Abstract: Objective To observe the neural protection of 3-n-butylphthalide (NBP) injection in focal cerebral ischemia-reperfusion rats. Methods 160 male Sprague-Dawley rats were randomly divided into sham group (n=10), ischemia- reperfusion group (IR group, n=50), high-dose NBP treatment group (high-dose group, n=50), middle-dose NBP treatment group (middle-dose group, n=25) and low-dose NBP treatment group (low-dose group, n=25). The later 4 groups were occluded the middle cerebral artery for 2 hours and reperfused. The sham group was sacrificed 24 hours after operation, and the other groups at 6, 12, 24, 48 and 72 hours after reperfusion, in which 5 of them were stained with TdT mediated dUTP Nick End Labeling (TUNEL) to observe the neuronal apoptosis, and immunohistochemistry to observe the expression of silent information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α); the other 5 of sham group, IR group and high-dose group were observed with quantitative real-time PCR of SIRT1 and PGC-1α. Results Compared with the IR group, the number of apoptotic cells decreased and the SIRT1 and PGC-1α positive cells increased in all NBP groups at each time (F>160.60, P<0.001), and it was the least of apoptotic cells and most of SIRT1 and PGC-1α positive cells in the high-dose group (P<0.05), while there was significant difference between the low-dose group and the middle-dose group, excluding 6 hours after reperfusion (P<0.05). Compared with IR group, the expression of SIRT1 and PGC-1α mRNA increased in the high-dose group at each time (t> 4.13, P<0.01). Conclusion NBP can protect brain from apoptosis in focal cerebral ischemia-reperfusion rats, which may relate to more expression of SIRT1 and PGC-1α.

Key words: cerebral ischemia-reperfuson, Butylphthalide, apoptosis, silent information regulation 2 homolog 1, peroxisome proliferator- activated receptor &gamma, coactivator-1α