1. Ginkgolide B prevents cathepsin-mediated cell death following cerebral ischemia/reperfusion injury.
- Author
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Qin XF, Lu XJ, Ge JB, Xu HZ, Qin HD, and Xu F
- Subjects
- Animals, Apoptosis drug effects, Brain Ischemia pathology, Brain Ischemia physiopathology, Cathepsin B metabolism, Cathepsin L metabolism, Cerebral Cortex drug effects, Cerebral Cortex pathology, Cerebral Cortex physiopathology, Down-Regulation drug effects, Male, Mice, Mice, Inbred ICR, Motor Activity drug effects, Motor Activity physiology, Necrosis drug therapy, Necrosis pathology, Reperfusion Injury pathology, Reperfusion Injury physiopathology, Severity of Illness Index, Brain Ischemia drug therapy, Cathepsins metabolism, Cell Death drug effects, Ginkgolides therapeutic use, Lactones therapeutic use, Neuroprotective Agents therapeutic use, Reperfusion Injury drug therapy
- Abstract
Ginkgolide B (GB) has been shown to exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanism by which GB prevents ischemic cell death remains unclear. Lysosomal proteases, including cathepsins B and L, have been implicated in ischemic cell death following reperfusion. Therefore, in the present study, we investigated the role of GB with respect to cathepsin-mediated cell death following I/R. Both the expression and enzymatic activity of cathepsins B and L were significantly increased in the ischemic cortex following cerebral I/R injury. We found that GB treatment markedly decreased the activity and expression of cathepsins B and L following I/R. Moreover, GB reduced necrotic and apoptotic cell death following I/R. These data strongly suggest that GB prevents cathepsin-mediated cell death following focal cerebral I/R injury, and they might provide new insights into the mechanism of the neuroprotective effects of GB.
- Published
- 2014
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