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@#Objective To analyze the protective mechanism of spinal cord ischemia-reperfusion injury mediated by N-methyl-D-aspartate (NMDA) receptor. Methods A total of 42 SD rats were randomly assigned to 4 groups: a non-blocking group (n=6), a saline group (n=12), a NMDA receptor blocker K-1024 (25 mg/kg) group (n=12) and a voltage-gated Ca2+ channel blocker nimodipine (0.5 mg/kg) group (n=12). The medications were injected intraperitoneally 30 min before ischemia. The neural function was evaluated. The neuronal histologic change of spinal cord lumbar region, the release of neurotransmitter amino acids and expression of spinal cord neuronal nitric oxide synthase (nNOS) were compared. Results At 8 h after reperfusion, the behavioral score of the K-1024 group was 2.00±0.00 points, which was statistically different from those of the saline group (5.83±0.41 points) and the nimodipine group (5.00±1.00 points, P<0.05). Compared with the saline group and nimodipine group, K-1024 group had more normal motor neurons (P<0.05). There was no significant difference in glutamic acid concentration in each group at 10 min after ischemia (P=0.731). The nNOS protein expression in the K-1024 group was significantly down-regulated compared with the saline group (P<0.01). After 8 h of reperfusion, the expression of nNOS protein in the K-1024 group was significantly up-regulated compared with the saline group (P<0.05). Conclusion K-1024 plays a protective role in spinal cord ischemia by inhibiting NMDA receptor and down-regulating nNOS protein expression; during the reperfusion, K-1024 has a satisfactory protective effect on spinal cord function, structure and biological activity of nerve cells.
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Objective Lipoxin A4 (LXA4) has been proved to have a good protective effect on spinal cord ischemia-reperfusion injury in rats, but whether autophagy is one of the protective mechanisms remains unclear. This study aims to investigate the effects of lipoxin A4 on rat spinal cord ischemia-reperfusion injury. Methods 48 rats were randomly divided into LXA4 group, ischemia-reperfusion group (SCII group) and sham group with 16 rats in each, and the models of each group were built accordingly. The rats in LXA4 group received intrathecal injection of 10μl LXA4 (300 pmol) 30 minutes after clamping the abdominal aorta. Three groups of rats were sacrificed by cervical dislocation 24 hours after reperfusion and the apoptosis-positive cells were then obtained. The spinal cord tissues of three groups of rats were stained and counted by LC3B fluorescence staining, and the expressions of LC3-II/LC3-I and GABARAP protein were detected by Western blot. Results There were few LC3B positive cells in the sham group. Compared to those in the sham group (73.40±19.42), the number of LC3B positive cells in SCII group (399.80±18.46) and LXA4 group (240.80±12.76) significantly increased (P<0.05), and the number in LXA4 group was significantly lower than that in SCII group (P<0.05). The ratio of LC3-II/LC3-I and the expression of GABARAP in SCII group and LXA4 group was significantly higher than those in sham group (P<0.05). The ratio of LC3-II/LC3-I in spinal cord tissue significantly declined compared with that of SCII group (P<0.05). Conclusion The autophagy is activated when SCII occurs, indicating that the autophagy is involved in SCII. After LXA4 is administered, autophagy is inhibited and SCII is alleviated.
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Objective: To observe the effects of ginsenoside Rg1 pretreatment on the expression of survivin protein and apoptosis after spinal cord ischemia-reperfusion injury (SCII) in rats so as to explore the possible mechanism of ginsenoside Rg1 on motor function recovery after SCII in rats. Methods: We selected 120 adult healthy SD rats to construct the model of SCII and randomly divided them into four groups: sham operation group, ischemia group, ischemia-reperfusion group, and drug group. Basso Beattie and Bresnahan score (BBB score) was used to evaluate the motor function of the hind limbs of the rats. The expressions of survivin protein and apoptosis-inducing factor (AIF) was observed by immunohistochemistry. The expression and activity of survivin protein and Caspase-9 in each group were observed and analyzed by Western blot and RT-PCR. Results: The intervention of ginsenoside Rg1 could increase the score of the motor function of the rat hind limbs. It could decrease the number of AIF positive cells, but increase the number of survivin protein positive cells. Ginsenoside Rg1 could decrease the expressions of survivin and Caspase-9, and decrease the apoptosis of nerve cells in SCII. Conclusion: Ginsenoside Rg1 could inhibit the expression of Caspase-9 by promoting the expression of survivin protein and decrease the apoptosis of rat SCII induced by the level of cytoplasmic AIF.
