INF-γ Cancer Research Results

INF-γ, interferon gamma: Click to Expand ⟱
Source:
Type:
IFN-γ is a cytokine produced primarily by activated T lymphocytes (CD4⁺ Th1, CD8⁺ cytotoxic T cells) and natural killer (NK) cells.
– It plays a central role in orchestrating immune responses against pathogens and tumor cells by enhancing antigen presentation and activating immune effector mechanisms.

– IFN-γ can promote antitumor immunity by activating macrophages, NK cells, and cytotoxic T lymphocytes.
– It enhances the presentation of tumor antigens, thereby facilitating the immune system’s ability to target and eliminate cancer cells.
• Its expression and signaling within the tumor microenvironment are generally associated with a robust immune response and, in many cases, a favorable prognosis—particularly in tumors deemed "immunologically hot."

• Dual Role:
– While IFN-γ typically supports immune-mediated tumor suppression, chronic exposure to IFN-γ within the tumor microenvironment may contribute to immune editing and the selection of tumor cell variants that are resistant to immune attack.
Scientific Papers found: Click to Expand⟱
3550- ALA,    Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?
- Review, AD, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner

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↓,

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

1806- NarG,    Naringin: Nanotechnological Strategies for Potential Pharmaceutical Applications
- Review, NA, 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↓,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   IL10↑, 1,   IL6↓, 1,   INF-γ↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   GSR↓, 1,   H2O2↓, 1,   lipid-P↓, 1,   MDA↓, 3,   NRF2↑, 3,   ROS↓, 3,   SOD↑, 3,  

Mitochondria & Bioenergetics ⓘ

AIF↓, 1,   ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

cAMP↑, 1,   LDH↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   Casp3↓, 2,   Casp9↓, 2,   iNOS↓, 2,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   STAT↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 3,   IL2↓, 2,   IL4↓, 2,   IL6↓, 2,   INF-γ↓, 3,   Inflam↓, 3,   NF-kB↓, 1,   PGE2↓, 2,   TNF-α↓, 4,  

Synaptic & Neurotransmission ⓘ

ChAT↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   eff↑, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 4,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 46

Scientific Paper Hit Count for: INF-γ, interferon gamma
2 Curcumin
1 Alpha-Lipoic-Acid
1 Naringin
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#:1170  State#:%  Dir#:1
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