Role of SOD1,PI3K/AKT Signaling Pathway in Protection of Propofol on Spinal Cord Ischemic Reperfusion Injury in Rabbit Model
10.3870/yydb.2014.10.005
- VernacularTitle:SOD1和 PI3K/AKT 信号转导通路在丙泊酚防治兔脊髓缺血-再灌注损伤中的作用
- Author:
Qijing YU
;
Hong TAO
;
Yunzhao YANG
- Publication Type:Journal Article
- Keywords:
Propofol;
Spinal cord;
Ischemia-reperfusion;
Superoxide dismutase
- From:
Herald of Medicine
2014;(10):1273-1277
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate roles of superoxide dismutase-1(SOD1),phosphatidylinositol 3-kinase (PI3K) /serine/ threonine protein kinase (AKT) signal transduction pathway in protection of propofol on spinal cord ischemic reperfusion injury (SCIRI) in rabbit model before and after ischemia. Methods Sixty Japanese male rabbits were randomly divided into 3 groups (n=20),namely sham-operation group (Group S),ischemia-reperfusion group (Group I/ R) and ischemia-reperfusion group with propofol treatment (Group P). Abdominal aorta of the rabbits in group I/ R and group P were blocked by clamp for 40 min and then the clamp was removed. Propofol (30 mg·kg-1 ) was intravenously infused 10 min before blocking the aorta and at the time of reperfusion. Normal saline was intravenously infused at the same time points in the other two groups. Four rabbits of each group were randomly executed 1,2,3,5,7 days after surgery. Spinal cord tissues at L3-L4 levles were harvested. Bioactivity of SOD1 was detected by ELISA and mRNA expression levels of SOD1,PI3K and AKT were detected by RT-PCR. Results On the 1st day after the surgery,the bioactivity of SOD1 increased significantly in Group I/ R and Group P as compared with that in Group S (P<0. 05). On the 2nd day,compared with Group S,the bioactivity of SOD1 increased significantly in Group P (P<0. 05),but there was no change in Group I/ R (P>0. 05). On the 3rd,the 5th and the 7th day,compared with Group S,the bioactivity of SOD1 decreased significantly in Group I/ R (P<0. 05),but there was no change in Group P (P>0. 05). Linear regression analysis indicated that there was a positive correlation between the changes of SOD1 activity and the mRNA expression of SOD1,PI3K and AKT respectively in spinal cord tissues. Conclusion Pre- and post-ischemic conditioning with propofol shows potent protective effects against SCIRI in the rabbit model. The mechanisms may be related to increased expression of SOD1 in the spinal cord tissues by activating PI3K/ AKT signal transduction pathway.
