkB/CREB pathway, inhibition of NLRP3/Caspase-1/GSDMD pathway,

1399-

BBR,

Rad,

Radiotherapy Enhancing and Radioprotective Properties of Berberine: A Systematic Review

Review,

NA,

*ROS↓, normal cells
*MDA↓, normal cells
*TNF-α↓, normal cells
*TGF-β↓, TGF-β1 normal cells
*IL10↑, normal cells
ROS↑, cancer cells
DNAdam↑, cancer cells
mtDam↑, cancer cells
MMP↓, cancer cells
Apoptosis↑, cancer cells
TumCCA↑, cancer cells
Hif1a↓, cancer cells
VEGF↓, cancer cells
RadioS↑, revealed radiosensitizing properties

2696-

BBR,

Berberine regulates proliferation, collagen synthesis and cytokine secretion of cardiac fibroblasts via AMPK-mTOR-p70S6K signaling pathway

in-vivo,

Nor,

 1-3 day-old SD rats

*α-SMA↓, It was demonstrated that treatment of cardiac fibroblasts with berberine resulted in deceased proliferation, and attenuated fibroblast α-smooth muscle actin expression and collagen synthesis.
*TGF-β1↓, protein secretion of TGFβ1 was inhibited; however, the protein secretion of IL-10 was increased in cardiac fibroblasts with berberine treatment.
*IL10↑,
*p‑AMPK↑, Mechanistically, the phosphorylation level of AMPK was increased
*p‑mTOR↓, phosphorylation levels of mTOR and p70S6K were decreased in berberine treatment group
*P70S6K↓,
*cardioP↑, protective effects of berberine on cellular behaviors of cardiac fibroblasts

2713-

BBR,

Berberine improved the microbiota in lung tissue of colon cancer and reversed the bronchial epithelial cell changes caused by cancer cells

in-vitro,

Nor,

BEAS-2B

Thirty-six BALB/c nude mice

*GutMicro↑, Berberine or probiotics significantly increased the alpha diversity of the lung microbiota
*IL6↑, Berberine increased IL-6 and IL-10 and decreased IL-17 and IFN-γ expression in lung tissue
*IL10↑,
*IL17↑,
*IFN-γ↑,
PDGF↓, In addition, HT29 and RKO CM had no significant effect on the expression of PDGF-β in BEAS-2B cells, while berberine significantly reduced its expression.
*RAD51↓, berberine protects lung cells against this stress by enhancing RAD51 expression.

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↓,

2749-

BetA,

Anti-Inflammatory Activities of Betulinic Acid: A Review

Review,

Nor,

Inflam↓, betulinic acid as a promissory lead compound with anti-inflammatory activity
*NO↓, BA can inhibit the production of NO, mainly in macrophages cultures stimulated with bacterial lipopolysaccharide (LPS) and/or interferon gamma (IFN-ɣ)
*IL10↑, (BA) has a broad-spectrum anti-inflammatory activity, significantly increasing IL-10 production, decreasing ICAM-1, VCAM-1, and E-selectin expression and inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB),
*ICAM-1↓,
*VCAM-1↓,
*E-sel↓,
*NF-kB↓,
*IKKα↓, BA blocks the NF-κB signaling pathway by inhibiting IκB phosphorylation and d
*COX2↓, BA also inhibits cyclooxygenase-2 (COX-2) activity and, therefore, decrease prostaglandin E2 (PGE2) synthesis
*PGE2↓,
*IL1β↓, The production of critical pro-inflammatory cytokines, such as IL-1β, IL-6, IL-8, IL-12, and TNF, is also decreased by BA treatment
*IL6↓,
*IL8↓,
*IL12↓,
*TNF-α↑,
*HO-1↑, induction of HO-1 enzyme activity is associated with the anti-inflammatory effect of BA, since SnPP, an inhibitor of HO-1, promoted a partial reversal of BA’s effect on NF-κB activity,
*IL10↑, BA also increased the amount of IL-10, a well-known anti-inflammatory cytokine
*IL2↓, decreasing the production of pro-inflammatory cytokines, such as IL-2, IL-6, IL-17, and IFN-γ
*IL17↓,
*IFN-γ↓,
*SOD↑, BA decreased the production of the inflammatory mediators described above at the inflammation site and increased enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GRd) in the liver
*GPx↑,
*GSR↑,
*MDA↓, BA decreased malondialdehyde (MDA) levels, a key mediator of oxidative stress and widely used as a marker of free radical mediated lipid peroxidation injury, at the inflammation site
*MAPK↓, BA downregulates MAPK signaling pathways (ERK1/2, JNK, and p38) in the paw edema tissue, which, in part, explains the inhibition of cytokine production (IL-1β and TNF), COX-2 expression, and PGE2 production (Figure 3).

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↓,

743-

Bor,

Boric Acid (Boron) Attenuates AOM-Induced Colorectal Cancer in Rats by Augmentation of Apoptotic and Antioxidant Mechanisms

in-vitro,

CRC,

rats

BAX↑,
Bcl-2↓,
GPx↑,
SOD↑,
Catalase↑,
MDA↓, in colon tissue homogenates
TNF-α↓,
IL6↓,
IL10↑,

5742-

Buty,

Butyrate: A Double-Edged Sword for Health?

