| Institution: | 1.Department of Neurosurgery,Eski?ehir Osmangazi University School of Medicine,Eskisehir,Turkey;2.Department of Anatomy,Eski?ehir Osmangazi University School of Medicine,Eskisehir,Turkey;3.Department of Biochemistry,Eski?ehir Osmangazi University School of Medicine,Eskisehir,Turkey;4.Department of Histology-Embryology,Eski?ehir Osmangazi University School of Medicine,Eskisehir,Turkey;5.Department of Physiology,Eski?ehir Osmangazi University School of Medicine,Eskisehir,Turkey |
| Abstract: | We hypothesized that dexanabinol can prevent neuronal death by protecting neuronal lysosomes from nitric oxide (NO)-mediated
toxicity, and in turn, by suppressing the release of cathepsins during cerebral ischemia. Focal cerebral ischemia was induced
in two sets of animals by permanent middle cerebral artery occlusion. The first set was used to monitor NO concentration and
cathepsin activity, while the second was used for histological examination with hematoxylin and eosin, and TUNEL staining.
In post-ischemic brain tissue, NO content and cathepsin B and L activity increased (p < 0.05). Dexanabinol treatment reduced NO concentration and cathepsin activity to the control level (p > 0.05). The number of eosinophilic and apoptotic neurons increased in the post-ischemic cerebral cortex (p < 0.05). However, dexanabinol treatment lowered both of these (p < 0.05). We conclude that dexanabinol might be a useful agent for the treatment of stroke patients. |
