Tags

Type your tag names separated by a space and hit enter

Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway.
World Neurosurg. 2019 Jul; 127:e624-e630.WN

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.

Authors+Show Affiliations

Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.Department of Emergency Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China.Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. Electronic address: zhaoqingping247@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30930327

Citation

Teng, Lu, et al. "Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats Via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway." World Neurosurgery, vol. 127, 2019, pp. e624-e630.
Teng L, Chen W, Yin C, et al. Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway. World Neurosurg. 2019;127:e624-e630.
Teng, L., Chen, W., Yin, C., Zhang, H., & Zhao, Q. (2019). Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway. World Neurosurgery, 127, e624-e630. https://doi.org/10.1016/j.wneu.2019.03.232
Teng L, et al. Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats Via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway. World Neurosurg. 2019;127:e624-e630. PubMed PMID: 30930327.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway. AU - Teng,Lu, AU - Chen,Weiguang, AU - Yin,Changyou, AU - Zhang,Hongtao, AU - Zhao,Qingping, Y1 - 2019/03/28/ PY - 2019/01/03/received PY - 2019/03/20/revised PY - 2019/03/21/accepted PY - 2019/4/2/pubmed PY - 2020/1/24/medline PY - 2019/4/2/entrez KW - Brain injury KW - Cerebral ischemia reperfusion KW - Dexmedetomidine KW - ERK/CREB pathway SP - e624 EP - e630 JF - World neurosurgery JO - World Neurosurg VL - 127 N2 - 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. SN - 1878-8769 UR - https://www.unboundmedicine.com/medline/citation/30930327/Dexmedetomidine_Improves_Cerebral_Ischemia_Reperfusion_Injury_in_Rats_via_Extracellular_Signal_Regulated_Kinase/Cyclic_Adenosine_Monophosphate_Response_Element_Binding_Protein_Signaling_Pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1878-8750(19)30912-X DB - PRIME DP - Unbound Medicine ER -