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Objectives: Orostachys japonicas (O. japonicus) has been known for its anti-tumor effect. In the present study, it was investigated whether O. japonicus EtOH extracts could induce apoptosis and autophagy which are part of the main mechanism related to anti-tumor effect in THP-1 cells.
Methods: Cells were treated with various concentrations of O. japonicus EtOH extracts (0-300μg/ml) for 24, 48, and 72h. Cell viability was evaluated by MTS/PMS assay and apoptosis rate was examined by flow cytometry and ELISA assay. The mRNA expression of apoptosis-related genes (Bcl-2, Mcl-1, Survivin, Bax) and autophagy-related gene (mTOR) was evaluated using real-time PCR. The protein expression of Caspase-3, Akt, LC3Ⅱ, Beclin-1, Atg5, NF-κB, p38, ERK was evaluated using western blot analysis.
Results: O. japonicus EtOH extracts inhibited cell proliferation and apoptosis rate was increased in both flow cytometry and ELISA assay. Bcl-2, Mcl-1, Survivin (anti-apoptosis factors) mRNA expressions were decreased and Bax (pro-apoptosis factor) mRNA level was increased. mTOR mRNA expressions was decreased and LC3Ⅱ protein expressions was increased. Activation of NF-κB was decreased and phosphorylation of p38 was increased.
Conclusion: O. japonicus is regarded to inhibit cell proliferation, to induce apoptosis and to regulate autophagy-related genes in THP-1 cells via NF-κB and p38 MAPK signaling pathway. This suggests O. japonicus could be an effective herb in treating acute myeloid leukemia.
Methods: Cells were treated with various concentrations of O. japonicus EtOH extracts (0-300μg/ml) for 24, 48, and 72h. Cell viability was evaluated by MTS/PMS assay and apoptosis rate was examined by flow cytometry and ELISA assay. The mRNA expression of apoptosis-related genes (Bcl-2, Mcl-1, Survivin, Bax) and autophagy-related gene (mTOR) was evaluated using real-time PCR. The protein expression of Caspase-3, Akt, LC3Ⅱ, Beclin-1, Atg5, NF-κB, p38, ERK was evaluated using western blot analysis.
Results: O. japonicus EtOH extracts inhibited cell proliferation and apoptosis rate was increased in both flow cytometry and ELISA assay. Bcl-2, Mcl-1, Survivin (anti-apoptosis factors) mRNA expressions were decreased and Bax (pro-apoptosis factor) mRNA level was increased. mTOR mRNA expressions was decreased and LC3Ⅱ protein expressions was increased. Activation of NF-κB was decreased and phosphorylation of p38 was increased.
Conclusion: O. japonicus is regarded to inhibit cell proliferation, to induce apoptosis and to regulate autophagy-related genes in THP-1 cells via NF-κB and p38 MAPK signaling pathway. This suggests O. japonicus could be an effective herb in treating acute myeloid leukemia.
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재료 및 방법
결과
고찰
결론
참고문헌
참고문헌 (31)
참고문헌 신청
De Kouchkovsky I / 2016 / Acute myeloid leukemia : a comprehensive review and 2016update / Blood cancer journal 6(7):e441
Eun-Hye Park / 2015 / Nationwide statistical analysis of myeloid malignancies in Korea: incidence and survival rate from 1999 to 2012 / Blood Research 50(4):204~217
Lowenberg B / 1999 / Acute myeloid leukemia / New England Journal of Medicine 341(14):1051~1062
Shah A / 2013 / Survival and cure of acute myeloid leukaemia in England, 1971‐2006 : a population-based study / British journal of haematology 162(4):509~516
Meyers J / 2013 / Medicare fee-for-service enrollees with primary acute myeloid leukemia : an analysis of treatment patterns, survival, and healthcare resource utilization and costs / Applied health economics and health policy 11(3):275~286
Eun-Hye Park / 2015 / Nationwide statistical analysis of myeloid malignancies in Korea: incidence and survival rate from 1999 to 2012 / Blood Research 50(4):204~217
Lowenberg B / 1999 / Acute myeloid leukemia / New England Journal of Medicine 341(14):1051~1062
Shah A / 2013 / Survival and cure of acute myeloid leukaemia in England, 1971‐2006 : a population-based study / British journal of haematology 162(4):509~516
Meyers J / 2013 / Medicare fee-for-service enrollees with primary acute myeloid leukemia : an analysis of treatment patterns, survival, and healthcare resource utilization and costs / Applied health economics and health policy 11(3):275~286
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UCI(KEPA) : I410-ECN-0101-2019-519-000946695