curcumin and gallocatechol

Previously, we observed curcumin improves aging-associated memory impairment in D-galactose (D-gal) and normal-aged (NA) mice. Evidence showed that multiple agents can be used in managing aging-induced memory dysfunction, drawn by the contribution of several pathways. Curcumin and Epigallocatechin 3 gallate (EGCG) combination substantially reduced the oxidative stress that commonly mediates aging. This study examined the combined effect of EGCG and curcumin on memory improvement in two recognized models, D-gal and normal-aged (NA) mice. The co-administration of EGCG and curcumin significantly (p < 0.05) increased retention time detected by passive avoidance (PA) and freezing response determined in contextual fear conditioning (CFC) compared to the discrete administration of EGCG or curcumin. Biochemical studies revealed that the combination of EGCG and curcumin remarkably ameliorated the levels (p < 0.05) of glutathione, superoxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxidation compared to the monotherapy of EGCG or curcumin in mice hippocampi. The behavioral and biochemical studies revealed that the combination of EGCG and curcumin showed better improvement in rescuing aging-associated memory disorders in mice. EGCG and curcumin combination could serve as a better choice in managing aging-related memory disorders.

Topics: Aging; Animals; Catechin; Curcumin; Galactose; Memory Disorders; Mice; Oxidative Stress

To fetch pathways involved in targetting Hsp90 through Curcumin and Epigallocatechin through Network pharmacological approach.. Hsp90 is a molecular chaperone involved in stabilizing inflammatory protein which may lead to chronic diseases. The herbal compounds Curcumin and Epigallocatechin processing antiinflammatory properties are known to follow a common pathway and control the expression of Hsp90.. To collect the gene targets of Hsp90, Curcumin and Epigallocatechin in order to understand protein-protein interactions of gene targets by constructing the interactome to identify the hub proteins. Hub proteins docking was performed with curcumin and epigallocatechin. Finally, hub proteins involvement with various human diseases were identified.. The gene targets of Hsp90, Curcumin and Epigallocatechin were obtained from there respective databases. Protein-protein interactions of Pkcδ-Nrf2 and Tlr4 pathway gene targets were collected from String database. Protein interaction network was constructed and merged to get intercession network in cytoscape and Cluego was used to predict the disease related target genes. Docking of ligands to target proteins was carried out using Autodock vina tool.. The main key regulators of Curcumin and Epigallocatechin were identified particularly from Pkcδ-Nrf2 and Tlr4 pathway.. The combined action of Curcumin and Epigallocatechin can reduce the expression of Hsp90 eventually controlling the inflammation.

Topics: Anti-Inflammatory Agents; Catechin; Curcumin; Drug Synergism; Flavonoids; HSP90 Heat-Shock Proteins; Humans; Inflammation; Molecular Chaperones; Molecular Docking Simulation; Network Pharmacology; NF-E2-Related Factor 2; Protein Interaction Mapping; Protein Kinase C-delta; Signal Transduction; Toll-Like Receptor 4

Certain phenolic phytochemicals can kill cancer cells. Possible interference from antioxidants is a concern, and this issue has not been studied appreciably. Therefore, the effect of ascorbate and N-acetylcysteine on the ability of epigallocatechin gallate (EGCG) and curcumin to kill HCT116 colon cancer cells was examined. EGCG and curcumin each caused DNA damage in the cells. The DNA-damaging ability of EGCG, but not curcumin, was hindered by either ascorbate or NAC, which was also shown in HT29 and SW480 colon cancer cells. Also, iron chelators (deferoxamine and 2,2'-dipyridyl) inhibited the ability of EGCG, but not curcumin, to cause damage to the DNA in HCT116 cells. Interestingly, curcumin, but not EGCG, increased the expression of growth arrest and DNA damage-inducible gene 153 and also heme oxygenase-1, and this stress gene upregulation by curcumin was antioxidant-insensitive. With prolonged incubation of HCT116 cells with either EGCG or curcumin, cell shrinkage, membrane blebbing, apoptotic bodies, and chromatin condensation/fragmentation were observed. These morphological changes were not apparent in EGCG-treated cells that had been pretreated with either ascorbate or NAC. However, the ascorbate and NAC pretreatments did not prevent the occurrence of the morphological changes in curcumin-treated cells. Thus, these findings suggest that ascorbate and NAC interfere with the ability of EGCG, but not curcumin, to kill HCT116 cells. This basic knowledge may help to better plan and optimize strategies for chemoprevention or chemotherapy.

Topics: Acetylcysteine; Antioxidants; Apoptosis; Ascorbic Acid; Catechin; Cell Line, Tumor; Colonic Neoplasms; Curcumin; DNA Damage; Drug Interactions; Gene Expression; HCT116 Cells; Heme Oxygenase-1; HT29 Cells; Humans; Iron Chelating Agents