Role of glycogen synthase kinase-3 beta in spinal cord ischemia/reperfusion injury in rats
10.3760/cma.j.issn.0254-1416.2014.11.010
- VernacularTitle:糖原合成酶激酶3β在大鼠脊髓缺血再灌注损伤中的作用
- Author:
Shuaiguo LYU
;
Tingkun LI
;
Changsheng LI
;
Xihua LU
;
Zhifeng LYU
;
Miaomiao LYU
;
Tieli DONG
- Publication Type:Journal Article
- Keywords:
Glycogen synthase kinase 3;
Reperfusion injury;
Spinal cord
- From:
Chinese Journal of Anesthesiology
2014;34(11):1323-1325
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of glycogen synthase kinase-3 beta (GSK-3β) in spinal cord ischemia/reperfusion (I/R) injury in rats.Methods Forty-eight male Sprague-Dawley rats,aged 3 months,weighing 250-300 g,were randomly divided into 3 groups (n =16 each) using a random number table:sham operation group (group S),group I/R and I/R+ GSK-3β inhibitor LiCl group (group LiCl).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 300 mg/kg.Spinal cord ischemia was induced by 45 min occlusion of the abdominal aorta followed by reperfusion.In I/R and LiCl groups,normal saline 5 ml and LiCl 15 mg/kg were injected,respectively,via the caudal vein at 30 min before ischemia.The animals were sacrificed at 48 h of reperfusion and the lumbar segment (L4-6) of spinal cords was removed for microscopic examination and for determination of neuronal apoptosis in the anterior horn of the spinal cord (by TUNEL),and the expression of interleukin-6 (IL-6),IL-8 and IL-10 was detected (by immunohistochemistry).The apoptosis rate was calculated.Results Compared with group S,the apoptosis rate was significantly increased,IL-6 and IL-8 expression was upregulated,and IL-10 expression was down-regulated in I/R and LiCl groups.Compared with group I/R,the apoptosis rate was significantly decreased,IL-6 and IL-8 expression was down-regulated,IL-10 expression was up regulated,and the pathological damage was attenuated in LiCl group.Conclusion Activated GSK-3β is involved in the development of spinal cord I/R injury possibly by promoting synthesis and release of inflammatory factors in rats.
