Curcumin And Apoptosis-Inducing Factor

Cancer is a terrible disease, characterized by uncontrolled growth of cells. There are many different forms of cancer, but they do have several commonalities, some of which appear to be affected by curcumin supplementation. Researchers have been studying curcumin as a beneficial herb in cancer treatment. It can affect cancer growth, development and spread at the molecular level. Studies have shown that it can reduce angiogenesis (growth of new blood vessels in tumors), metastasis (spread of cancer), as well as contributing to the death of cancerous cells. Multiple studies have shown that curcumin can reduce the growth of cancerous cells in the laboratory and inhibit the growth

While Turmeric (Curcumin) can be taken in capsule form with water it is not readily passed into the stomach and small intestine then into the blood to be made available to the body. The liver and gastrointestinal tract quickly metabolize Curcumin and make it available to the kidneys to excrete. The constituent Curcumin, needs fat to be made bioavailable to the body. Studies have shown adding Piperine (black pepper) to Curcumin and fat makes Curcumin 2,000% more bioavailable. Bioavailable Curcumin will permeate the blood brain barrier where it will be stable enough to effect a change in

Curcumin is a very active compound and is responsible for the yellow color of turmeric which has antioxidant and anti-inflammatory properties that can have a significant effect on osteoarthritis by the protection of chondrocytes. The aim of this study was to evaluate the effectiveness of curcumin in reducing the symptoms of patients with osteoarthritis of the knee. In this interventional study, curcumin and placebo will be prescribed to the groups and a random number table will be used for treatment allocation by the statistical analyzer. Patients and researchers will not know the group of the patients and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) will be completed for patients in 0 and 6 weeks of drug using. In this study, WOMAC questionnaire will be completed for 80 patients (40 patients in curcumin group and 40 patients in the placebo group) with knee osteoarthritis in 0 and 6

Annexing V FITIC/PI was used to detect for the involvement of apoptosis based upon externalization of phospholipid phosphatidylserine (PS) and permeabilization of nuclear membrane for staining with PI. PS is a biomarker of early apoptotic stage, Annexin V has specific and high affinity for the anionic PS, when PS is exposed on cell surface Annexing V binds to it. PS indicates intermediate stages of apoptosis. Caspases-3 activation, nuclear fragmentation and mitochondrial membrane flux preceded PS translocation [46]. From Fig.5 sonicated pectin induced dose apoptosis and reduced proportion of viable cells. The 400W sonicated pectin was more potent apoptosis inducer than 200W sonicated pectin. control cells had 89.29% viable cells 3.14% early apoptotic cells and 6.50% late apoptosis, 400W sonicated pectin at 0.1 and 0.5mg/ml induced significant reduction in viable cells to 70.90%, early apoptotic cells were 4.84% and late apoptosis 14.94% in the cells as shown in Fig.5b, on the other hand, 0.5mg/ml led to 50.79% viable cells, 22.65 %early apoptotic cells and 19.56% late apoptotic cells as shown in Fig.

Resistance to apoptosis will be assayed via western blot for Thyroid, FTC cells with mutations, and PTC with mutations treated and not treated with siFLRT3 knockouts with antibodies specific for caspase-3 , actin and FLRT3. The appearance of caspase-3 indicates DNA damage and subsequent apoptosis, since caspase is a DNA repairing protein that is cleaved when cells undergo apoptosis. Additionally, resistance to apoptosis will be calculated using a TUNEL-assay protocol [4] for FTC cells harboring mutations, and PTC cells containing mutations treated and not treated with siFLRT3 and infrared radiation. TUNEL assays quantify apoptosis by using TdT enzymes to bind to the 3’ end of DNA in order to gauge the amount of DNA fragmentation, a marker of apoptosis. We will evaluate FLRT3’s impact on motility for FTC cell lines with / mutations by testing for metastasis over various time intervals. Metastasis in vivo experiments will be performed by injecting immunodeficient mice in the tail with PTC cells containing either or / mutations and checking for metastasis to the lymph nodes at various time intervals[5]. PTC cells with / / mutations will be generated by performing a mouse knock out by isolating embryonic stem cells from / containing white mouse blastocysts and subsequently introducing ∆flrt3::neoR containing plasmids with homologous primers attached into the cells

It is the phycocyanin in spirulina that has the anti-cancer effect. A recent study shows that the phycocyanin kills cancerous blood cells.

