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| 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 -may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog). 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 curcumin can act as a pro-oxidant when blue light is applied - 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↑">SOD↑, GSH↑, Catalase↑, - lowers Inflammation : 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
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| SOD, or superoxide dismutase, is an important antioxidant enzyme that plays a crucial role in protecting cells from oxidative stress. It catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide. SOD Isoforms: There are three main isoforms of SOD: SOD1 (cytosolic): Often found to be overexpressed in certain tumors, which may help cancer cells survive in oxidative environments. SOD2 (mitochondrial): Plays a critical role in protecting mitochondria from oxidative damage. Its expression can be upregulated in some cancers, contributing to tumor growth and resistance to therapy. SOD3 (extracellular): Its role in cancer is less well understood, but it may have implications in the tumor microenvironment and metastasis. The expression levels of SOD can serve as a prognostic indicator in some cancers. For example, high levels of SOD expression have been associated with poor prognosis in certain types of tumors, potentially due to their role in promoting tumor cell survival and resistance to therapies. |
| 3795- | CUR, | Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence |
| - | Review, | AD, | NA |
| 3794- | CUR, | Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities |
| - | Review, | AD, | NA |
| 2819- | CUR, | Chemo, | Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury |
| - | Review, | Var, | NA |
| 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 |
| 2810- | CUR, | Effect of curcuminoids on oxidative stress: A systematic review and meta-analysis of randomized controlled trials |
| - | Review, | Nor, | NA |
| 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 |
| 3581- | CUR, | Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease |
| - | NA, | AD, | NA |
| 3574- | CUR, | The effect of curcumin (turmeric) on Alzheimer's disease: An overview |
| - | Review, | AD, | NA |
| 128- | CUR, | RES, | Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer |
| - | in-vivo, | Pca, | NA |
| 4827- | QC, | CUR, | Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin |
| - | Review, | Var, | NA |
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
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