title: ROS mediates baicalin-induced apoptosis in human promyelocytic leukemia HL-60 cells through the expression of the Gadd153 and mitochondrial-dependent pathway.
abstract: BACKGROUND
  Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of leukemia. In this study, we investigated the effects of baicalin (a compound obtained from Scutellaria baicalensis Georgi and S. rivularis Benth Labiateae) on the viability, induction of apoptosis and associated mechanism in human leukemia HL-60 cells.
  
  
  METHODS
  The cell viability and apoptosis was examined by flow cytometric analysis. The results showed that baicalin induced cytotoxicity in a dose- and time-dependent manner through the activation of caspase-3, as shown by treatment of HL-60 cells with an inhibitor of caspase-3 (z-VAD-fmk). Baicalin increased the levels of ROS, Ca2+ and decreased mitochondrial membrane potential in HL-60 cells. Western blot demonstrated that baicalin promoted the levels of Gadd153, Bax, cytochrome c and caspase-3 and -12, but decreased the levels of Grp78 and Bcl-2 in HL-60 cells.
  
  
  CONCLUSIONS
  Baicalin was found to induce apoptosis in HL-60 cells through multiple pathways.
authors.affiliation: Department of Clinical Pathology, Cheng Hsin Rehabilitation Medical Center, Taipei, Taiwan, ROC.
authors.forename: Hsu-Fung
authors.initials: HF
authors.lastname: Lu
authors.forename: Shu-Ching
authors.initials: SC
authors.lastname: Hsueh
authors.forename: Yung-Tsuan
authors.initials: YT
authors.lastname: Ho
authors.forename: Ming-Ching
authors.initials: MC
authors.lastname: Kao
authors.forename: Jai-Sing
authors.initials: JS
authors.lastname: Yang
authors.forename: Tsan-Hung
authors.initials: TH
authors.lastname: Chiu
authors.forename: Shau-Yen
authors.initials: SY
authors.lastname: Huamg
authors.forename: Ching-Chung
authors.initials: CC
authors.lastname: Lin
authors.forename: Jing-Gung
authors.initials: JG
authors.lastname: Chung
mesh_terms: D000590:Amino Acid Chloromethyl Ketones / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism; D053454:Caspase 12 / Q000378:metabolism; D053148:Caspase 3 / Q000096:biosynthesis / Q000378:metabolism; D061945:Caspase Inhibitors; D002470:Cell Survival / Q000187:drug effects; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D000091342:Endoplasmic Reticulum Chaperone BiP; D004790:Enzyme Induction / Q000187:drug effects; D005419:Flavonoids / Q000494:pharmacology*; D005434:Flow Cytometry; D018922:HL-60 Cells; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D018832:Molecular Chaperones / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D051742:Transcription Factor CHOP / Q000096:biosynthesis*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000590:Amino Acid Chloromethyl Ketones; C494826:BAX protein, human; D061945:Caspase Inhibitors; D015853:Cysteine Proteinase Inhibitors; C497249:DDIT3 protein, human; D000091342:Endoplasmic Reticulum Chaperone BiP; D005419:Flavonoids; C000717247:HSPA5 protein, human; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; C096713:benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; D051742:Transcription Factor CHOP; C038044:baicalin; D045304:Cytochromes c; D053454:Caspase 12; D053148:Caspase 3; D002118:Calcium