科研之友
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摘要
Parkinsons disease is the second most common neurodegenerative disease, and environmental toxins such as rotenone play an important role in causing degeneration of dopaminergic neurons. Melatonin, a major secretory product of pineal, is recently reported to protect against rotenone-induced cell death in animal models. Yet, the mechanism involved in this protection needs to be elucidated. Here, we report that rotenone treatment (0100 mu m) decreased cell survival of Hela cells in a dose-dependent manner. At concentrations ranging from 0.1 to 100 mu m, rotenone induced a dose-dependent increase in the expression of microtubule-associated protein 1 light chain 3 (LC3)-II, a protein associated with the autophagosomal membrane. Knockdown of Bax or Omi using shRNA inhibited 1 mu m rotenone-induced autophagy. To determine whether melatonin would protect cells against rotenone-induced cell death and autophagy, we pretreated Hela cells with 250 mu m melatonin for 24 hr in the presence of rotenone. Melatonin inhibited Bax expression and the release of the omi/HtrA2 into the cytoplasm induced by 1 mu m rotenone. Melatonin 250 mu m treatment also suppressed cell death induced by 0.1100 mu m rotenone and protected against the formation of LC3-II in cells exposed to 1 mu m rotenone. This work demonstrates a novel role for melatonin as a neuroprotective agent against rotenone.
- 出版日期2012-1
- 单位中山大学
