Hemoglobin-Induced Nitric Oxide Synthase Overexpression and Nitric Oxide Production Contribute to Blood–Brain Barrier Disruption in the Rat
作者： Shuo Yang , Yizhao Chen , Xinqing Deng , Weiping Jiang , Bing Li
DOI: 10.1007/S12031-013-9990-Y
关键词:
摘要: Hemoglobin (Hb) released from extravasated erythrocytes may have a critical role in the process of blood–brain barrier (BBB) disruption and subsequent edema formation after intracerebral hemorrhage (ICH). Excessive nitric oxide (NO) production synthesized by synthase (NOS) has been well documented to contribute BBB disruption. However, considerably less attention focused on NO Hb-induced This study was designed examine hypothesis that NOS overexpression excessive changes tight junction (TJ) proteins dysfunction. infused with stereotactic guidance into right caudate nucleus male Sprague Dawley rats. Then, we investigated effect Hb permeability, TJ (claudin-5, occludin, zonula occludens-1 (ZO-1), junctional adhesion molecule-1 (JAM-1)), iron deposition, expression inducible (iNOS) endothelial (eNOS), as production. injection caused significant increase permeability. Significant reduction claudin-5, ZO-1, JAM-1 observed evidenced PCR immunofluorescence. After decrease at early stage, occludin showed fivefold mRNA level 7 days. deposition detectable 48 h days time-dependent manner. The iNOS eNOS levels dramatically increased concomitantly large quantities released. Furthermore, enhanced or immunoreactivity co-localized diffused diminished claudin-5 staining. We concluded overexpressed induced disruption, which provide an important potential therapeutic target treatment ICH.
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