title: Correlation between nitric oxide and early brain injury after subarachnoid hemorrhage.
abstract: BACKGROUND
  Early brain injury (EBI) has recently been identified as the main factor of poor prognosis for subarachnoid hemorrhage (SAH), and apoptosis has an important function in EBI. Although nitric oxide (NO) and caspase-12, a specific molecule related to endoplasmic reticulum (ER) stress-induced apoptosis signaling pathways, are involved in brain injury after SAH, the relationship between NO and ER stress has not been reported yet. We examined the NO and caspase-12 contents and investigated the relationship between NO and ER stress-induced apoptosis.
  
  
  METHODS
  Sprague-Dawley rats (n = 90), weighing 300 g to 350 g, were used for the SAH model. SAH was induced in rats by blood injection into the prechiasmatic cistern. NO, caspase-12, and apoptosis were measured by nitrate reductase method, real-time polymerase chain reaction, and terminal deoxynucleotidy1 transferase-mediated dUTP nick-end labeling staining, respectively, at different time points after SAH. Pearson correlation coefficients were used to examine correlation.
  
  
  RESULTS
  NO level of cerebrospinal fluid significantly increased in the SAH group at 3, 24, 48, and 72 h compared with other groups. Caspase-12 also significantly increased at 1, 3, 6, 24, 48, and 72 h. Cell apoptosis significantly increased at 24, 48, and 72 h. A significant correlation between the number of apoptotic neurons and caspase-12 was found. NO was also correlated with caspase-12.
  
  
  CONCLUSIONS
  Our results suggest that NO is involved in the pathophysiological events of EBI after SAH by increasing caspase-12, which results in neuronal apoptosis.
authors.affiliation: 1Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Zhao
authors.forename: Qi
authors.initials: Q
authors.lastname: Liu
authors.forename: Yunxiang
authors.initials: Y
authors.lastname: Ji
authors.forename: Ganggang
authors.initials: G
authors.lastname: Wang
authors.forename: Xuejun
authors.initials: X
authors.lastname: He
authors.forename: Weidong
authors.initials: W
authors.lastname: Tian
authors.forename: Hui
authors.initials: H
authors.lastname: Xu
authors.forename: Ting
authors.initials: T
authors.lastname: Lei
authors.forename: Yezhong
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000134:cerebrospinal fluid* / Q000209:etiology* / Q000473:pathology; D053454:Caspase 12 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D005260:Female; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D020287:In Situ Nick-End Labeling; D008297:Male; D009474:Neurons / Q000648:ultrastructure; D009569:Nitric Oxide / Q000134:cerebrospinal fluid*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000401:mortality; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D009569:Nitric Oxide; D053454:Caspase 12
keywords: NO; caspase-12; early brain injury; subarachnoid hemorrhage