Abstract

Ischemic cerebrovascular disease is a global health problem. According to the World Health Organization, ischemic stroke is actually the most common cause of death in the world. ActA/smads signaling pathways was shown to be required for the differentiation-associated physiological apoptosis of stroke. Although smad7 is an important regulator of ActA/smads signaling via a negative feedback circuit, its effects have not been well understood. This experiment primarily investigated the apoptosis in ischemic cerebral injury by targeting silence of smad7. In this study, we used nerve growth factor (NGF) and oxygen–glucose deprivation (OGD) to stimulate PC12 cells and convert them into neurons in order to establish an ischemia in vitro model. Combined with the small interfering technology of smad7, we also used flow cytometric (FCM) and 4,6-diamidino-2-phenylindole(DAPI) to identify apoptosis rate. The results show that OGD 16 h apoptosis rate was 25.53%, while OGD 16 h combined with sismad7 apoptosis rate was 16.76%. It was also observed that the apoptosis rate decreased in ischemic injury when sismad7 was targeted. This study therefore provides a reference for further study of ActA/smads signaling pathways on acute ischemic brain damage.

Key words: Oxygen–glucose deprivation (OGD), ischemia tolerance model, smad7,ActA/Smad pathway.