title: Effects of portulacerebroside a on apoptosis of human leukemia HL60 cells and p38/JNK signaling pathway.
abstract: Acute myeloid leukemia is known as one of the most malignant diseases. We aimed at exploring the effect of portulacerebroside A (PCA) on the apoptosis in human leukemia HL60 cells and clarify the possible mechanisms involved in. By MTT analysis, we found that PCA (1-100 μM) inhibited the cell viability in a time- and dose-dependent manner, and cell cycle was arrested at G0/G1 period. PCA treatment from 5 to 50 μM dose-dependently induced apoptosis from 12.7 ± 1.56% to 52.7 ± 6.214% of HL60 cells. Mitochondrial membrane potential (MMP) was decreased and reactive oxygen species (ROS) accumulated obviously. mRNA expressions and protein levels of Bax/Bcl-2, caspase-3 and caspase-9 were elevated significantly. ERK1/2, JNK1/2 and p38 MAPK pathway were blocked detected by western blot analysis. In conclusion, PCA can act as a new agent for leucocythemia treatment.
authors.affiliation: Department of Hematology, Shanghai Children's Hospital, Shanghai Jiao Tong University China.
authors.forename: Qidong
authors.initials: Q
authors.lastname: Ye
authors.affiliation: Department of Hematology, Shanghai Children's Hospital, Shanghai Jiao Tong University China.
authors.forename: Na
authors.initials: N
authors.lastname: Zhang
authors.affiliation: Department of Hematology, Shanghai Children's Hospital, Shanghai Jiao Tong University China.
authors.forename: Kai
authors.initials: K
authors.lastname: Chen
authors.affiliation: Department of Hematology, Shanghai Children's Hospital, Shanghai Jiao Tong University China.
authors.forename: Jiashi
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Hematology, Shanghai Children's Hospital, Shanghai Jiao Tong University China.
authors.forename: Hui
authors.initials: H
authors.lastname: Jiang
mesh_terms: D000972:Antineoplastic Agents, Phytogenic / Q000302:isolation & purification / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D059447:Cell Cycle Checkpoints / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002554:Cerebrosides / Q000302:isolation & purification / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D005963:Glucosylceramides / Q000302:isolation & purification / Q000494:pharmacology*; D018922:HL-60 Cells; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010766:Phosphorylation; D031822:Portulaca / Q000737:chemistry; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D051017:Apoptosis Regulatory Proteins; D002554:Cerebrosides; D005963:Glucosylceramides; D017382:Reactive Oxygen Species; C000611839:portulacerebroside A; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Portulacerebroside A; apoptosis; leucocythemia; p38/JNK
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