Abstract: AIM: To explore the effect of propyl gallate on neurological dysfunction with injury after ce-rebral ischemia-reperfusion, and the effect on neuronal apoptosis and BDNF expression.METHODS: Middle cerebral artery occlusion models of rat transient focal ischemia were induced by inserting a filament through right internal carotid artery for 1 h .Rats were grouped as follows:control, sham operation, model, vehicle, PG 23.5 μmol/kg, PG 47 μmol/kg, PG 94 μmol/kg. Rats received intraperitoneal injections of PG immedi-ately after reperfusion, and the same volume physiolog-ical saline for vehicle group.Neuronogical behavior was evaluated by Longa's scoring method .Each rat re-ceived an injection every day and coronal brain sections were collected after l d, 2 d, 4 d, 7 d of reperfusion. Neuronal apoptosis in the boundary zone of the infarcts was evaluated by TUNEL staining .The expression of BDNF was investigated by immunohistochemistry and Western-blot with corresponding antibodies. RESULTS: Neurological deficits of model group and TUNEL positive neurons were observed at each time point and peaked at 1 d (P<0.01 compared to 2 d, 4 d, 7 d) .BDNF immunoreactivity increased to its peak at l d (P<0.01 compared to 2 d, 4 d, 7 d) and then decreased gradually in the boundary zone of the in-farcts.PG 47 μmol/kg and PG 94 μmol/kg could re-duce those damage and neurological deficits significant-ly (P<0.01) ;Furthermore, PG 47 μmol/kg and PG 94 μmol/kg markedly reduced the number of TUNEL positive neurons and increased the immunoreactivity of BDNF at 1d (P<0.01 compared to model) .Dose of 94 μmol/kg PG was more effective .CONCLUSION: The increasing expression of BDNF after cerebral isch-emia-reperfusion injury possibly affect the recovery of the boundary zone of the infarcts;the possible mecha-nism of propyl gallate could protect neurons from isch-emia-reperfusion injury may involve its upregulation of BDNF.

Key words: propyl gallate, cerebral ischemia-reperfusion, BDNF, neuronal apoptosis