Effect of dexmedetomidine on hippocampal BDNF/TrκB signaling pathway in a rat model of cerebral ischemia-reperfusion injury
10.3760/cma.j.cn131073.20240313.01119
- VernacularTitle:右美托咪定对脑缺血再灌注大鼠海马BDNF/TrκB信号通路的影响
- Author:
Simayi ALIMUJIANG
1
;
Li QU
;
Xuan ZHAO
;
Guiping XU
Author Information
1. 新疆医科大学研究生学院，乌鲁木齐 830011
- Keywords:
Dexmedetomidine;
Brain;
Reperfusion injury;
Brain-derived neurotrophic factor;
Receptor protein-tyrosine kinases
- From:
Chinese Journal of Anesthesiology
2024;44(11):1381-1385
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the effect of dexmedetomidine on the hippocampal brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrκB) signaling pathway in a rat model of cerebral ischemia-reperfusion (I/R).Methods:Forty-five clean-grade healthy Sprague-Dawley rats, half male and half female, aged 5-6 months, weighing 200-250 g, were divided into 3 groups ( n=15 each) using a random number table method: sham operation group (group S), cerebral I/R group (group I/R), and dexmedetomidine + I/R group (group Dex). A rat model of cerebral I/R injury was established by occluding the middle cerebral artery for 90 min followed by restoring perfusion. In group Dex, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before ischemia, while the equal volume of normal saline was intraperitoneally injected in S and I/R groups. Neurological deficit scores were evaluated at 12 h of reperfusion. The rats were anesthetized and sacrificed, and the hippocampus was isolated for determination of the percentage of cerebral infarct size (by TTC method), expression of BDNF and TrκB (by Western blot), and expression of BDNF mRNA and TrκB mRNA (by real-time polymerase chain reaction) and for microscopic examination of cell apoptosis (by TUNEL method). Results:Compared with group S, the neurological deficit scores and percentage of cerebral infarct size were significantly increased, the number of apoptotic hippocampal neurons was increased, and the expression of BDNF and TrκB protein and mRNA was down-regulated in I/R and Dex groups ( P<0.05). Compared with group I/R, the neurological deficit scores and percentage of cerebral infarct size were significantly decreased, the number of apoptotic hippocampal neurons was reduced, and the expression of BDNF and TrκB protein and mRNA was up-regulated in group Dex ( P<0.05). Conclusions:The mechanism by which dexmedetomidine alleviates cerebral I/R injury may be related to activating hippocampal BDNF/TrκB signaling pathways in rats.
