Lu Teng1, Weiguang Chen2, Changyou Yin1, Hongtao Zhang1, Qingping Zhao3. 1. Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. 2. Department of Emergency Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. 3. Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. Electronic address: zhaoqingping247@163.com.
Abstract
OBJECTIVE: To investigate the mechanism of dexmedetomidine (Dex) in improving brain damage induced by cerebral ischemia-reperfusion injury in rats. METHODS: Rats were randomly divided into a sham operation group, ischemia-reperfusion group, Dex group, piracetam group, and yohimbine + Dex group, with 12 rats per group. 2,3,5-Triphenyltetrazolium chloride staining was used to analyze cerebral infarct size. Hematoxylin-eosin staining and immunohistochemistry were used to observe brain damage caused by ischemia-reperfusion. Cognitive and memory functions was detected by Morris water maze test, and the expression of phosphorylated extracellular signal-regulated kinases 1 and 2 (ERK1/2) and phosphorylated cyclic adenosine monophosphate response element binding protein (CREB) were measured by Western blot. RESULTS: Cognitive dysfunction was improved in the Dex group and the piracetam group compared with the ischemia-reperfusion group. Compared with the ischemia-reperfusion group, infarct size and neuronal cell death rates were decreased in the Dex group and the piracetam group. The expression of phosphorylated ERK1/2 and phosphorylated CREB in the Dex group was increased, whereas the expression of phosphorylated ERK1/2 and phosphorylated CREB in the yohimbine + Dex group was lower than in the Dex group (P < 0.05). CONCLUSIONS: Dex improved ischemic brain damage by promoting signal transduction of the ERK/CREB pathway, which may provide new ways for clinical treatment of cerebral ischemia-reperfusion injury.
OBJECTIVE: To investigate the mechanism of dexmedetomidine (Dex) in improving brain damage induced by cerebral ischemia-reperfusion injury in rats. METHODS:Rats were randomly divided into a sham operation group, ischemia-reperfusion group, Dex group, piracetam group, and yohimbine + Dex group, with 12 rats per group. 2,3,5-Triphenyltetrazolium chloride staining was used to analyze cerebral infarct size. Hematoxylin-eosin staining and immunohistochemistry were used to observe brain damage caused by ischemia-reperfusion. Cognitive and memory functions was detected by Morris water maze test, and the expression of phosphorylated extracellular signal-regulated kinases 1 and 2 (ERK1/2) and phosphorylated cyclic adenosine monophosphate response element binding protein (CREB) were measured by Western blot. RESULTS:Cognitive dysfunction was improved in the Dex group and the piracetam group compared with the ischemia-reperfusion group. Compared with the ischemia-reperfusion group, infarct size and neuronal cell death rates were decreased in the Dex group and the piracetam group. The expression of phosphorylated ERK1/2 and phosphorylated CREB in the Dex group was increased, whereas the expression of phosphorylated ERK1/2 and phosphorylated CREB in the yohimbine + Dex group was lower than in the Dex group (P < 0.05). CONCLUSIONS:Dex improved ischemic brain damage by promoting signal transduction of the ERK/CREB pathway, which may provide new ways for clinical treatment of cerebral ischemia-reperfusion injury.