Effect of ulinastatin on expression of metabotropic glutamate receptor Ⅱ during cerebral ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2019.03.012
- VernacularTitle:乌司他丁对大鼠脑缺血再灌注时代谢型谷氨酸受体Ⅱ表达的影响
- Author:
Lidong DOU
1
;
Jie WANG
;
Kaiwei WANG
;
Hongqi LIN
Author Information
1. 河南省人民医院麻醉科
- Keywords:
Trypsin inhibitor;
Reperfusion injury;
Brain;
Receptor;
glutamate
- From:
Chinese Journal of Anesthesiology
2019;39(3):296-299
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of ulinastatin on the expression of metabotropic glutamate receptor Ⅱ ( mGluRⅡ) during cerebral ischemia-reperfusion ( I∕R) in rats. Methods Forty-eight male Sprague-Dawley rats, aged 6-8 weeks, weighing 230-280 g, were divided into 3 groups ( n=16 each) by a random number table method: sham operation group (S group), cerebral I∕R group (I∕R group) and ulinastatin group ( U group) . The model of cerebral I∕R injury was established by occluding the right middle cerebral artery using a nylon thread with a rounded tip inserted into internal carotid artery and advanced cranially until resistance was met. Middle cerebral artery occlusion was maintained for 2 h followed by 24-h reperfusion. Ulinastatin 100000 U∕kg was injected via the tail vein immediately after onset of reperfusion in group U. The neurological deficit score ( NDS) was assessed after 24 h of reperfusion. The rats were then sacrificed, and brain tissues were obtained for determination of brain infarction ( by TTC staining) , expression of IκB-α in cerebral ischemic penumbra ( by Western blot) and expression of mGluRⅡ in cerebral ischemic penumbra ( by immunofluorescent staining) . The percentage of cerebral infarct vol-ume was calculated. Results Compared with S group, the NDS and percentage of cerebral infarct volume were significantly increased, the expression of mGluRⅡ in cerebral ischemic penumbra was up-regulated, and the expression of IκB-α in cerebral ischemic penumbra was down-regulated in I∕R and U groups ( P<0. 05). Compared with I∕R group, the NDS and percentage of cerebral infarct volume were significantly de-creased, the expression of mGluRⅡ in cerebral ischemic penumbra was down-regulated, and the expres-sion of IκB-α in cerebral ischemic penumbra was up-regulated in U group ( P<0. 05) . Conclusion The mechanism by which ulinastatin mitigates cerebral I∕R injury may be related to inhibiting the expression of mGluR Ⅱ in cerebral ischemic penumbra of rats.