Review,

Var,

HCAR2↑, Another major GPCR activated by butyrate is GPR109A (
Inflam↓, anti-inflammatory properties of butyrate are also achieved through inhibition of the production of proinflammatory enzymes and cytokines
HDAC↓, Butyrate functions as an HDAC inhibitor
*IFN-γ↓, animal studies reported that the proinflammatory cytokines IFN-γ, TNF-α, IL-1β, IL-6, and IL-8 are inhibited, whereas IL-10 and TGF-β are upregulated in response to butyrate
*TNF-α↓,
*IL1β↓,
*IL6↓,
*IL8↓,
*IL10↑,
*TNF-β↑,
*NF-kB↓, butyrate is at least in part due to inhibition of the activation of a transcription factor known as NF-κB (
*ROS↓, by rescuing the redox machinery and controlling reactive oxygen species,
PPARγ↓, Further studies also showed that butyrate is capable of activating PPAR-γ (67), which is a member of the nuclear hormone receptor family and highly expressed in colonic epithelial cells,
Weight↓, although a large body of evidence has suggested the effect of butyrate on alleviating high fat diet–induced obesity and insulin resistance, a few studies showed an opposite effect.

5739-

Buty,

Butyrate as a promising therapeutic target in cancer: From pathogenesis to clinic (Review)

Review,

Var,

GutMicro↑, Butyrate, a short-chain fatty acid, is generated through gut microbial fermentation of dietary fiber.
*Inflam↓, Butyrate, a primary anti-inflammatory SCFA, exhibits a multifaceted role in mitigating inflammation
*IL6↓, It inhibits the production of pro-inflammatory cytokines and chemokines, such as IL-6, TNF-α and IL-17, which helps to prevent colon cancer
*TNF-α↓,
*IL17↓,
*IL10↑, while promoting IL-10 production
*ROS↝, regulates the production of reactive oxygen species (ROS)
COX2↓, butyrate has been observed to suppress inflammation by inhibiting the expression of cyclooxygenase-2 mRNA in colonic tissues (60).
NLRP3↓, butyrate exhibits the highest efficiency in the negative regulation of NLRP3
Imm↑, Enhancement of the immunotherapeutic effect
HDAC↓, Inhibition of HDAC activity in cells
TumCCA↑, Butyrate has been found to induce cell cycle arrest in the G0/G1 phase in a dose-dependent manner in vitro in numerous tumors, including colon, liver, lung and bladder cancer,
Apoptosis↑, butyrate-induced apoptosis is accompanied by elevated ROS levels and caspase activity (126)
ROS↑,
Casp↑,
mtDam↑, suggests that ROS can induce mitochondrial membrane damage, release Cyt c from damaged mitochondria, and enhance apoptosis via the Cyt c/caspase-3 pathway
Cyt‑c↑,
eff↑, Clostridium butyricum is an anaerobic bacterium classified as a probiotic due to its production of butyric acid (139)
chemoP↑, butyrate not only alleviates the side effects associated with conventional chemotherapeutic agents such as oxaliplatin, irinotecan and 5-fluorouracil (149-151), but it also enhances the efficacy of both chemotherapy and immunotherapy
ChemoSen↑,
eff↑, metformin has been demonstrated to enhance the biosynthesis of butyrate while concurrently inhibiting the progression of CRC
RadioS↑, Butyrate significantly enhanced radiation-induced cell death and enhanced treatment effects compared with administration of radiation alone.
HCAR2↑, Activation of cell-surface receptors (GPR41, GPR43 and GPR109A);

5987-

Chit,

Chitin, Chitosan, and Glycated Chitosan Regulate Immune Responses: The Novel Adjuvants for Cancer Vaccine

Review,

Var,

other↝, A common method for the synthesis of chitosan is the deacetylation of chitin using sodium hydroxide in excess as a reagent and water as a solvent
other↝, molecular weight of chitosan is between 3800 and 20,000 Daltons. The degree of deacetylation (%DD) ranges from 60% to 100%.
*Weight↝, chitosan and fat is not very well understood and has not been proved clinically yet, chitosan has been used as an effective complement to help lose weight during diet period or to stabilise one's weight
*toxicity↓, Since they are biocompatible, biodegradable, mucoadhesive, and nontoxic, with antimicrobial, antiviral, and adjuvant properties, chitin and chitosan have been widely applied in medicine and pharmacy
*Bacteria↓,
*BioAv↑,
DDS↑, Combined with drugs such as doxorubicin, paclitaxel, docetaxel, and norcantharidin, chitin and chitosan are used as drug carriers.
*Wound Healing↑, Moreover, chitin has some unusual properties that accelerate healing of wounds in humans
*other↝, Because of its mucoadhesive properties, chitin and chitosan are widely applied for mucosal routes of administration, that is, oral, nasal, and ocular mucosa, which are noninvasive routes.
*Imm↑, hypothesized that a viscous chitosan solution, when administered subcutaneously, would not only provide immune stimulation as previously
eff↑, With the development of nanotechnology, chitosan have shown its unique advantages when combined with nanoparticles.
*BioAv↝, Chitosan is soluble in diluted acids but is relatively insoluble in water [66, 67]. The poor solubility of chitosan poses limitations for its biomedical applications.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was formed
eff↑, Chitosan nanoparticles (CNPs) can be administrated through noninvasive routes such as oral, nasal, pulmonary, and ocular routes
NK cell↑, CNP remarkably increased the killing activities of NK cells activity
IL2↑, CNP also significantly promoted the production of Th1 (IL-2 and IFN-γ) and Th2 (IL-10) cytokines
IFN-γ↑,
IL10↑,

