Abstract
Though we have reported the neuroprotective effect of exogenous ActA on oxygen-glucose deprivation (OGD) injury, the endogenous role of Smad6 remains not well understood. Smad6 is an important regulator of the ActA/smads signaling via a negative feedback circuit. In this study, nerve growth factor (NGF) and OGD were used to stimulate (rat adrenal pheochromocytoma) PC12 cells converting them into neurons to establish an ischemia in vitro model. Combined with the small interfering technology of Smad6 and FCM, Hoechst and Western blot were used to identify the apoptosis rate. The effect of silencing of Smad6 with siRNA was observed. These results showed that the apoptosis rate was 21.54% by 16-h OGD. For the combined Smad6-siRNA, the apoptosis rate was 10.55%. The expression of procaspase-3 protein was increased by Smad6-siRNA.The expression of ActA and p300 was also increased. The apoptosis rate was decreased in the ischemic injury with Smad6-siRNA. At the same time, it provided a reference to study the mechanism of Smad6 and its signaling in response to the acute ischemic damage.
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