First, the α-2,6 sialylation can block the apoptosis mechanism40-41. Apoptosis is the mechanism of programmed cell death of multicellular organisms. The apoptosis process is induced by binding of cell galectins42-43. Galectins are a type of lectin and lectins are a class of proteins which can bind to specific proteins, via interacting with specific glycans. These galectins bind galactose of cell surface glycans to initiate the killing mechanism. It has been reported that α-2,6 sialyation significantly blocks galectin binding and inhibit apoptosis and this leads to the undesirable growth of cancer cells44-45. The α-2,6 sialyation also significantly blocks apoptosis pathways which use FAS46 and TNFR147 cell receptors.

Hypothesis: Specific concentrations of tannic acid eluting from collagen beads can be used to selectively trigger cell death in ER+ and HER2+ breast cancer cells and not healthy mammary cells over a period of several months.

Studies have shown that CN is a unique homodimeric disintegrin that is able to bind to many integrins. This ability gives CN an advantage among other disintegrins as they are only able to bind to a single integrin. Integrins are expressed in wound healing, tissue remodeling, angiogenesis, tumor growth, and metastasis (Schmitmeier et al. 2003). Furthermore, they are also ECM protein receptors, thus, they are involved in bidirectional signaling in the cell. As a result, integrins are able to modify a cell by altering migration, degradation, and proliferation among other functions (Swenson et al. 2004). Correspondingly, CN is heavily researched upon in order to combat illnesses. Disintegrins are able to bind to fibrinogen receptors, inhibiting fibrinogen platelet aggregation and decreasing tumor metastasis (Zhou

Therefore, then prompt caspase three and other effector caspases that cause apoptosis. By utilizing this data, experiments have been carried out that try to induce apoptosis in cancer cells by activation of the p53 gene. One particular examination was done on the human osteosarcoma cell line Saos-2, which is deficient in p53. According to Schuler (2000), an introduction of the p53 gene led to apoptosis through an intrinsic pathway. Subsequently subjecting p53 to gene treatment might be of enormous importance in the battle against leukemia.

In this study, scientist found that there are levels of free radicals reactivity of the compounds that are being produced in the cell; some with least reactivity such as H2O2, and some are highly reactive such as OH. The free radicals can affect the cell negatively. One of the element that generates free radicals and causes oxidative stress is cadmium. It increases lipid peroxidation and/or changes intracellular glutathione levels. However, investigators found that some plants such as curcumin is a natural drug that works

In vitro: Mocetinostat was found to potently target human HDAC1 but also had inhibitory activity against HDAC2, HDAC3, and HDAC11. In cells, mocetinostat could inhibit only a fraction of the total HDAC activity. Moreover, mocetinostat induced hyperacetylation of histones, selectively induced apoptosis, and caused cell cycle blockade in various human cancer cell lines. Mocetinostat also showed potent and selective antiproliferative activities against various human cancer cell lines [1].

Curcumin is a standout amongst the most intense remedial agents related to turmeric. Free radicals and irritation are believed to assume a noteworthy part in aging and curcumin influences both.

DJ-1 protects against mtDNA damage, mitophagy and cell death. DJ-1 is a multifunctional protein that protects cells from oxidative stress via several molecular processes including regulating gene transcription, mediating cell signal transduction pathways, stabilizing cytoprotective proteins and scavenging ROS (3). DJ-1 is expressed in human primary alveolar type II cells (preliminary data) and we have recently postulated that plays a role in the antioxidant defense system in the lung (REF). The importance of DJ-1 can be supported by several observations. First, DJ-1 mutations are pathogenic (4), second, oxidation of cysteine and methionine residues within DJ-1 was reported as a sensor of its activity (5) and third, the novel oxidized

Chemo-protective effects of cruciferous vegetables is comprehensively studied on intentions of reducing the onset of prostate cancer. Cruciferous vegetables contain many bioactive compounds. The anti-carcinogenic engagements of cruciferous vegetables are frequently related to the glucosinolate (sulfur-containing chemicals) component of these vegetables. The substrate components of glucosinolates are biologically active compounds that are being studied for possible anticancer effects in foods such as broccoli, Brussels sprouts, cabbage, radishes, and wasabi. Compounds of the cruciferous nature have revealed anticancer effects in cells and animals, but the results of studies with humans result in controversial properties.