title: The role of rosiglitazone in the proliferation of vascular smooth muscle cells after experimental subarachnoid hemorrhage.
abstract: BACKGROUND
  Recent evidence has demonstrated that rosiglitazone can attenuate cerebral vasospasm following subarachnoid hemorrhage (SAH). Some studies have shown that rosiglitazone can suppress inflammation and immune responses after SAH. However, the precise molecular mechanisms by which cerebral vasospasm is attenuated is not clear.
  
  
  METHODS
  In this study, SAH was created using a "double hemorrhage" injection rat model. Rats were randomly divided into three groups and treated with saline (control group), untreated (SAH group), or treated with rosiglitazone. Using immunocytochemistry, hematoxylin and eosin (HE) staining, and measurement of the basilar artery, we investigated the formation of pathologic changes in the basilar artery, measured the expression of caveolin-1 and proliferating cell nuclear antigen (PCNA), and investigated the role of rosiglitazone in vascular smooth muscle cell (VSMC) proliferation in the basilar artery after SAH.
  
  
  RESULTS
  In this study, we observed significant pathologic changes in the basilar artery after experimental SAH. The level of vasospasm gradually increased with time during the 1st week, peaked on day 7, and almost recovered on day 14. After rosiglitazone treatment, the level of vasospasm was significantly attenuated in comparison with the SAH group. Immunocytochemistry staining showed that caveolin-1 expression was significantly increased in the rosiglitazone group, compared with the SAH group. Inversely, the expression of PCNA showed a notable decrease after rosiglitazone treatment.
  
  
  CONCLUSIONS
  The results indicate that rosiglitazone can attenuate cerebral vasospasm following SAH. Up-regulation of caveolin-1 by rosiglitazone may be a new molecular mechanism for this response, which is to inhibit proliferation of VSMCs after SAH, and this study may provide a novel insight to prevent delayed cerebral vasospasm (DCVS).
authors.affiliation: Department of Neurosurgery, the First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
authors.forename: Mao-Feng
authors.initials: MF
authors.lastname: Cheng
authors.forename: Jin-Ning
authors.initials: JN
authors.lastname: Song
authors.forename: Dan-Dong
authors.initials: DD
authors.lastname: Li
authors.forename: Yong-Lin
authors.initials: YL
authors.lastname: Zhao
authors.forename: Ji-Yang
authors.initials: JY
authors.lastname: An
authors.forename: Peng
authors.initials: P
authors.lastname: Sun
authors.forename: Xian-Hua
authors.initials: XH
authors.lastname: Luo
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000187:drug effects* / Q000473:pathology; D051242:Caveolin 1 / Q000187:drug effects / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077154:Rosiglitazone; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D045162:Thiazolidinediones / Q000494:pharmacology*; D015854:Up-Regulation; D014661:Vasoconstriction / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*; D020301:Vasospasm, Intracranial / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control
chemical_list: C495537:Cav1 protein, rat; D051242:Caveolin 1; D018809:Proliferating Cell Nuclear Antigen; D045162:Thiazolidinediones; D014665:Vasodilator Agents; D000077154:Rosiglitazone