1574-

Citrate,

Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway

in-vitro,

Lung,

A549

5,10,15mM

in-vitro,

Melanoma,

WM983B

in-vivo,

NA,

4 g/kg citrate twice a day for 4 week

mice. Plasma levels in chronically treated animals were approximately 3 mM

TumCG↓,
eff↑, additional benefit accrued in combination with cisplatin
T-Cell↑, significantly higher infiltrating T-cells
p‑IGF-1R↓, citrate inhibited IGF-1R phosphorylation
p‑Akt↓, inhibited AKT phosphorylation
PTEN↑, activated PTEN
p‑eIF2α↑, increased expression of p-eIF2a p-eIF2a was decreased when PTEN was depleted
OCR↓, citrate treatment of A549 cells dramatically reduced oxygen consumption
ROS↓, observed a decrease in ROS in A549
ECAR∅, acidification rate (ECAR) and found it to be unchanged
IL1↑, s (e.g. interleukin-1, tumor necrosis factor-alpha, etc) and anti-inflammatory cytokines (e.g. interleukin-10 and interleukin 1 receptor antagonist) are activated
TNF-α↑,
IL10↑,
IGF-1R↓, Citrate Inhibits IGF-1R Activation And Its Downstream Pathway
eIF2α↑, eIF2α activity was increased in A549 cells after citrate treatment
PTEN↑, PTEN was activated
TCA↓,
Glycolysis↓, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
selectivity↑, citrate may inhibit tumor growth via inhibiting glycolysis and the TCA cycle and that this effect appears to be selective to tumor tissue.
*toxicity∅, Chronic citrate treatment was non-toxic as evidenced by gross pathology in numerous organs (liver, lung, spleen and kidney)
Dose∅, corresponding to approximately 56 g of citrate in a 70 kg person

3795-

CUR,

Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence

Review,

AD,

*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.

2919-

LT,

Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence

Review,

Var,

RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration

3528-

Lyco,

The Importance of Antioxidant Activity for the Health-Promoting Effect of Lycopene

Review,

Nor,

Review,

AD,

Review,

Park,

*antiOx↑, the antioxidant effect of lycopene
*ROS↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*BioAv↝, human body cannot synthesize lycopene. It must be supplied with the diet
*Half-Life↑, half-life of lycopene in human plasma is 12–33 days
*BioAv↓, bioavailability decreases with age and in the case of certain diseases
*BioAv↑, heat treatment process of food increases the bioavailability of lycopene
*cardioP↑, positive effect on cardiovascular diseases, including the regulation of blood lipid levels
*neuroP↑, beneficial effects in nervous system disorders, including neurodegenerative diseases such as Parkinson′s disease and Alzheimer′s disease
*H2O2↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*VitC↑, ability to regenerate non-enzymatic antioxidants such as vitamin C and E.
*VitE↑,
*GPx↑, increase in cardiac GSH-Px activity and an increase in cardiac GSH levels
*GSH↑,
*MPO↓, also a decrease in the level of cardiac myeloperoxidase (MPO), cardiac H2O2, and a decrease in cardiac glutathione S transferase (GSH-ST) activity.
*GSTs↓,
*SOD↑, increasing the activity of GSH-Px and SOD in the liver
*NF-kB↓, reducing the expression of NF-κB mRNA in the heart
*IL1β↓, decreased the level of IL-1β and IL-6 and increased the level of anti-inflammatory IL-10 in the heart
*IL6↓,
*IL10↑,
*MAPK↓, inhibited the activation of the ROS-dependent pro-hypertrophic mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling pathways.
*Akt↓,
*COX2↓, decrease in the levels of pro-inflammatory mediators in heart: COX-2, TNF-α, IL-6, and IL-1β and an increase in the anti-inflammatory cardiac TGF-β1.
*TNF-α↓,
*TGF-β1↑,
*NO↓, reduced NO levels in heart and cardiac NOS activity
*GSR↑, increase in the level of cardiac and hepatic SOD, CAT, GSH, GPx, and glutathione reductase (GR)
*NRF2↑, It also activated nuclear factor-erythroid 2 related factor 2 (Nrf2). This affected the downstream expression of HO-1 [97].
*HO-1↑,
*TAC↑, Researchers observed an increase in the liver in TAC and GSH levels and an increase in GSH-Px and SOD activity
*Inflam↓, study showed that lycopene was anti-inflammatory
*BBB↑, Lycopene is a lipophilic compound, which makes it easier to penetrate the blood–brain barrier.
*neuroP↑, Lycopene had also a neuroprotective effect by restoring the balance of the NF-κB/Nrf2 pathway.
*memory↑, lycopene on LPS-induced neuroinflammation and oxidative stress in C57BL/6J mice. The tested carotenoid prevented memory loss

1708-

Lyco,

The Anti-Cancer Activity of Lycopene: A Systematic Review of Human and Animal Studies

Review,

Var,

OS↑, reduced prostate cancer-specific mortality in men at high risk for prostate cancer
ChemoSen↑, improved the response to docetaxel chemotherapy in advanced castrate-resistant prostate cancer
QoL↑, lycopene improved the quality of life, and provided relief from bone pain and control of lower urinary tract symptoms
PSA∅, PSA stabilisation in prostate cancer
eff↑, Lycopene co-supplementation with vitamin E also showed an improvement in the results of prostate cancer treatment
AntiCan↑, lycopene intake showed a strong protective effect against stomach cancer, regardless of H. pylori status
AntiCan↑, A lycopene-rich diet was shown to reduce the incidence of pancreatic cancer in humans by 31%
angioG↓,
VEGF↓,
Hif1a↓,
SOD↑,
Catalase↑,
GPx↑,
GSH↑,
GPx↑,
GR↑,
MDA↓,
NRF2↑,
HO-1↑,
COX2↓,
PGE2↓,
NF-kB↓,
IL4↑,
IL10↑,
IL6↓,
TNF-α↓,
PPARγ↑,
TumCCA↑, G(0)/G(1) phase
FOXO3↓,
Casp3↑,
IGF-1↓, breast cancer,crc
p27↑,
STAT3↓,
CDK2↓,
CDK4↓,
P21↑,
PCNA↓,
MMP7↓,
MMP9↓,

4529-

MAG,

Effectiveness of Magnolol, a Lignan from Magnolia Bark, in Diabetes, Its Complications and Comorbidities—A Review

