1-1-diphenyl-2-picrylhydrazyl and Leukemia

Natural products can be a source of biomolecules with antioxidant activity which are able to prevent oxidative stress-induced diseases and show antitumor activity, making them important sources of new anticancer drug prototypes. In this context, this study aimed to analyze the chemical composition of an ethanol extract of

Topics: Antineoplastic Agents, Phytogenic; Antioxidants; Biphenyl Compounds; Calcium; Caspase 3; Cell Proliferation; Cell Survival; Dose-Response Relationship, Drug; Erythrocytes; G2 Phase Cell Cycle Checkpoints; Humans; Inhibitory Concentration 50; Jurkat Cells; K562 Cells; Leukemia; Lipid Peroxidation; Malondialdehyde; Membrane Potential, Mitochondrial; Oxidative Stress; Phytochemicals; Phytotherapy; Picrates; Plant Extracts; Plant Leaves; Plants, Medicinal; S Phase Cell Cycle Checkpoints; Senna Plant

Fresh loquat leaves have been used as folk health herb in Asian countries for long time, although the evidence supporting their functions is still minimal. This study aimed to clarify the chemopreventive effect of loquat tea extract (LTE) by investigating the inhibition on proliferation, and underlying mechanisms in human promyelocytic leukemia cells (HL-60). LTE inhibited proliferation of HL-60 in a dose-dependent manner. Molecular data showed that the isolated fraction of LTE induced apoptosis of HL-60 as characterized by DNA fragmentation; activation of caspase-3, -8, and -9; and inactivation of poly(ADP)ribose polymerase. Moreover, LTE fraction increased the ratio of pro-apoptotic Bcl-2-associated X protein (Bax)/anti-apoptotic myeloid cell leukemia 1 (Mcl-1) that caused mitochondrial membrane potential loss and cytochrome c released to cytosol. Thus, our data indicate that LTE might induce apoptosis in HL-60 cells through a mitochondrial dysfunction pathway. These findings enhance our understanding for chemopreventive function of loquat tea.

Topics: Antineoplastic Agents; Apoptosis; bcl-2-Associated X Protein; Beverages; Biphenyl Compounds; Cell Proliferation; Eriobotrya; Free Radical Scavengers; HL-60 Cells; Humans; Leukemia; Membrane Potential, Mitochondrial; Myeloid Cell Leukemia Sequence 1 Protein; Picrates; Plant Extracts; Up-Regulation

The purpose of this study was to assess whether a methanol extract isolated from the greater celandine Chelidonium majus L. (CME) had antioxidant effect and was able to inhibit proliferation and to induce apoptosis in leukemia cells in vitro.. The potential antioxidant activity of CME was proved by the 1,1-diphenyl- 2-picrylhydrazyl (DPPH) radical scavenging assay. The cytotoxicity of CME was measured by the cell growth inhibition assay using murine leukemia L1210 cell line and human promyelocytic HL-60 leukemia cells. Apoptosis-inducing effect was determined by fluorescence microscopy (chromatin condensation and nuclear DNA fragmentation).. In the DPPH assay CME acted as a scavenger of DPPH free radical. The results on antiproliferative properties assessment clearly demonstrated that CME had a cytotoxic effect towards both leukemia cell lines in a dose-dependent manner. In addition, the human promyelocytic HL-60 cells were more sensitive to CME treatment than the L1210 cells.. We concluded that the extract of C. majus L. had a strong antioxidant potential and exerted the antiproliferative activity via apoptosis on leukemia cells. CME due to the presence of the isoquinoline alkaloids and the flavonoid components may play an important role in both cancer chemoprevention through its antioxidant activity and modern cancer chemotherapy as cytotoxic and apoptosis-inducing agent.

Topics: Animals; Antineoplastic Agents, Phytogenic; Antioxidants; Apoptosis; Biphenyl Compounds; Chelidonium; Dose-Response Relationship, Drug; Free Radical Scavengers; HL-60 Cells; Humans; Leukemia; Leukemia L1210; Mice; Microscopy, Fluorescence; Picrates; Plant Extracts