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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.
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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.
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Objective To observe the mechanisms of bone marrow mesenchymal stem cells (BMSCs) transfected with neurotrophin-3 in treating nanoparticle repaired spinal cord ischemia-reperfusion (I/R) injury of adult rat. Methods BMSCs were transfected into NT-3 with nanoparticle carrier and transplanted into 80 adult rats on the spinal cord I/R injury model. Then the rats were divided into four groups: sham group, NS group, BMSCs and BMSCs+NT-3. The BBB scoring system, the neurons cell apoptosis, levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were observed and compared between the four groups. Results The BBB score of the BMSCs+NT-3 group was significantly higher than those of BMSCs and NS group , but was lower obviously than the Sham group. TUNEL-apoptosis cells were significantly decreased in the BMSCs + NT-3 group compared to BMSCs and NS groups, but was more significantly lower than the Sham group. The contents of MDA and MPO of the NS group were significantly higher than the BMSCs group. The contents of the BMSCs + NT-3 group were lower than those of the BMSCs group, but lower significantly than the Sham group (P < 0.05). Conclusion BMSCs transfected with NT-3 with nanoparticle carrier could be induced each other. When transplanted into SCI , they can repair spinal cord by alleviating neuron cells apoptosis and inhibiting the lipid peroxidation of free radicals.
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Objective To investigate the effect of salvia mihiorrhiza on spinal cord ischemia reperfusion injury after surgical treatment in patients with cervical canal stenosis. Methods Retrospective analysis of 64 cases had cervical canal stenosis in the last 5 years in our hospital. Sixty-four cases were randomly divided into the salvia mihiorrhiza group(31 cases)and the control group(33 cases). The therapeutic effect was assessed using JOA grade system. Results In the salvia mihiorrhiza group,the JOA average score was 8. 8 ±2. 6 before surgical treatment, after two weeks of surgical treatment it was 13. 7 ± 2. 4. The JOA improvement ratio was (61. 5 ± 2. 9) % . In the control group,the JOA average score was 9. 1 ±2. 2 before surgical treatment,after two weeks of surgical treatment it was 13. 4 ± 2. 3. The JOA improvement ratio was (60. 5 ± 2.2)% .The JOA improvement ratio in the salvia mihiorrhiza group was significantly higher than that in the control group (P < 0. 05) . Conclusions Salvia mihiorrhiza has protective effect on spinal cord ischemia reperfusion injury.
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@#ObjectiveTo explore the atorvastatin impact of pretreatment on spinal cord ischemia-reperfusion injured model of rabbits.MethodsThe animal model was induced by occlusion abdominal aorta. Spinal cord was performed for 45 min ischemia and neuronal function was evaluated at 2 h, 6 h, 12 h, and 24 h after reperfusion. The contents of malonydialdehyde (MDA), superoxide dismutase (SOD) and myeloperoxidase (MPO) were assayed 24 h after reperfusion.ResultsThe neuronal function decreased significantly 12 h and 24 h after reperfusion. The activity of SOD significantly enhanced, MDA contents and the activity of MPO decreased at medium-dose and high-dose atorvastatin.ConclusionAtorvastatin has protective effect on the spinal cord ischemia-reperfusion injury of rabbits.
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@#Objective To observe the changes of MEP(motor evoked pontential) and neurologic function after Erigeron beviscapus(EBHM) preconditioning on spinal cord ischemia-reperfusion injury in rabbits, and provide substructural experimental theory.Methods Twenty-four domestic rabbits were randomly divided into four groups with six rabbits each. In sham group (group A) only the abdominal aorta was exposed. In the blank group (group B), the abdominal aorta was occluded 40 minute followed by reperfusion. In the methylprednisolone group (group C), it was occluded 30 minute before the abdominal, methylprednisolone (30 mg/kg) was injected into the rabbit by vein, which was used for two days after the surgeon. In the EBHM group (group D), EBHM(50 mg/kg) was injected into the rabbit by vein, the following procedure was the same as group C. MEP was measured in each observed point and neurologic function was observed everyday for 7days.Results At every observed point after SCI, the MEP changed regularly, and compared with group B, there was significant difference in groups C and D(P<0.05). 7 days later, the neurologic function changed significantly in each group(P<0.05).Conclusion MEP monitoring can reflect the early change on spinal cord ischemia-reperfusion injury. EBHM preconditioning can protect the rabbit from spinal cord ischemia reperfusion injury.
