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蛛网膜下腔出血后交通性脑积水患者脑脊液中转化生长因子-β1水平的升高

Elevation of transforming growth factor-beta 1 level in cerebrospinal fluid of patients with communicating hydrocephalus after subarachnoid hemorrhage.

作者信息

Kitazawa K, Tada T

机构信息

Department of Neurosurgery, Shinshu University, School of Medicine, Matsumoto, Japan.

出版信息

Stroke. 1994 Jul;25(7):1400-4. doi: 10.1161/01.str.25.7.1400.

Abstract

BACKGROUND AND PURPOSE

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional polypeptide that controls the production of extracellular matrix protein. Platelets store a large quantity of TGF-beta 1, which is released at hemorrhage. We recently reported that human recombinant TGF-beta 1 induced communicating hydrocephalus in mice. The aim of this study was to determine whether TGF-beta 1 is related to the development of communicating hydrocephalus after subarachnoid hemorrhage (SAH).

METHODS

TGF-beta 1 in the cerebrospinal fluid of 24 patients with SAH was measured with enzyme-linked immunosorbent assay. The levels were compared between hydrocephalic and nonhydrocephalic groups. Western blot analysis was performed to determine active TGF-beta 1 in the cerebrospinal fluid.

RESULTS

TGF-beta 1 rapidly decreased from the onset of SAH. The level of TGF-beta 1 of 13 patients showing ventricular dilatation with periventricular low density on computed tomographic scan was 1.07 +/- 0.37 ng/mL on days 12 through 14, which was significantly higher than 0.52 +/- 0.21 ng/mL in patients without ventricular dilatation (P < .02). Furthermore, the TGF-beta 1 level of patients who had undergone ventriculoperitoneal shunt (n = 11) was 1.11 +/- 0.09 ng/mL on days 12 through 14, which was also higher than the level of the nonshunt group (n = 13) (0.56 +/- 0.22 ng/mL; P < .01). A 25-kD band was demonstrated by Western blot analysis in the cerebrospinal fluid of a patient with SAH.

CONCLUSIONS

Our results strongly suggest that TGF-beta 1 plays an important role in generating communicating hydrocephalus after SAH.

摘要

背景与目的

转化生长因子-β1(TGF-β1)是一种控制细胞外基质蛋白产生的多功能多肽。血小板储存大量TGF-β1,在出血时释放。我们最近报道,人重组TGF-β1可诱导小鼠发生交通性脑积水。本研究旨在确定TGF-β1是否与蛛网膜下腔出血(SAH)后交通性脑积水的发生有关。

方法

采用酶联免疫吸附测定法检测24例SAH患者脑脊液中的TGF-β1。比较脑积水组和非脑积水组的水平。进行蛋白质印迹分析以确定脑脊液中活性TGF-β1。

结果

SAH发病后TGF-β1迅速下降。13例计算机断层扫描显示脑室扩张伴脑室周围低密度的患者在第12至14天的TGF-β1水平为1.07±0.37 ng/mL,显著高于无脑室扩张患者的0.52±0.21 ng/mL(P<.02)。此外,接受脑室腹腔分流术的患者(n = 11)在第12至14天的TGF-β1水平为1.11±0.09 ng/mL,也高于未分流组(n = 13)(0.56±0.22 ng/mL;P<.01)。蛋白质印迹分析在1例SAH患者的脑脊液中显示出一条25-kD的条带。

结论

我们的结果强烈提示,TGF-β1在SAH后交通性脑积水的发生中起重要作用。

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