Dl-3-n-butylphthalide Cardioprotection In Acute Myocardial Infarction

Objective Dl-3-n-butylphthalide (NBP), an established natural antioxidant for clinicalstroke treatment in China, can reportedly reduce beta-amyloid-induced neuronaltoxicity in cultured neuronal cells, and attenuate neurodegenerative changes in agedrats. This study is to observe the effection of Dl-3-n-butylphthalide (NBP) on the sizeand myocardial apoptosis after myocardial infarction in rats.Methods64male SD rats were randomly divided into sham operation group (8rats),model group (28rats), and NBP group (28rats). For those undergoing ischemia, somerats were given saline by intraperitoneal injection (control group,0.5ml*bid.d-1), or Dl-3-n-butylphthalide (NBP,80mg*bid.kg-1.d-1) by oral gavage. For those undergoingsham surgeries, some rats were also given saline by intraperitioneal injection, or DL-3-n-butylphthalide. Those rats with pre-treatment lasted1week until being killed. Themodel and NBP groups were made into MI model by ligation of the left anteriordescending (LAD) coronary artery, but not Rats in sham-operated. Model group andNBP group were taken heart specimens at1h,4h,8h and12h after coronary arteryligation (7rats at each time point). Size of MI was analyzed by TTC staining.Cardiomyocyte apoptosis was analyzed by TUNEL in myocardial infarct border zone.Electron perspective microscopy was applicated in observing junction ultrastructure ineach group after myocardial infarction. Accordingly with it, the expression of Bcl-2protein and Bax protein were detected by Western-bloting and the ratio of Bcl-2/Baxwas calculated. Results Compared with model group, Butylphthalide significantly inhibitedMitochondria infaction, reduced acute myocardial infarct size (P<0.05) andcardiomyocyte apoptosis (p <0.05), while significantly increased expression of Bcl-2protein and the ratio of Bcl-2/Bax.Conclusion Butylphthalide has a significant cardioprotective effect by increasing theexpression of the Bcl-2protein and the ratio of Bcl-2/Bax, decreasing Mitochondriainfaction, reducing myocardial infarct size and cardiomyocyte apoptosis in rats withacute myocardial infarction process.