Protective effects of 20‐hydroxyecdysone on CoCl 2 ‐induced cell injury in PC12 cells

• Published in: Journal of cellular biochemistry Vol. 111; no. 6; pp. 1512 - 1521
• Main Authors: Hu, J., Zhao, T.Z., Chu, W.H., Luo, C.X., Tang, W.H., Yi, L., Feng, H.
• Format: Journal Article
• Language: English
• Published: 15.12.2010
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.22877

Abstract 20‐Hydroxyecdysone, which is found in the rhizomes, roots and the stems of many plants, is an ecdysteroid hormone that regulates molting in insects. We have previously shown that 20‐Hydroxyecdysone could alleviate neurological deficits induced by subarachnoid hemorrhage in rabbits. Thus, we hypothesized that 20‐Hydroxyecdysone might protect neurons against hypoxic–ischemic injury. In present study, the effects of 20‐Hydroxyecdysone on cobalt chloride (CoCl 2 )‐induced cellular injury in PC12 cells was investigated. The incubation of PC12 cells with CoCl 2 reduced the cell viability, increased the rate of apoptosis. However, when cells were treated with 20‐Hydroxyecdysone before or after CoCl 2 exposure, the CoCl 2 ‐induced cellular injuries were significantly ameliorated. In addition, 20‐Hydroxyecdysone dramatically reduced the CoCl 2 ‐induced production of reactive oxygen species (ROS), decreased the depolarization of the mitochondrial membrane, inhibited the release of cytochrome c into the cytosol and increased the Bax/Bcl‐2 ratio. Furthermore, 20‐Hydroxyecdysone eliminated the CoCl 2 ‐induced activation of caspase‐3. Taken together, these results indicate that 20‐Hydroxyecdysone may protect PC12 cells against CoCl 2 ‐induced cell injury by inhibiting ROS production and modulating components of the mitochondrial apoptosis pathway. Based on our results, 20‐Hydroxyecdysone may be a potential candidate for intervention in hypoxic–ischemic brain injuries such as stroke. J. Cell. Biochem. 111: 1512–1521, 2010. © 2010 Wiley‐Liss, Inc.