Jiang-quan Han1, Kui-ying Yu, Min He. 1. Department of Neurology, Fifth Affiliated Hospital, Zunyi Medical College, Guangdong. gdshanjq@163.com
Abstract
OBJECTIVE: To observe the effects of puerarin (Pue) on the neurocyte apoptosis and the p-Akt (Ser473) expression in the ischemic penumbra of rats with cerebral ischemia/reperfusion (I/R). METHODS: The 48 Sprague-Dawley rats were randomly divided into four groups, i.e., the sham-operation group, the I/R group, the Pue treatment group, and the Pue + LY294002 treatment group (Pue + LY), 12 in each group. The cerebral I/R rat model was established by Longa's suture method. Pue and Pue + specific P13K kinase inhibitor, i.e., LY294002 were administered. The score of the neurological deficit was estimated 1 h followed by 24 h reperfusion. The infarct volume was measured using TTC staining. The number of apoptotic neurons were detected using Tunel method. The expressions of p-Akt (Ser473) was detected using immunohistochemical assay, and the images were analyzed. RESULTS: The score of the neurological deficit decreased more obviously, the number of apoptosis decreased more significantly, the expressions of p-Akt (Ser473) increased more significantly in the Pue group than in the I/R group (all P < 0.05). The score of the neurological deficit increased more obviously, the number of apoptosis increased more significantly, the expression of p-Akt (Ser473) decreased more significantly in the Pue + LY group than in the Pue group (all P < 0.05). CONCLUSION: Pue reduced the apoptosis of neurocytes and had protective effects against cerebral I/R injury possibly through activating the PI3K/Akt signaling pathway.
OBJECTIVE: To observe the effects of puerarin (Pue) on the neurocyte apoptosis and the p-Akt (Ser473) expression in the ischemic penumbra of rats with cerebral ischemia/reperfusion (I/R). METHODS: The 48 Sprague-Dawley rats were randomly divided into four groups, i.e., the sham-operation group, the I/R group, the Pue treatment group, and the Pue + LY294002 treatment group (Pue + LY), 12 in each group. The cerebral I/R rat model was established by Longa's suture method. Pue and Pue + specific P13K kinase inhibitor, i.e., LY294002 were administered. The score of the neurological deficit was estimated 1 h followed by 24 h reperfusion. The infarct volume was measured using TTC staining. The number of apoptotic neurons were detected using Tunel method. The expressions of p-Akt (Ser473) was detected using immunohistochemical assay, and the images were analyzed. RESULTS: The score of the neurological deficit decreased more obviously, the number of apoptosis decreased more significantly, the expressions of p-Akt (Ser473) increased more significantly in the Pue group than in the I/R group (all P < 0.05). The score of the neurological deficit increased more obviously, the number of apoptosis increased more significantly, the expression of p-Akt (Ser473) decreased more significantly in the Pue + LY group than in the Pue group (all P < 0.05). CONCLUSION:Pue reduced the apoptosis of neurocytes and had protective effects against cerebral I/R injury possibly through activating the PI3K/Akt signaling pathway.