Silymarin Protects Umbilical Cord-Derived Mesenchymal Stem Cells against Apoptosis Induced by Serum-Deprivation / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 1422-1426, 2015.
Artigo
em Chinês
| WPRIM
| ID: wpr-274023
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protection of silymarin against the human mesenchymal stem cell (MSC) apoptosis induced by serum deprivation and its underlying mechanism.</p><p><b>METHODS</b>Human umbilical cord MSCs were cultured in the absence of serum, and the silymain of different concentration (1-10 µg/ml) was added into the medium. MTT test was performed to observe the cell proliferation status. After being cultured for 72 hours, the cells were collected, and flow cytometry with Annexin-V-PI double-staining was used to detect the apoptotic cells from the control and silymarin-treated groups. Furthermore, the intracellular contents of BAX and BCL-2 were detected by Western blot for exploring the potential mechanism.</p><p><b>RESULTS</b>The silymarin promoted the proliferation of human UC-MSCs in a dose-dependent manner, reaching its maximal at a dose of 5 µg/ml. Moreover, silymarin could inhibit the serum deprivation-induced apoptosis of MSCs and, the inhibitory rate reached up to 30% when it was added at a concentration of 5 µg/ml. The content of intracellular BAX was obviously elevated after serum-deprivation treatment, and this increase could be blunted by the addition of silymarin. Meanwhile, the content of BCL-2 was not obviously changed.</p><p><b>CONCLUSION</b>The silymarin can stimulate MSC growth and inhibit the apoptosis of MSCs probably by the mitochondria pathway.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Silimarina
/
Cordão Umbilical
/
Meios de Cultura Livres de Soro
/
Apoptose
/
Proteínas Proto-Oncogênicas c-bcl-2
/
Biologia Celular
/
Proliferação de Células
/
Proteína X Associada a bcl-2
/
Células-Tronco Mesenquimais
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Experimental Hematology
Ano de publicação:
2015
Tipo de documento:
Artigo
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