Review,

Diabetic,

*AntiDiabetic↑,
*glucose↓, magnolol administered to rats with type 2 diabetes reduced fasting blood glucose and plasma insulin levels, without affecting their body weight
*SOD↑, increase in SOD and CAT activity
*Catalase↑,
*ROS↓, Magnolol acts as a free radical scavenger which was proven in numerous in vitro and in vivo studies
*MDA↓, decrease in MDA level
*GPx↑, increase in SOD, CAT and GPx activities, decrease in MDA level and CYP2E1 activity in the liver
*CYP2E1↓,
*AGEs↓, decrease in AGEs level in kidney glomeruli
*IL10↑, increase in IL-10 level in the plasma
*neuroP↑, numerous reports on the protective effect of magnolol on the nervous system, it can be assumed that this lignan may also have neuroprotective effects in the course of diabetes
*GutMicro↑, In the case of the intestinal microflora, honokiol had a beneficial effect on obtaining microbiota homeostasis increasing the amount of Akkermansia bacteria and reducing the amount of Oscillospira bacteria

2243-

MF,

Pulsed electromagnetic fields increase osteogenetic commitment of MSCs via the mTOR pathway in TNF-α mediated inflammatory conditions: an in-vitro study

in-vitro,

Nor,

mesenchymal stem cells (MSCs)

*eff↑, PEMF exposure increased cell proliferation and adhesion
*mTOR↑, PEMFs contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.
*Akt↑,
*PKA↑, PEMFs increase the activity of certain kinases belonging to known intracellular signaling pathways, such as the protein kinase A (PKA) and the MAPK ERK1/2
*MAPK↑,
*ERK↑,
*BMP2↑, PEMFs stimulation also upregulates BMP2 expression in association with increased differentiation in mesenchymal stem cells (MSCs
*Diff↑,
*PKCδ↓, Decrease in PKC protein (involved on Adipogenesis)
*VEGF↑, Increase on VEGF (involved on angiogenesis)
*IL10↑, PEMF induced a significant increase of in vitro expression of IL-10 (that exerts anti-inflammatory activity)

3536-

MF,

Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis

Review,

Arthritis,

Review,

Stroke,

*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

3475-

MF,

A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells

in-vitro,

Nor,

HT22

Review,

AD,

*Apoptosis↓, PEMF exposure improved viability of HT22 cells after excitotoxicity and reduced lactate dehydrogenase release and cell death.
*LDH↓,
*neuroP↑, PEMF exposure indicated that the neuroprotective effects of PEMF were related to modulation of the eCB metabolic system.
*toxicity∅, Recent studies have shown that PEMF is a safe and non-invasive approach for management of several neurological diseases, including Alzheimer's disease
*IL1β↓, Previous studies have shown that PEMF could modulate inflammation after traumatic brain injury by inhibiting production of pro-inflammatory factor IL-1β
*Inflam↓, PEMF influences neuroinflammation via elevation of anti-inflammatory IL-10 and reduction of pro-apoptotic tumor necrosis factor
*IL10↑,
*TNF-α↓,

3474-

MF,

Pulsed electromagnetic fields potentiate the paracrine function of mesenchymal stem cells for cartilage regeneration

in-vitro,

Nor,

 2 mT and 3 mT amplitudes

 mesenchymal stem cell (MSC

*Inflam↓, PEMF-induced CM was capable of enhancing the migration of chondrocytes and MSCs as well as mitigating cellular inflammation and apoptosis.
*Apoptosis↓,
*other↑, modulating the paracrine function of MSCs for the enhancement and re-establishment of cartilage regeneration in states of cellular stress.
*PGE2↓, studies showing PEMF inhibition of the PGE2 and cycloxigenase-2 (COX-2) pathways, reducing the expression of pro-inflammatory cytokines (IL-6, IL-8) while augmenting anti-inflammatory factors (cAMP, IL-10) in synovial fibroblasts from bovine and ost
*COX2↓,
*IL6↓,
*IL8↓,
*cAMP↑,
*IL10↑,

500-

MF,

Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent

in-vitro,

AML,

THP1

 wkEMF (<50 μT), mdEMF (<250 μT) and stEMF (<4.8 mT), 16.7Hz

compared to healty blood cells

ROS↑, only in THP1 cells, not in normal cells ***
Prx6↑, 2x
DHCR24↑, 6x
IL10↑, 6x

220-

MFrot,

MF,

Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation

in-vitro,

Melanoma,

B16-F10

 0.4 T, 7.5 Hz

 mouse cell line

OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,

204-

MFrot,

MF,

Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization

in-vivo,

AD,

 0.2T, 4Hz

 reduced aluminum deposition in the brains of AD mice

*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice

1806-

NarG,

Naringin: Nanotechnological Strategies for Potential Pharmaceutical Applications

Review,

NA,

Inflam↓, anti-inflammatory, antioxidant, antiapoptotic, anticancer and antiulcer effects
antiOx↓,
AntiCan↑,
BioAv↓, clinical application of naringin is severely restricted due to its susceptibility to oxidation, poor water solubility, and dissolution rate. low bioavailability (approximately 8.8%) when administered orally
BioAv↓, In addition, naringin shows instability at acidic pH, is enzymatically metabolized by β-glycosidase in the stomach and is degraded in the bloodstream when administered intravenously
BioAv↑, limitations, however, have been overcome thanks to the development of naringin nanoformulations.
INF-γ↓, The report indicates decreased levels of proinflammatory cytokines (INF-γ, IL-6, and TNF-α) with an increase in IL-10 (anti-inflammatory cytokine), and the attenuation of serum rheumatoid factor (RF-factor) levels and C-reactive protein (CRP)
IL6↓,
TNF-α↓,
IL10↑,
CRP↓,

