Salidroside inhibits H2O2-induced apoptosis in PC 12 cells by preventing cytochrome c release and inactivating of caspase cascade

  1. Lei Cai1,
  2. Hua Wang2,
  3. Qin Li2,
  4. Yunfei Qian1,
  5. Wenbing Yao1,*

Article first published online: 29 SEP 2008

DOI: 10.1111/j.1745-7270.2008.00463.x

Issue

Acta Biochimica et Biophysica Sinica

Acta Biochimica et Biophysica Sinica

Volume 40, Issue 9, pages 796–802, September 2008

Additional Information

How to Cite

Cai, L., Wang, H., Li, Q., Qian, Y. and Yao, W. (2008), Salidroside inhibits H2O2-induced apoptosis in PC 12 cells by preventing cytochrome c release and inactivating of caspase cascade. Acta Biochimica et Biophysica Sinica, 40: 796–802. doi: 10.1111/j.1745-7270.2008.00463.x

Author Information

  1. 1

    School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China

  2. 2

    Yangtze River Pharmacy Group, Guangzhou Hairui Pharmaceutical Company, Guangzhou 510663, China

* *Corresponding author: Tel, 86-25-83271218; Fax, 86-25-83271218; E-mail, wbyao@cpu.edu.cn

Publication History

  1. Issue published online: 29 SEP 2008
  2. Article first published online: 29 SEP 2008
  3. Received: March 11, 2008; Accepted: June 17, 2008

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Keywords:

  • salidroside;
  • hydrogen peroxide;
  • apoptosis;
  • PC 12 cells

We used a rat pheochromocytoma (PC 12) cell line to study the effects of salidroside on hydrogen peroxide (H2O2)-induced apoptosis. In PC12 cells, H2O2-induced apoptosis was accompanied by the down-regulation of Bcl-2, the up-regulation of Bax, the release of mitochondrial cytochrome c to cytosol, and the activation of caspase-3, -8 and -9. However, salidroside suppressed the down-regulation of Bcl-2, the up-regulation of Bax and the release of mitochondrial cytochrome c to cytosol. Moreover, salidroside attenuated caspase-3, -8 and -9 activation, and eventually protected cells against H2O2-induced apoptosis. Taken together, these results suggest that treatment of PC12 cells with salidroside can block H2O2-induced apoptosis by regulating Bcl-2 family members and by suppressing cytochrome c release and caspase cascade activation.

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