Title:Dexmedetomidine Attenuates Spinal Cord Ischemia-reperfusion
Injury in Rabbits by Decreasing Oxidation and Apoptosis
Volume: 23
Issue: 6
Author(s): Bingbing Liu, Yatong Liang, Weihua Huang, Hui Zhang, Daiwei Zhou*Xiaoshan Xiao*
Affiliation:
- Department of Anesthesiology,
Guangdong Second Provincial General Hospital; Zhuhai High-Tech Zone People’s Hospital; Zhuhai, China
- Department of Anesthesiology, Guangdong Second Provincial General Hospital; The Second School of
Clinical Medicine, Southern Medical University; Guangzhou, China
Keywords:
Spinal cord injury, ischemia-reperfusion injury, dexmedetomidine, apoptosis, Bcl-2, oxidative stress.
Abstract:
Background: In brain ischemia, dexmedetomidine (DEX) prevents glutamate
and norepinephrine changes, increases nerve conduction, and prevents apoptosis, but
the mechanisms are poorly understood.
Objective: This study aimed at examining the protective effect and function of DEX on
spinal cord ischemia-reperfusion injury (SCIRI) and whether the effect is mediated by
oxidative stress and apoptosis (with the involvement of Bcl-2, Bax, mitochondria, and
Caspase-3).
Methods: Rabbits were randomly divided into the sham group, infusion/reperfusion (I/R)
group, and DEX+I/R group. SCIRI was induced by occluding the aorta just caudal to the
left renal artery for 40 min, followed by reperfusion. DEX was continuously administered
for 60 min before clamping. The animals were evaluated for neuronal functions. Spinal
cord tissues were examined for SOD activity and MDA content. Bcl-2, Bax, and
Caspase-3 expressions were detected by western blotting. TUNEL staining was used for
apoptosis.
Results: With the extension of reperfusion time, the hind limbs’ neurological function in
the DEX+I/R group gradually improved, but it became worse in the I/R group (all P<0.05
vs. the other time points within the same groups). Compared with I/R, DEX decreased
MDA and increased SOD (P<0.01), upregulated Bcl-2 protein expression (P<0.05),
downregulated Bax expression (P<0.05), decreased caspase-3 expression (P<0.05),
prevented histological changes in neurons, and decreased the apoptotic index of the
TUNEL labeling (P<0.05).
Conclusion: DEX could attenuate SCIRI in rabbits by improving the oxidative stress
status, regulating the expression of apoptosis-related proteins, and decreasing neuronal
apoptosis.
