Electrical Stimulation Of Fastigial Nucleus And Cellular Apoptosis In Injured Region
Previous studies have indicated that electrical stimulation of the cerebellar fastigial nucleus in rats may reduce brain infarct size, increase the expression of Ku70 in cerebral ischemia/reperfusion region, and decrease the number of apoptotic neurons. In vitro studies have confirmed that Ku70 can mediate cellular apoptosis by interfering Bax. Dr. Jingli Liu and her team, the First Hospital Affiliated to Guangxi Medical University, China, presumed that the protective effect of Ku70 on cerebral ischemia/reperfusion injury after electrical stimulation of the cerebellar fastigial nucleus is likely to be related to Bax-mediated cellular mitochondrial apoptosis pathway. A study from this team published in Neural Regeneration Research (Vol. 9, No. 7, 2014) demonstrated that there was no co-localization of Ku70 with TUNEL-positive cells in the cerebral ischemia/reperfusion region, however, Ku70 partly co-localized with Bax protein in the cytoplasm of rats with cerebral ischemia/reperfusion injury. Therefore, they considered that the anti-apoptotic activity of Ku70 in the cytoplasm of rats subjected to electrical stimulation of the cerebellar fastigial nucleus is related to the co-localization of Ku70 with Bax.
Immunofluorescence double staining revealed that electrical stimulation of the left cerebellar fastigial nucleus at 72 hours before cerebral ischemia/reperfusion injury resulted in co-localization of most Ku70 with Bax in the injured brain tissue.