Effect of ulinastatin on activity of JAK2/STAT3 signaling pathway during focal cerebral ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2018.05.009
- VernacularTitle:乌司他丁对大鼠局灶性脑缺血再灌注时JAK2/STAT3信号通路活性的影响
- Author:
Xiaoxi CHEN
1
;
Xiaoqiang LIAN
;
Huansen HUANG
;
Lin RUAN
;
Lingzhi WANG
Author Information
1. 510260,广州医科大学附属第二医院麻醉科
- Keywords:
Trypsin inhibitors;
Reperfusion injury;
Brain;
Janus kinase 2;
STAT3 transcription factor
- From:
Chinese Journal of Anesthesiology
2018;38(5):545-547
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of ulinastatin on the activity of Janus kinase 2/signaling transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Forty-eight clean-grade healthy adult male Sprague-Dawley rats,aged 6-8 weeks,weighing 230-280 g,were divided into 3 groups (n=16 each) using a random number table:sham operation group (S group),cerebral I/R group (I/R group) and ulinastatin group (U group).Focal cerebral I/R was induced by occlusion of the middle cerebral artery for 2 h followed by reperfusion.Ulinastatin 100 000 U/kg was injected via the femoral vein immediately after beginning of cerebral ischemia in group U.Neurologic deficit was evaluated and scored (NDS) at 24 h of reperfusion.The rats were then sacrificed and brains were removed for measurement of the cerebral infarct size (by TTC staining) and for determination of the expression of total JAK2,total STAT3 and phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) in the cerebral cortex.Results Compared with S group,NDS and cerebral infarct size were significantly increased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was up-regulated in I/R group and U group (P<0.05).Compared with I/R group,NDS and cerebral infarct size were significantly decreased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was down-regulated in U group (P<0.05).There was no significant difference in the expression of total JAK2 and total STAT3 in the cerebral cortex between three groups (P>0.05).Conclusion Ulinastatin can inhibit the activity of JAK2/STAT3 signaling pathway during cerebral I/R,which may be involved in the brain protective mechanism of ulinastatin in rats.