Mechanism of rat osteosarcoma cell apoptosis induced by a combination of low-intensity ultrasound and 5-aminolevulinic acid in vitro

Y. N. Li, Q. Zhou, B. Yang, Z. Hu, J. H. Wang, Q. S. Li, W. W. Cao

Research output: Contribution to journalArticle

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Abstract

We investigated the killing effect of low-intensity ultrasound combined with 5-aminolevulinic acid (5-ALA) on the rat osteosarcoma cell line UMR-106. Logarithmic-phase UMR-106 cells were divided into a control group, ultrasound group and 5-ALA group. The cell apoptotic rate, production of reactive oxygen species, and the change in mitochondrial membrane potential were analyzed by flow cytometry; ultrastructural changes were observed by transmission electron microscopy. Using low-intensity ultrasound at 1.0 MHz and 2.0 W/cm2 plus 5-ALA at a concentration of 2 mM, the apoptotic rate of the sonodynamic therapy group was 27.2 ± 3.4% which was significantly higher than that of the control group, ultrasound group, and 5-ALA group (P < 0.05). The production of reactive oxygen species was 32.6 ± 2.2% and the decrease in mitochondrial membrane potential was 39.5 ± 2.5%. The 33342 staining showed nuclear condensation and fragmentation in the ultrasound group and 5-ALA group. Structural changes in the cell membrane, mitochondria, Golgi apparatus, and other organelles observed by transmission electron microscopy included formation of apoptotic bodies. The killing effect of low-intensity ultrasound combined with 5-ALA on UMR-106 cells was significant. Cell apoptosis played a vital role in the killing effect, and the mitochondria pathway contributed to the apoptosis of UMR-106 cells.

Original languageEnglish (US)
Pages (from-to)9604-9613
Number of pages10
JournalGenetics and Molecular Research
Volume14
Issue number3
DOIs
StatePublished - Aug 14 2015

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Aminolevulinic Acid
Osteosarcoma
Apoptosis
Mitochondrial Membrane Potential
Transmission Electron Microscopy
Reactive Oxygen Species
Mitochondria
Control Groups
Golgi Apparatus
Group Psychotherapy
Organelles
In Vitro Techniques
Flow Cytometry
Cell Membrane
Staining and Labeling
Cell Line

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics

Cite this

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title = "Mechanism of rat osteosarcoma cell apoptosis induced by a combination of low-intensity ultrasound and 5-aminolevulinic acid in vitro",
abstract = "We investigated the killing effect of low-intensity ultrasound combined with 5-aminolevulinic acid (5-ALA) on the rat osteosarcoma cell line UMR-106. Logarithmic-phase UMR-106 cells were divided into a control group, ultrasound group and 5-ALA group. The cell apoptotic rate, production of reactive oxygen species, and the change in mitochondrial membrane potential were analyzed by flow cytometry; ultrastructural changes were observed by transmission electron microscopy. Using low-intensity ultrasound at 1.0 MHz and 2.0 W/cm2 plus 5-ALA at a concentration of 2 mM, the apoptotic rate of the sonodynamic therapy group was 27.2 ± 3.4{\%} which was significantly higher than that of the control group, ultrasound group, and 5-ALA group (P < 0.05). The production of reactive oxygen species was 32.6 ± 2.2{\%} and the decrease in mitochondrial membrane potential was 39.5 ± 2.5{\%}. The 33342 staining showed nuclear condensation and fragmentation in the ultrasound group and 5-ALA group. Structural changes in the cell membrane, mitochondria, Golgi apparatus, and other organelles observed by transmission electron microscopy included formation of apoptotic bodies. The killing effect of low-intensity ultrasound combined with 5-ALA on UMR-106 cells was significant. Cell apoptosis played a vital role in the killing effect, and the mitochondria pathway contributed to the apoptosis of UMR-106 cells.",
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Mechanism of rat osteosarcoma cell apoptosis induced by a combination of low-intensity ultrasound and 5-aminolevulinic acid in vitro. / Li, Y. N.; Zhou, Q.; Yang, B.; Hu, Z.; Wang, J. H.; Li, Q. S.; Cao, W. W.

In: Genetics and Molecular Research, Vol. 14, No. 3, 14.08.2015, p. 9604-9613.

Research output: Contribution to journalArticle

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AU - Li, Y. N.

AU - Zhou, Q.

AU - Yang, B.

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AU - Cao, W. W.

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