Sirtuin 1 activation protects against early brain injury after experimental subarachnoid hemorrhage in rats

• DOI: 10.1038/cddis.2016.292
• Publication Date: 2016-10-13T12:52:52Z
• Authors: Xiang-Sheng Zhang; Qi Wu; Ling-Yun Wu; Zhen-Nan Ye; Tian-Wei Jiang; Wei Li; Zong Zhuang; Meng-Liang Zhou; Xin Zhang; Chun-Hua Hang
• Keywords: Sirtuin 1; Gliosis

Abstract Increasing evidence indicates that sirtuin 1 (SIRT1) is implicated in a wide range of cellular functions, such as oxidative stress, inflammation and apoptosis. The aim this study was to investigate the change SIRT1 brain after subarachnoid hemorrhage (SAH) its role on SAH-induced early injury (EBI). In first set experiments, rats were randomly divided into sham group SAH groups at 2, 6, 12, 24, 48 72 h. expression evaluated by western blot analysis, immunohistochemistry immunofluorescence. another SIRT1-specific inhibitor (sirtinol) activator (activator 3) exploited EBI. It showed protein level markedly elevated stage peaked 24 h SAH. could be observed neurons microglia, enhanced mainly located Administration sirtinol inhibited activation pathways SAH, while 3 addition, inhibition exacerbate forkhead transcription factors O class-, nuclear factor-kappa B- p53-induced damage, neuroinflammation neuronal apoptosis, leading aggravated contrast, treatment reduce B-, apoptosis protect against These results suggest plays an important neuroprotection EBI deacetylation subsequent oxidative, inflammatory apoptotic pathways. might new promising molecular target for