Function of SOD1, SOD2, and PI3K/AKT signaling pathways in the protection of propofol on spinal cord ischemic reperfusion injury in a rabbit model

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• 作者：Qi Jing Yu ; ^{yqj721103@sina.com" class="auth_mail" title="E-mail the corresponding author} ; Yunzhao Yang
• 关键词：Spinal cord ; Ischemia-reperfusion ; Propofol ; Superoxide dismutase 1 (SOD1) ; Superoxide dismutase 2 (SOD2)
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：1 March 2016
• 年：2016
• 卷：148
• 期：Complete
• 页码：86-92
• 全文大小：1219 K

文摘

To verify that co-application of propofol preconditioning and postconditioning protects spinal cord from ischemia/reperfusion injury by enhancing the different subtypes of SOD activity, which is related to PI3K/AKT signal pathway.

Materials and methods

60 rabbits were randomly equally assigned to 3 groups: Group S, sham-operation group; Group I/R., ischemia/reperfusion group; Group P, ischemia/reperfusion group with propofol treatment. Four rabbits per group were randomly executed at the time-points: days 1, 2, 3, 5, and 7 post-surgery. Spinal cord tissues at L3 to L4 levels were harvested. The bioactivities of SOD₁ and SOD₂, and the mRNA expression levels of SOD₁, SOD₂, PI3K, and AKT were detected.

Key findings

On day 1, the bioactivity of SOD₁ increased significantly in Group I/R or Group P compared with Group S (P < 0.05). On day 2, compared with Group S, the bioactivity of SOD1 increased significantly in Group P (P < 0.05). On days 3, 5, and 7, the bioactivity of SOD₁ decreased significantly respectively in Group I/R compared with Group S (P < 0.05). On all timepoints, the bioactivity of SOD₂ decreased significantly in Group I/R compared with Group S (P < 0.05). There was a positive correlation between the SOD₁ activity and the respective mRNA expression of SOD₁, PI3K, and AKT.

Significance

Co-application of propofol preconditioning and postconditioning resulted in potent protective effects against spinal cord ischemia/reperfusion injury, which was associated with the increased expression of SOD₁ in spinal cord tissues by activating PI3K/AKT signal pathway.