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      INTRACELLULAR Ca^2+ RELEASE MEDIATES URSOLIC ACID-INDUCED APOPTOSIS IN HUMAN LEUKEMIC HL-60 CELLS

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      https://www.riss.kr/link?id=A30059975

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      The effect of ursolic acid(UA)on tumor cell apoptosis was investigated using HL-60 human promyelocytic leukemia cells as a model cellular system. Treatment with UA resulted in a concemtration-dependent decreased cell viability assessed by MTT assay. UA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which UA induced celldeath was through apotosis. The intracellular Ca^2+ level was increased by treatment with UA. Intracellular Ca^2+ inhibitors, such as intracellular Ca^2+, release blockers(dantrolene, TMB-8 and ruthenium red) and an intracellular Ca^2+ chelator(BAPTA/AM),significantly blocked the UA-induced increased intracellular Ca^2+ concentration. These inhibitors also blocked the effect of UA on cell viability and apoptosis. These results suggest that enhanced intracellular Ca^2+ signals may be involved in UA-induced apoptosis in HL-60 cells.lnt.J.Cancer 73:725-728,1997.
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      The effect of ursolic acid(UA)on tumor cell apoptosis was investigated using HL-60 human promyelocytic leukemia cells as a model cellular system. Treatment with UA resulted in a concemtration-dependent decreased cell viability assessed by MTT assay. U...

      The effect of ursolic acid(UA)on tumor cell apoptosis was investigated using HL-60 human promyelocytic leukemia cells as a model cellular system. Treatment with UA resulted in a concemtration-dependent decreased cell viability assessed by MTT assay. UA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which UA induced celldeath was through apotosis. The intracellular Ca^2+ level was increased by treatment with UA. Intracellular Ca^2+ inhibitors, such as intracellular Ca^2+, release blockers(dantrolene, TMB-8 and ruthenium red) and an intracellular Ca^2+ chelator(BAPTA/AM),significantly blocked the UA-induced increased intracellular Ca^2+ concentration. These inhibitors also blocked the effect of UA on cell viability and apoptosis. These results suggest that enhanced intracellular Ca^2+ signals may be involved in UA-induced apoptosis in HL-60 cells.lnt.J.Cancer 73:725-728,1997.

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