摘要
目的探讨蛛网膜下腔出血（subarachnoid hemorrhage，SAH）后蛛网膜纤维化的发生机制。方法实验大鼠分成对照组、实验组、治疗组，使用放射免疫法（RIA）测定蛛网膜中透明质酸（HA）、层黏连蛋白（LN）、Ⅲ型前胶原氨基端肽（PⅢNP）、Ⅳ型胶原的含量。应用电镜观察蛛网膜细胞的形态及蛛网膜胶原纤维分布情况。结果RIA测量的4种细胞外基质中，PⅢNP在出血后增高最明显，LN与HA也明显升高，而Ⅳ型胶原变化不明显。应用地塞米松治疗后PⅢNP明显降低。电镜下发现蛛网膜细胞在出血后其生物活性增强，蛛网膜下腔的胶原纤维在1周左右开始明显增多，持续3周以上，地塞米松治疗后蛛网膜细胞线粒体密度相对较低，蛛网膜胶原纤维较稀疏。结论蛛网膜下腔出血后细胞外基质明显增加，参与蛛网膜纤维化。地塞米松可减轻蛛网膜下腔出血后蛛网膜纤维化，为防治蛛网膜下腔出血后脑积水提供新的思路。
Objective To study the mechanism of arachnoidal fibrosis after subarachnoid hemorrhage. Methods Rats were divided into control group, experiment group and treatment group. Radioimmunoassay （RIA） was employed to detect the levels of hyaluronie acid, Iaminin, type m preeollagen and type Ⅳ collagen in the araehnoid membrane. In the meantime, araehnoid cell＇s morphology and collagen distribution in the subaraehnoid space were investigated by electron microscope. Results Results of RIA detection showed increase of Type HI preeollagen level （peak at the second week）, obvious higher levels of LN and HA but insignificant change of type Ⅳcollagen after subarachnoid hemorrhage. However, dexamethasone treatment decreased type Ⅲpreeollagen level. Electron microscope found that araehnoid cells presented aeeentruated bioaetivity after subaraehnoid hemorrhage, with significant increase of araehnoidal collagen fibers from one week after subaraehnoid hemorrhage, continuing for 3 weeks. Dexamethasone treatment resulted in low density of mitochondria and sparsed araehnoidal collagen fibers. Conclusions Extracellular matrix （ECM） increases in araehnoid membrane after subaraelmoid hemorrhage and participates in araehnoid fibrosis. Dexamethasone can relieve araelmoidal fibrosis after subaraehnoid hemorrhage, as provides fresh way for prevention and treatment of post hemorrhagic hydrocephalus.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2008年第7期502-505,共4页
Chinese Journal of Trauma
基金
国家自然科学基金资助项目（30370497）