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

1662-

PBG,

The immunomodulatory and anticancer properties of propolis

Review,

Var,

IL6↓, suppressing the proinflammatory cytokines IL-6 and IL-12 but overexpressing the immune-tolerant cytokine IL-10.
IL12↓,
IL10↑,
CSCs↓, Propolis may Decrease Cancer Stem Cells Population
PAK1↓, artepillin C, a major component in Brazilian green propolis extract, can completely suppress the growth of human neurofibromatosis-associated tumor xenografts in mice through the blocking of oncogenic PAK1 signaling
VEGF↓, royal jelly and Chinese red propolis suppressed both VEGF-induced HUVEC proliferation and migration,
MMP2↓, CAPE from propolis could effectively suppress the adhesion and invasion potential of human hepatocellular carcinoma cells (SK-Hep1) by totally abolishing the expression of MMP-2 and MMP-9.
MMP9↓,
NF-kB↓, It was postulated that such action was related to the inhibition of the NFÎºB pathway
Hif1a↓, Brazilian green propolis and found that some compounds significantly inhibited the expression of the HIF-1α protein and HIF-1 downstream target genes such as glucose transporter 1, hexokinase 2, and VEGF-A
ChemoSen↑, the group with combined usage of paclitaxel and propolis achieved the lowest tumor weight compared to those with paclitaxel alone, propolis alone, or untreated controls
RadioS↑, complementary therapy to mainstream anticancer chemotherapies or radiotherapies.

3250-

PBG,

Allergic Inflammation: Effect of Propolis and Its Flavonoids

Review,

NA,

*SOD↑, increase in antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase, peroxiredoxin, and heme oxygenase-1
*GPx↑,
*Catalase↑,
*Prx↑,
*HO-1↑,
*Inflam↓, anti-inflammatory properties of propolis may be based on the following mechanisms:
*TNF-α↓, (1) suppression of the release of inflammatory cytokines, such as TNF-α and IL-1β;
*IL1β↓,
*IL4↑, (2) increase in production of anti-inflammatory cytokines such as IL-4 and IL-10;
*IL10↑,
*TLR4↓, (3) prevention of TLR4 activation;
*LOX1↓, (4) suppression of LOX, COX-1 and COX-2 gene expression
*COX1↓,
*COX2↓,
*NF-kB↓, (5) suppression of NF-κB and AP-1 activities;
*AP-1↓,
*ROS↓, CAPE treatment reduced ROS levels in the airway microenvironmen
*GSH↑, GSH level increased after CAPE treatment in an animal allergic asthma model
*TGF-β↓, significantly limiting secretion of eotaxin-1, TGF-β1, TNF-α, IL-4, IL-13, monocyte chemoattractant protein-1, IL-8, matrix metalloproteinase-9, and alpha-smooth muscle actin expression
*IL8↓,
*MMP9↓,
*α-SMA↓,
*MDA↓, (MDA) production and protein carbonyl (PC) levels significantly decreased

4220-

PI,

Piperine ameliorated memory impairment and myelin damage in lysolecethin induced hippocampal demyelination

in-vivo,

AD,

 male Wistar rats

in-vivo,

MS,

*memory↑, piperine improved the memory performance and myelin repair in the hippocampal demyelination model
*iNOS↓, Piperine inhibited iNOS expression concomitant with enhanced expression levels of Nrf2, HO1 and the total antioxidant capacity in the hippocampal tissue.
*NRF2↑,
*HO-1↑,
*TAC↑,
*TNF-α↓, Piperine treatment significantly reduced the gene expression level of TNF-α, IL1-β, NF-κB, and glial activation in the injured area;
*IL1β↓,
*NF-kB↓,
*IL10↑, however, the mRNA level of IL-10, Foxp3, BDNF and MBP were significantly increased
*FOXP3↑,
*BDNF↑,
other↑, piperine as a promising therapeutic target in MS patients

3597-

PI,

Chronic diseases, inflammation, and spices: how are they linked?

Review,

AD,

Review,

Park,

Review,

Var,

*NF-kB↓, downregulation of inflammatory pathways such as NF-κB, MAPK, AP-1, COX-2, NOS-2, IL-1β, TNF-α, PGE2, STAT3
*MAPK↓,
*AP-1↓,
*COX2↓,
*NOS2↓,
*IL1β↓, Parkinson’s disease ↓IL-1β, ↓TNF-α
*TNF-α↓,
*PGE2↓,
*STAT3↓,
*IL10↑, Arthritis ↑IL-10
*IL4↓, Asthma ↓IL-4, -5, ↓NF-κB
*IL5↓,
P53↑, Breast cancer ↑p53, ↓MMP-9,-2, ↓c-Myc, ↓VEGF
MMP9↓,
MMP2↓,
cMyc↓,
VEGF↓,
STAT3↓, Gastric cancer ↓STAT3
survivin↓, Triple negative breast cancer ↓Survivin, ↓p65
p65↓,

3025-

RosA,

Rosmarinic acid alleviates intestinal inflammatory damage and inhibits endoplasmic reticulum stress and smooth muscle contraction abnormalities in intestinal tissues by regulating gut microbiota

in-vivo,

IBD,

*GutMicro↑, RA upregulated the abundance of Lactobacillus johnsonii and Candidatus Arthromitus sp SFB-mouse-NL and downregulated the abundance of Bifidobacterium pseudolongum, Escherichia coli, and Romboutsia ilealis.
*ROCK1↓, RA downregulated the expressions of ROCK, RhoA, CaM, MLC, MLCK, ZEB1, ZO-1, ZO-2, occludin, E-cadherin, IL-1β, IL-6, TNF-α, GRP78, PERK, IRE1, ATF6, CHOP, Caspase12, Caspase9, Caspase3, Bax, Cytc, RIPK1, RIPK3, MLKL
*Rho↓,
*CaMKII ↓,
*Zeb1↓,
*ZO-1↓,
*E-cadherin↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*GRP78/BiP↓,
*PERK↓,
*IRE1↓,
*ATF6↓,
*CHOP↓,
*Casp12↓,
*Casp9↓,
*BAX↓,
*Casp3↓,
*Cyt‑c↓,
*RIP1↓,
*MLKL↓,
*IL10↑, upregulated the expression of IL-10 and Bcl-2.
*Bcl-2↑,
*ER Stress↓, RA inhibited the inflammation, which is caused by tight junction damage, by repairing intestinal flora dysbiosis, relieved endoplasmic reticulum stress, inhibited cell death

