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Acta Neurochirurgica
Published in: Acta Neurochirurgica 11/2014

01-11-2014 | Experimental Research - Vascular

The role of rosiglitazone in the proliferation of vascular smooth muscle cells after experimental subarachnoid hemorrhage

Authors: Mao-Feng Cheng, Jin-Ning Song, Dan-Dong Li, Yong-Lin Zhao, Ji-Yang An, Peng Sun, Xian-Hua Luo

Published in: Acta Neurochirurgica | Issue 11/2014

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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).
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Metadata
Title
The role of rosiglitazone in the proliferation of vascular smooth muscle cells after experimental subarachnoid hemorrhage
Authors
Mao-Feng Cheng
Jin-Ning Song
Dan-Dong Li
Yong-Lin Zhao
Ji-Yang An
Peng Sun
Xian-Hua Luo
Publication date
01-11-2014
Publisher
Springer Vienna
Published in
Acta Neurochirurgica / Issue 11/2014
Print ISSN: 0001-6268
Electronic ISSN: 0942-0940
DOI
https://doi.org/10.1007/s00701-014-2196-4

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