茜草根 추출물이 HL-60 세포주의 세포자멸사 기전에 미치는 영향
Influence of Rubiae Radix Extract on the Mechanism of Apoptosis in HL-60 Cells
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Rubiae radix belonging to the family Rubiaceae have been used in traditional medicine to blood stasis and hemostasis. In this study, we reported that methanol extract of Rubiae radix (RRME) induced apoptotic cell death through MAPKs activation in human promylocytic leukemia (HL-60) cells. The cytotoxic activity of activity of RRME in HL-60 cells was increased in a dose-dependent manner. RRME was cytotoxic to HL-60 cells, with IC50 of 8 ㎍/mL. Treatment of RRME to HL-60 cells showed apoptotic bodies, and the fragmentation of DNA, suggesting that these cells underwent apoptosis. Caspase-3 activity and PARP cleavage were time-dependently increased the expression of Bcl-2 and Bax. And ratio of Bax/Bcl-2 protein expression. Activation of p38 and JNK were increased 6 hr after RRME treatment in HL-60 cells, but activation of ERK was reduced 24 hr after treatment. Taken together, these results suggest that RRME induces apoptotic cell death through activation of p38 and JNK in HL-60 cells.
Abstract
Rubiae radix belonging to the family Rubiaceae have been used in traditional medicine to blood stasis and hemostasis. In this study, we reported that methanol extract of Rubiae radix (RRME) induced apoptotic cell death through MAPKs activation in human promylocytic leukemia (HL-60) cells. The cytotoxic activity of activity of RRME in HL-60 cells was increased in a dose-dependent manner. RRME was cytotoxic to HL-60 cells, with IC50 of 8 ㎍/mL. Treatment of RRME to HL-60 cells showed apoptotic bodies, and the fragmentation of DNA, suggesting that these cells underwent apoptosis. Caspase-3 activity and PARP cleavage were time-dependently increased the expression of Bcl-2 and Bax. And ratio of Bax/Bcl-2 protein expression. Activation of p38 and JNK were increased 6 hr after RRME treatment in HL-60 cells, but activation of ERK was reduced 24 hr after treatment. Taken together, these results suggest that RRME induces apoptotic cell death through activation of p38 and JNK in HL-60 cells.
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