3660-

SFN,

Sulforaphane - role in aging and neurodegeneration

Review,

AD,

*antiOx↑, antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB
*Inflam↓,
*NRF2↑, increased Nrf2 expression and nuclear localization after SFN treatment
*NF-kB↓,
*HDAC↓, inhibiting HDAC and DNA methyltransferases a
*DNMTs↓,
*neuroP↑, prevent neurodegeneration.
*AntiAge↑, “miraculous” drug to prevent aging and neurodegeneration.
*DNMT1↓, decrease the expression of DNA methyltransferases (DNMTs), especially DNMT1 and DNMT3b.
*DNMT3A↓,
*memory↑, SFN prevented the memory impairment induced by OKA in rats.
*HO-1↑, restored Nrf2 and antioxidant protein (GCLC, HO-1) expression
*ROS↓, diminished the oxidative stress by attenuating ROS and NO levels, and increased GSH concentration.
*NO↓,
*GSH↑,
*NF-kB↓, reducing NF-κB and TNF-α, and by rising IL-10
*TNF-α↓,
*IL10↑,

3318-

SIL,

Pharmaceutical prospects of Silymarin for the treatment of neurological patients: an updated insight

Review,

AD,

Review,

Park,

*hepatoP↑, widely studied as a hepatoprotective drug for various liver disorders.
*neuroP↑, research studies have shown its putative neuroprotective nature against various brain disorders, including psychiatric, neurodegenerative, cognitive, metabolic and other neurological disorders
*TLR4↓, Silymarin treatment has shown anti-inflammatory action in AD models by suppressing toll-like receptor 4 (TLR4) pathways and decreasing the increased mRNA levels of TNF-α, IL-1β and NF-κB
*TNF-α↓,
*IL1β↓,
*NF-kB↓,
*memory↑, improvement in memory los
*cognitive↑, finally leading to normal cognitive functions
*NRF2↑, upregulating the Nrf-2/HO-1 signaling in mice model
*HO-1↑,
*ROS↓, inhibition of oxidative stress in the brain
*Akt↑, Figure 4
*mTOR↑,
*SOD↑,
*Catalase↑,
*GSH↑,
*IL10↑,
*IL6↑,
*NO↓,
*MDA↓,
*AChE↓,
*MAPK↓,
*BDNF↑, Silymarin supplementation improved learning and memory in diabetes-induced cognitively impaired rats by elevating BDNF levels

3300-

SIL,

Toward the definition of the mechanism of action of silymarin: activities related to cellular protection from toxic damage induced by chemotherapy

Review,

Var,

*ROS↓, silymarin and silibinin protect the liver from oxidative stress and sustained inflammatory processes, mainly driven by Reactive Oxygen Species (ROS) and secondary cytokines
*SOD↑, Silymarin administered to patients with chronic alcoholic liver disease significantly enhanced the low SOD activity measured in the patientsâ erythrocytes and lymphocytes.
*hepatoP↑,
*AST↓, Wistar albino rats 50 mg/kg oral silymarin ↓ AST, ALT; ↓MDA (lipid peroxidation); ↑SOD, GSH, CAT; ↑GST and GR
*ALAT↓,
*lipid-P↓,
*GSH↑,
*Catalase↑,
*GSTs↑,
*GSR↑,
*TNF-α↓, ↓hepatic TNF, IFN-Î³, IL-4, IL-2; ↓hepatic NF-kB activation; ↑hepatic IL-10
*IFN-γ↓,
*IL4↓,
*IL2↓,
*NF-kB↓,
*IL10↑,
*Inflam↓, Anti-Inflammatory
COX2↓, NSCLC ↓ NF-kB activation; ↓COX-2; ↑apoptosis; ↑doxorubicin efficacy
Apoptosis↑,
ChemoSen↑,
PGE2↓, ↓prostaglandin E 2
VEGF↓, ↓VEGF

2213-

SK,

Shikonin attenuates cerebral ischemia/reperfusion injury via inhibiting NOD2/RIP2/NF-κB-mediated microglia polarization and neuroinflammation

in-vivo,

Stroke,

 MCAO/R rats

*neuroP↑, Shikonin treatment significantly reduced brain infarction volume and improved neurological function in MCAO/R rats.
*Inflam↓, Shikonin treatment significantly reduced microglial proinflammatory phenotype and levels of proinflammatory markers (inducible-NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α),
*iNOS↓,
*TNF-α↓,
*IL1β↓, interleukin-1 beta (IL-1β), and IL-6), increased microglial anti-inflammatory phenotype and levels of anti-inflammatory markers (Arginase-1 (Arg1), transforming growth factor-beta (TGF-β), and IL-10),
*IL6↓,
*ARG↑,
*TGF-β↑,
*IL10↑,
*NF-kB↓, reversed the expression of Nucleotide-binding oligomerization domain 2 (NOD2) and phosphorylation receptor interacting protein 2 (p-RIP2), and suppressed nuclear factor kappa-B (NF-κB) signaling activation in the ischemic penumbra regions.
*eff↓, Furthermore, overexpression of NOD2 markedly attenuated the neuroprotective effects of Shikonin treatment in MCAO/R rats.

