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Cycloheximide reduces the size of lesion caused in rats by a photothrombotic model of brain injury

1997; Taylor & Francis; Volume: 19; Issue: 1 Linguagem: Inglês

10.1080/01616412.1997.11740779

1743-1328

Alexander Kharlamov, Jin‐Yang Joo, Tolga Uz, Hari Manev,

Eicosanoids and Hypertension Pharmacology

A reproducible brain lesion can be triggered in rats by treating them systematically with rose bengal and irradiating their skulls with light. This procedure is often referred to as the photothrombotic model of stroke/ injury. Recently we reported that in this model some cells show signs of apoptosis, programmed cell death. Apoptosis can be attenuated by inhibitors of macromolecular synthesis. In the work described here, we tested the hypothesis that the protein synthesis inhibitor cycloheximide will reduce the actual size of a photothrombotic brain lesion. Ten male rats were treated subcutaneously with 2.5 mg kg-I cycloheximide; 10 rats received saline. One hour later, a photothrombotic injury was induced in the left cortex in all animals; they were sacrificec! 24 h after photothrombo~is. Nissl staining and computer-assisted analyses were used to assess the volume of the lesion, and to count the Nissl-positive cells. Both assays revealed significant protective action of cycloheximide treatment. In line with previous reports in which we described the occurrence of apoptosis in the model of photothrombotic brain injury our results with cycloheximide suggest that this model of focal brain ischemia can be used to test the neuroprotective efficacy of putative antiapoptotic compounds. [Neural Res 1997; 19: 92-96]