Male Sprague-Dawley rats were divided into 6 groups: sham group, I/R group, nimodipine and MXYF (58, 116 and 232 mg/kg respectively) groups. Cerebral ischemia model was induced by middle cerebral artery occlusion for 2 h followed by reperfusion for 48 h. Neurological functional score was evaluated according to the method of Zea longa’s score and the infarct area was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining at 48 h after reperfusion. The protein expression of cytochrome c (cyt-c), Bcl-2, Bax, caspase-9, caspase-3 and caspase-7 were analyzed by western blot and the mRNA expression of Caspase-9, Caspase-3 and Caspase-7 were determined by the reverse transcription-polymerase chain reaction.
Oral administration of MXYF (116 and 232 mg/kg) significantly reduced the neurological functional score and attenuated the cerebral infarct area. Western blot analysis showed that the expression of Bcl-2 is enhanced and Bax expression is inhibited after treatment with MXYF (116 and 232 mg/kg), leading to significant increase of the ratio between Bcl-2 and Bax. Furthermore, the protein expression of cyt-c, caspase-9, caspase-3 and caspase-7 was significantly inhibited while the mRNA expression of caspase-9, caspase-3 and caspase-7 but not cyt-c was markedly inhibited in the MXYF (116 and 232 mg/kg) treatment groups compared with the I/R group.
The above data suggested that MXYF has potential neuroprotective activities by the regulation of apoptotic pathway, MXYF is a promising agent in treatment of stroke.