3409-

TQ,

Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives

in-vivo,

Nor,

50 mg/kg

Forty adult male rats

*MDA↓, increased levels of malondialdehyde, TGF-β, CRP, NF-κB, TNF-α, IL-1β and caspase-3 associated with reduced levels of GSH, cyt-c oxidase, Nrf2 and IL-10. However, exposure of rats’ brain tissues to thymoquinone resulted ameliorated all these ef
*TGF-β↓,
*CRP↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*GSH↑,
*NRF2↑,
*IL10↑,
*neuroP↑, thymoquinone remediates sodium nitrite-induced brain impairment through several mechanisms including attenuation of oxidative stress
*ROS↓,
*Apoptosis↓,
*Inflam↓, TQ activates the Nrf2/ARE antioxidant mechanisms in its anti-inflammatory activity

3557-

TQ,

Thymoquinone protects against lipopolysaccharides-induced neurodegeneration and Alzheimer-like model in mice.

in-vivo,

AD,

 thirty-five Swiss mice

*Inflam↓, Thymoquinone is a known anti-inflammatory agent with a strong antioxidant activity.
*antiOx↑,
*cognitive↑, LPS significantly impaired performance in the Y-maze and NORT and induced behavioural abnormalities, compared to control. These were all ameliorated by treatment with TQ (15-30mg/kg).
*TNF-α↓, TQ also significantly (P<0.05) reduced the concentration of LPS-induced TNF-α, IL-1β, AChE and expressions of amyloid-beta, microglia and β-secretase/mRNA in hippocampus and prefrontal cortex.
*IL1β↓,
*AChE↓,
*IL10↑, TQ increased IL-10/mRNA, ChaT, synaptophysin in hippocampus and PFC
*ChAT↑,
*Aβ↓, depleted synaptic protein and Aβ accumulation.

3559-

TQ,

Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease

Review,

AD,

Review,

Var,

*antiOx↑, promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory,
*Inflam↓, anti-inflammatory activity of TQ is mediated through the Toll-like receptors (TLRs)
*AChE↓, In addition, it shows anticholinesterase activity and prevents α-synuclein induced synaptic damage.
AntiCan↑, NS plant, has been proven to have a wide range of pharmacological interventions, including antidiabetic, anticancer, cardioprotective, retinoprotective, renoprotective, neuroprotective, hepatoprotective and antihypertensive effects
*cardioP↑,
*RenoP↑,
*neuroP↑,
*hepatoP↑,
TumCG↓, potential ability to inhibit tumor growth by stimulating apoptosis as well as by suppression of the P13K/Akt pathways, cell cycle arrest and by inhibition of angiogenesis
Apoptosis↑,
PI3K↓,
Akt↑,
TumCCA↑,
angioG↓,
*NF-kB↓, TQ inhibits nuclear translocation of NF-kB which subsequently blocks the production of NF-kB mediated neuroinflammatory cytokines
*TLR2↓, TQ administration at different doses (10, 20, 40 mg/kg) significantly down-regulated the mRNA expression of TLR-2, TLR-4, MyD88, TRIF and their downstream effectors Interferon regulatory factor 3 (IRF-3)
*TLR4↓,
*MyD88↓,
*TRIF↓,
*IRF3↓,
*IL1β↓, TQ also inhibits LPS induced pro-inflammatory cytokine release like IL-1B, IL-6 and IL-12 p40/70 via its interaction with NF-kB
*IL6↓,
*IL12↓,
*NRF2↑, Nuclear erythroid-2 related factor/antioxidant response element (Nrf 2/ARE) being an upstream signaling pathway of NF-kB signaling pathway, its activation by TQ
*COX2↓, TQ also inhibits the expression of all genes regulated by NF-kB, i.e., COX-2, VEGF, MMP-9, c-Myc, and cyclin D1 which distinctively lowers NF-kB activation making it a potentially effective inhibitor of inflammation, proliferation and invasion
*VEGF↓,
*MMP9↓,
*cMyc↓,
*cycD1/CCND1↓,
*TumCP↓,
*TumCI↓,
*MDA↓, it prevents the rise of malondialdehyde (MDA), transforming growth factor beta (TGF-β), c-reactive protein, IL1-β, caspase-3 and concomitantly upregulates glutathione (GSH), cytochrome c oxidase, and IL-10 levels [92].
*TGF-β↓,
*CRP↓,
*Casp3↓,
*GSH↑,
*IL10↑,
*iNOS↑, decline of inducible nitric oxide synthase (iNOS) protein expression
*lipid-P↓, TQ prominently mitigated hippocampal lipid peroxidation and improved SOD activity
*SOD↑,
*H2O2↓, TQ is a strong hydrogen peroxide, hydroxyl scavenger and lipid peroxidation inhibitor
*ROS↓, TQ (0.1 and 1 μM) ensured the inhibition of free radical generation, lowering of the release of lactate dehydrogenase (LDH)
*LDH↓,
*Catalase↑, upsurge the levels of GSH, SOD, catalase (CAT) and glutathione peroxidase (GPX)
*GPx↑,
*AChE↓, TQ exhibited the highest AChEI activity of 53.7 g/mL in which NS extract overall exhibited 84.7 g/mL, which suggests a significant AChE inhibition.
*cognitive↑, Most prominently, TQ has been found to regulate neurite maintenance for cognitive benefits by phosphorylating and thereby activating the MAPK protein, particularly the JNK proteins for embryogenesis and also lower the expression levels of BAX
*MAPK↑,
*JNK↑,
*BAX↓,
*memory↑, TQ portrays its potential of spatial memory enhancement by reversing the conditions as observed by MWM task
*Aβ↓, TQ thus, has been shown to ameliorate the Aβ accumulation
*MMP↑, improving the cellular activity, inhibiting mitochondrial membrane depolarization and suppressing ROS

