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 100 000 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 mGluR Ⅱ in cerebral ischemic penumbra (by immunofluorescent staining). The percentage of cerebral infarct volume 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 decreased, the expression of mGluRⅡ in cerebral ischemic penumbra was down-regulated, and the expression 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. Key words: Trypsin inhibitor; Reperfusion injury; Brain; Receptor, glutamate

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