Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema
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Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema
Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema
解放军医学杂志(英文版)1992年第3期 页码:217-221
Affiliations:
1. Department of Neurosurgery Changzheng Hospital
2. Second Military Medical University
3. ,Shanghai,200433
4. Department of Pathophysiology
Author bio:
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DOI:
中图分类号:
纸质出版:1992
Accepted:
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Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema[J]. 解放军医学杂志(英文版), 1992,(3):217-221.
[1]宫钦志,朱诚,徐仁宝,杨中坚,谭金兴,乐颖影.Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema[J].Journal of Medical Colleges of PLA,1992(03):217-221.
Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema[J]. 解放军医学杂志(英文版), 1992,(3):217-221.DOI:
[1]宫钦志,朱诚,徐仁宝,杨中坚,谭金兴,乐颖影.Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema[J].Journal of Medical Colleges of PLA,1992(03):217-221.DOI:
Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema
摘要
Abstract
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正
>
The high-affinity glucocorticoid binding sites(HAGS)and the low-affinity glucocor-ticoid binding sites(LAGS)with steroid specificity were demonstrated in cerebral cytosol ofrats by using the radioligand binding assay.The equilibrium dissocation constant(Kd)of HAGSand LAGS were(2.78+0.71)×10
-8
mol/L and(2.12±1.06)×10
-6
mol/L respectively as esti-mated by Scatchard and Pseudoseatchard analysis.Glucocorticoid receptors(GR)in the trau-matized(left)hemisphere cytosol were decreased more significantly than those in both the con-trol(right)hemisphere cytosol at 6 h postinjury and normal brain tissue(P
<
0.05)
but Kd ofGR showed no significant changes.GR of liver cytosol at 6h postinjury were more markedly de-creased than normal hepatic cytosol
but Kd of GR underwent no significant changes.These da-ta demonstrate that high-dose glucocorticoid(GC)used in the treatment of traumatic brain ede-ma might maintain target-cell reactions by increasing the production of GC receptor complexesand is most likely to be mediated by LAGS.
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