Showing Research Papers: 1 to 40 of 40

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 40

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 199

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 7, Catalase↑, 9, CYP2E1↓, 1, GPx↑, 9, GSH↑, 11, GSR↑, 3, GSTs↓, 1, GSTs↑, 2, H2O2↓, 2, HO-1↑, 7, Keap1↓, 1, lipid-P↓, 5, MDA↓, 9, MPO↓, 3, NQO1↑, 1, NRF2↑, 8, Prx↑, 1, ROS?, 1, ROS↓, 16, ROS↝, 1, SOD↑, 13, TAC↑, 2, VitC↑, 1, VitE↑, 1,

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 3, AMPK↑, 2, p‑AMPK↑, 1, cAMP↑, 1, cMyc↓, 1, glucose↓, 1, LDH↓, 2, LDL↓, 1, NADPH↓, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↓, 1, Akt↑, 2, Apoptosis↓, 3, BAX↓, 2, Bcl-2↑, 1, BMP2↑, 1, Casp12↓, 1, Casp3↓, 4, Casp9↓, 1, Cyt‑c↓, 1, iNOS↓, 3, iNOS↑, 1, JNK↓, 1, JNK↑, 1, p‑JNK↓, 1, MAPK↓, 5, MAPK↑, 2, MLKL↓, 1, p‑p38↓, 1, RIP1↓, 1,

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1, SOX9↑, 1,

Transcription & Epigenetics ⓘ

other↓, 1, other↑, 2, other↝, 1,

Protein Folding & ER Stress ⓘ

ATF6↓, 1, CHOP↓, 2, ER Stress↓, 2, GRP78/BiP↓, 1, IRE1↓, 1, PERK↓, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1, LC3II↑, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1, DNMT1↓, 1, DNMT3A↓, 1, DNMTs↓, 1, RAD51↓, 1,

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 2, ERK↓, 1, ERK↑, 1, GSK‐3β↓, 1, HDAC↓, 1, MSCs↑, 1, mTOR↓, 1, mTOR↑, 3, p‑mTOR↓, 1, P70S6K↓, 1, STAT3↓, 2,

Migration ⓘ

5LO↓, 1, AP-1↓, 2, ARG↑, 2, CDK5↓, 1, COL2A1↑, 1, E-cadherin↓, 1, E-sel↓, 1, MMP2↓, 1, MMP9↓, 3, PKA↑, 1, PKCδ↓, 1, Rho↓, 1, ROCK1↓, 1, TGF-β↓, 4, TGF-β↑, 2, TGF-β1↓, 1, TGF-β1↑, 2, TumCI↓, 1, TumCP↓, 1, TXNIP↓, 1, VCAM-1↓, 1, Zeb1↓, 1, ZO-1↓, 1, ZO-1↑, 1, α-SMA↓, 2,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, angioG↝, 1, LOX1↓, 1, NO↓, 6, VEGF↓, 2, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 10, CRP↓, 2, FOXP3↑, 1, ICAM-1↓, 1, IFN-γ↓, 3, IFN-γ↑, 1, IKKα↓, 1, p‑IKKα↓, 1, IL1↓, 2, IL10↑, 32, IL12↓, 2, IL17↓, 3, IL17↑, 1, IL1β↓, 19, IL2↓, 2, IL23↓, 1, IL4↓, 2, IL4↑, 3, IL5↓, 1, IL5↑, 1, IL6↓, 15, IL6↑, 2, IL8↓, 4, Imm↑, 2, Inflam↓, 16, p‑IκB↓, 1, MCP1↓, 1, MyD88↓, 2, NF-kB↓, 20, p‑p65↓, 1, PGE2↓, 5, TLR2↓, 1, TLR4↓, 4, TNF-α↓, 24, TNF-α↑, 1, TNF-β↑, 1, TRIF↓, 1,

Synaptic & Neurotransmission ⓘ

AChE↓, 5, BDNF↑, 4, ChAT↑, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

AGEs↓, 1, Aβ↓, 4, BACE↓, 1, NLRP3↓, 1, β-Amyloid↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 3, BioAv↝, 4, Dose↝, 2, eff↓, 1, eff↑, 4, Half-Life↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 3, ALP↓, 2, AST↓, 3, BG↓, 1, CRP↓, 2, GutMicro↑, 5, IL6↓, 15, IL6↑, 2, LDH↓, 2, NOS2↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 2, AntiCan↑, 1, AntiDiabetic↑, 2, cardioP↑, 3, cognitive↑, 4, hepatoP↑, 6, memory↑, 7, neuroP↑, 12, OS↑, 1, RenoP↑, 1, toxicity↓, 2, toxicity∅, 3, Weight↝, 1, Wound Healing↑, 2,

Infection & Microbiome ⓘ

Bacteria↓, 1, IRF3↓, 1,
Total Targets: 198

Scientific Paper Hit Count for: IL10, Interleukin-10

7 Magnetic Fields
4 Berberine
3 Propolis -bee glue
3 Thymoquinone
2 Boron
2 Butyrate
2 Lycopene
2 Magnetic Field Rotating
2 Piperine
2 Silymarin (Milk Thistle) silibinin
1 Silver-NanoParticles
1 Aloe anthraquinones
1 Baicalein
1 Baicalin
1 Radiotherapy/Radiation
1 Betulinic acid
1 Selenium
1 chitosan
1 Citric Acid
1 Curcumin
1 Luteolin
1 Magnolol
1 Naringin
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Shikonin

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#:562  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

IL10 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Home Page