Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (10): 1736-1740.doi: 10.3969/j.issn.1673-8225.2011.10.006

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Hydrogen sulfide protects human bone marrow mesesenchymal stem cells against cisplatin-induced damage

Li Jing-chun1, 2, Huang Gang1, Yong Bi-cheng1, Xu Ming-hong1, Wang Yao-fei1, Zhang Long-juan2   

  1. 1Department of Orthopedic-Oncology, 2Laboratory of Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou  510080, Guangdong Province, China
  • Received:2010-10-01 Revised:2010-12-20 Online:2011-03-05 Published:2011-03-05
  • Contact: Huang Gang, Doctor, Associate professor , Associate chief physician, Department of Orthopedic-Oncology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China ganghuang@163.net
  • About author:Li Jing-chun★, Studying for master’s degree, Department of Orthopedic- Oncology, Laboratory of Surgery, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China jingchun999@yahoo.com.cn
  • Supported by:

    Natural Science Foundation of Guangdong Province, No. 07001667*

Abstract:

BACKGROUND: Due to serious myelosuppression caused by hemopoietic stem cell damage when using cisplatin chemo-treatment, there is no effective cytoprotective agent of chemo-treatment to lessen its adverse reaction.
OBJECTIVE: To explore the protection of hydrogen sulfide (H2S) against cisplatin–induced human bone marrow mesesenchymal stem cells (hBMSCs) damage.
METHODS: Sodium hydrosulfide (NaHS) as a H2S donor. hBMSCs treated with different concentrations of sodium hydrosulfide and cisplatin for 48 hours, the cell survival rate was measured by MTT assay; the morphological change of apoptotic cells was tested by using the chromatin dye Hoechst 33258; the proteins expression were detected with Western blot techniques.
RESULTS AND CONCLUSION: MTT detection showed that cisplatin chould reduce the survival rate of BMSCs, and NaHS dose-dependently blocked the inhibition of hBMSCs cells growth induced by cisplatin. When hBMSCs cells were treated by both NaHS (0.5, 1 mmol/L) and cisplatin (20 mg/L) for 48 hours, the NF-κB (p65) was up-regulated, but the IκB-α was down-regulated. When hBMSCs cells were treated by both NaHS (1 mmol/L) and cisplatin (20 mg/L) for 6 hours, the level of phosphorylated protein kinase 1/2 was significantly ascended. The results showed that H2S chould protect hBMSCs against cisplatin-induced damage, which may be associated with the activation of protein kinase-NF-κB signaling pathway.

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