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@#Objective To explore the effects of erythropoietin (EPO) on the neural function recovery and the expressions of nuclear factor-κB (NF-κB) in rabbit spinal cord after ischemia-reperfusion injury. Methods 24 rabbits were randomized into 3 groups: EPO treatment group, ischemia-reperfusion (I/R) group and sham group with 8 rabbits in each group. The rabbit model of spinal cord ischemia-reperfusion injury was established with Tetik's method. The changes of neural functional recovery of rabbits of 3 groups were observed through Tarlov's scale at different time points post-operation. The expressions of NF-κB were tested with immunohistochemistry. Results The grade of nerve function improved distinctly in EPO treatment group (P<0.01).The expression of NF-κB in EPO group was lower than that of I/R group (P<0.01).Conclusion EPO can significantly improve the motor function of hind limbs in rabbits after spinal cord ischemia-reperfusion injury, which might be related with inhibition of the expressions of NF-κB.
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@# Objective To observe the effect of aprotinin preconditioning on nitric oxide (NO), nitric oxide synthase (NOS) and oxyradical during spinal cord ischemia-reperfusion injury in rabbits.Methods 21 rabbits were randomly divided into the aprotinin treatment group (8 rabbits), control group (8 rabbits) and sham operative group (5 rabbits). The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. In the treatment group, aprotinin was given at 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in the control group, the ischemia-reperfusion duration between aprotinin treatment group and control group remained same. The sham operative group was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and 8 h, 24 h after ischemia-reperfusion, lumbar segment was harvested to detect content of NO, malondialdehyde (MDA), induced nitric oxide synthase (iNOS) and superoxide dismutase (SOD) of spinal cord.Results 8 h after spinal cord ischemia-reperfusion, compared with the control group, the content of NO, MDA and the activity of iNOS were less, and the activity of SOD was more in the aprotinin treatment group ( P<0.05).Conclusion Aprotinin pretreatment can reduce the content of NO, MDA and descend the activity of NOS. Moreover aprotinin pretreatment can ascend the activity of SOD and improve apoptosis of nerve cell.
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@#Objective To observe the effect of pretreatment of aprotinin on nitric oxide (NO) and nitric oxide synthase (NOS) contents after ischemia-reperfusion injury of spinal cord in rabbits.Methods 45 rabbits were randomly divided into aprotinin treatment group (group A), normal saline control group (group B) and pseudo-surgical operation group (group C) with 15 rabbits in each group. The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. Aprotinin was given 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in group B, the ischemia-reperfusion duration between group A and group B remained same. The group C was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and at 8 h, 24 h after ischemia-reperfusion, lumbar segment spinal cords were harvested to detect contents of NO and NOS of spinal cord.Results After 8 h of ischemia-reperfusion,the contents of NO, total NOS (TNOS), and induced NOS (iNOS) in group A and group B were more than that before ischemia (P＜0.05). After 8 h of ischemia-reperfusion, there was a significant difference in the contents of NO, TNOS, iNOS between group A and group B (P＜0.05～0.01). After 24 h of ischemia-reperfusion, there was a significant difference too between group A and group B (P＜0.01). After 8 h and 24 h ischemia-reperfusion, the contents of NO, TNOS, iNOS in group A and group B were more than that in group C (P＜0.01).Conclusion During the ischemia-reperfusion, more NO produced is an important factor of spinal cord injury. Aprotinin can decrease the contents of NO and ischemia-reperfusion injury to spinal cord of rabbits.
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@#Objective To investigate the effect of regional captopril infusion on ischemia-reperfusion (I-R) injury of spinal cord in rabbits. Methods 32 rabbits were divided randomly into four groups, the group A (sham operated, no I-R injury), the group B (control group, only with I-R injury), the group C (I-R injury + intra-aortic infusion of hypothermic normal saline), and the group D (I-R injury + infusion of normal saline plus 4mg/kg captopril). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Hemodynamic data were measured in every group. The spinal cord function was assessed 24, 48 and 96 hours after aortic declamping according to Tarlov's Scale. Spinal cords were harvested for histological analysis. Results There were no significant differences in blood pressure and heart rate among four groups. The neurological status in the groups C and D was significantly superior to that of the group B (P<0.01). In the group B, all animals were paraplegic with Tarlov's Scale of 0 or 1. Three of 8 animals in the group C were paraplegic with Tarlov's Scale of 0 or 1, and only one animal in the group D. Compared to the group B, there were more normal neurons in the anterior horn of spinal cords in the groups C and D (P<0.01). Conclusion Regional infusion of hypothermic normal saline contained captopril can provide sufficient spinal cord protection against ischemia.