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ABM: To investigate the effects ofβ-aescin on apoptosis induced by transient focal brain ischemia in rats. METHODS: Rats were pretreated with β-aescin for 7 d and then subjected to brain ischemia/reperfusion (I/R) injury induced by a middle cerebral artery occlusion. After 2 h ischemia and 24 h reperfusion, Hematoxylin-Eosin (HE) staining, in situ end-labeling of nuclear DNA fragmentation (TUNEL) were employed to determine the level of apoptosis. The expressions of caspase-3 and Bcl-2 in the cortex were determined by immunohistochemistry and Western blot. The release of cytochrome c was analyzed by Western blot. RESULTS: The increased numbers of HE- and TUNEL-positive staining cells were significantly observed at 24 h after reperfusion. The immunoreactivity was inhibited by β-aescin (30, 60 mg/kg) (P<0.01 or P<0.05 vs vehicle-treated). After cerebral I/R, cytochrome c was released into the cytosol and caspase-3 was activated, whereas Bcl-2 expression was inhibited. β-Aescin (30, 60 mg/kg) markedly in
ABT: To investigate the effects of β-aescin on apoptosis induced by transient focal brain ischemia in rats. METHODS: Rats were pretreated with β-aescin for 7 d and then subjected to brain ischemia / reperfusion (I / R) injury induced by a middle Cerebral occlusion occlusion. After 2 h ischemia and 24 h reperfusion, Hematoxylin-Eosin (HE) staining, in situ end-labeling of nuclear DNA fragmentation (TUNEL) were employed to determine the level of apoptosis. The expressions of caspase-3 and Bcl -2 in the cortex were determined by immunohistochemistry and Western blot. RESULTS: The increased numbers of HE- and TUNEL-positive staining cells were significantly observed at 24 h after reperfusion. The immunoreactivity was inhibited by β-aescin (30, 60 mg / kg) (P <0.01 or P <0.05 vs vehicle-treated). After cerebral I / R, cytochrome c was released into the cytosol and caspase-3 was activated, 2 expression was inhibited. Β-Aescin (30, 60 mg / kg) markedly in