Hua Fang1, Jing-Chao Zhang1, Miao Yang1, Hua-Feng Li2, Jian-Ping Zhang3, Fang-Xiang Zhang1, Quan-Yun Wang4, Ru-Rong Wang4, Jin Liu4. 1. Department of Anesthesiology, Guizhou Provincial People's Hospital, Guiyang 550002, Guizhou Province, China; Department of Anesthesiology, Affiliated People's Hospital of Guizhou Medical University, Guiyang 550002, Guizhou Province, China. 2. Department of Anesthesiology, West China Second University Hospital, Chengdu 610041, Sichuan Province, China. 3. Department of Anesthesiology, Guizhou Provincial People's Hospital, Guiyang 550002, Guizhou Province, China; Department of Anesthesiology, Affiliated People's Hospital of Guizhou Medical University, Guiyang 550002, Guizhou Province, China. Electronic address: albatrossa@126.com. 4. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China.
Abstract
OBJECTIVE: To observe the effects of perfusion of the gastrodin in abdominal aorta for alleviating the spinal cord ischemia reperfusion injury (SCIRI). METHODS: A total of 36 New Zealand white rabbits were divided randomly into sham-operated group (group S), control group (group C) and gastrodin group (group G), 12 rabbits for each group. Aorta abdominalis infrarenalis blocking method was applied to establish the SCIRI model. The changes of motor evoked potentials (MEPs) before the ischemia and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of the gastrodin were respectively recorded, and the neurologic function score before the ischemia, on the 6 h, 12 h and 24 h of the reperfusion of the gastrodin were assessed. And the changes of the concentration of serum neuron specific enolase (NSE), interleukin (IL)-lβ and IL-8 were measured before the ischemia, after 45 min of ischemia, and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of gastrodin. Then the levels of spinal cord nerve cells mitochondrial superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total antioxidant capacity (T-AOC) and mitochondrial swelling degree (MSD) were tested and the histopathologic changes in spinal cord tissues were observed. RESULTS: The levels of the NSE, IL-lβ, IL-8, ROS, MDA and MSD of group C were all significantly elevated after the ischemia (P < 0.01); the levels of the spinal nerve cell mitochondria SOD, GSH-PX and T-AOC were all significantly reduced (P < 0.01), MEPs and spinal cord tissue pathology were damaged significantly (P < 0.01). The rate of motor neuron abnormalities and the damages of spinal cord tissue pathology of group G were significantly milder than those of group C (P < 0.01); the levels of NSE, IL-lβ, IL-8, ROS, MDA and MSD were significantly lower than those of group C (P < 0.01), but the levels of SOD, GSH-PX and T-AOC were all significantly higher than those of group C (P < 0.01), and the recovery of neurologic function score during the reperfusion of gastrodin was significantly faster than group C (P < 0.01). CONCLUSIONS: Perfusion of the gastrodin in abdominal aorta can alleviate the spinal cord ischemia reperfusion injury by promoting the mitochondrial antioxidant capacity and inhibiting the inflammatory reaction.
OBJECTIVE: To observe the effects of perfusion of the gastrodin in abdominal aorta for alleviating the spinal cord ischemia reperfusion injury (SCIRI). METHODS: A total of 36 New Zealand white rabbits were divided randomly into sham-operated group (group S), control group (group C) and gastrodin group (group G), 12 rabbits for each group. Aorta abdominalis infrarenalis blocking method was applied to establish the SCIRI model. The changes of motor evoked potentials (MEPs) before the ischemia and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of the gastrodin were respectively recorded, and the neurologic function score before the ischemia, on the 6 h, 12 h and 24 h of the reperfusion of the gastrodin were assessed. And the changes of the concentration of serum neuron specific enolase (NSE), interleukin (IL)-lβ and IL-8 were measured before the ischemia, after 45 min of ischemia, and on 30 min, 60 min, 6 h, 12 h and 24 h of reperfusion of gastrodin. Then the levels of spinal cord nerve cells mitochondrial superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total antioxidant capacity (T-AOC) and mitochondrial swelling degree (MSD) were tested and the histopathologic changes in spinal cord tissues were observed. RESULTS: The levels of the NSE, IL-lβ, IL-8, ROS, MDA and MSD of group C were all significantly elevated after the ischemia (P < 0.01); the levels of the spinal nerve cell mitochondria SOD, GSH-PX and T-AOC were all significantly reduced (P < 0.01), MEPs and spinal cord tissue pathology were damaged significantly (P < 0.01). The rate of motor neuron abnormalities and the damages of spinal cord tissue pathology of group G were significantly milder than those of group C (P < 0.01); the levels of NSE, IL-lβ, IL-8, ROS, MDA and MSD were significantly lower than those of group C (P < 0.01), but the levels of SOD, GSH-PX and T-AOC were all significantly higher than those of group C (P < 0.01), and the recovery of neurologic function score during the reperfusion of gastrodin was significantly faster than group C (P < 0.01). CONCLUSIONS: Perfusion of the gastrodin in abdominal aorta can alleviate the spinal cord ischemia reperfusion injury by promoting the mitochondrial antioxidant capacity and inhibiting the inflammatory reaction.