Expression profile of catechol-O-methyltransferase in rats after subarachnoid hemorrhage
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Expression profile of catechol-O-methyltransferase in rats after subarachnoid hemorrhage
Journal of Army Medical UniversityVol. 33, Issue 20, Pages: 2157-2161(2011)
作者机构:
重庆医科大学附属第一医院神经外科
作者简介:
基金信息:
DOI:
CLC:R-322;R345;R743.35
Published:2011,
Published Online:30 October 2011,
稿件说明:
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HE ZHAOHUI, SUN XIAOCHUAN, GUO ZONGDUO, et al. Expression profile of catechol-O-methyltransferase in rats after subarachnoid hemorrhage. [J]. Journal of army medical university, 2011, 33(20): 2157-2161.
DOI:
HE ZHAOHUI, SUN XIAOCHUAN, GUO ZONGDUO, et al. Expression profile of catechol-O-methyltransferase in rats after subarachnoid hemorrhage. [J]. Journal of army medical university, 2011, 33(20): 2157-2161.DOI:
Expression profile of catechol-O-methyltransferase in rats after subarachnoid hemorrhage
Objective To investigate the expression pattern of mRNA and protein of catechol-O-methy-ltransferase (COMT)
plasma content of catecholamine (CA)
diameter and wall thickness
of basilar artery in early period after subarachnoid hemorrhage (SAH) in rats
and to investigate the significance of COMT expression in early period after SAH. Methods Rat SAH model was established by single blood injection to prechiasmatic cistern. RT-PCR and Western blotting were adopted to detect mRNA and protein expression of COMT respectively in the striatum corpora at 6
12
24
48
and 72 h after SAH. Plasma content of CA was determined by high performance liquid chromatography
and the diameter and wall thickness of basilar artery in rats were measured after SAH in corresponding time points. Results Compared with the control group
COMT expression in rats in SAH group began to rise at 6 h
reached peak at 12 h
then decreased continually at 24 h and 48 h
and finally returned close to the level of control group at 72 h. The expression of COMT at 6
12
24 and 48 h after SAH was significantly higher than that of control group (
P
<
0.01) and that of sham group at corresponding time points (
P
<
0.01). After SAH modeling
CA content in SAH group began to rise 6 h after SAH and reached peak at 24 h
and decreased after 24 h to 72 h. The contents in each time points were higher than that in control group and those in sham operation group at corresponding time points (
P
<
0.01). The caliber constriction and wall thickening aggravated obviously 12 h after modeling (
P
<
0.01)
reached the peak at 24 h (
P
<
0.01) and last to 48 h (
P
<
0.01). The caliber and wall thickness of basilar artery reached nearly normal size 72 h after SAH modeling (
P
>0.05). Conclusion Experimental SAH induces COMT upregulation in early stage after injury. And plasma CA content is increased obviously accompanied with cerebral vasospasm (CVS)
which may be associated with insufficient elevated expression of COMT in early stage after experimental SAH.