Antioxidation of quercetin against spinal cord injury in rats

Objective : To observe the effect of quercetin on experimental spinal cord injury (SCI) in rats. Methods: Sixty Sprague-Dawley rats were randomly divided into four groups : Group A only for laminectomy, Group B for laminectomy with SCI, Group C for SCI and intraperitoneal injection with a bolus of 200 mg/kg quercetin and Group D for SCI and intraperitoneal injection of saline. SCI model was made by using modified Aliens method on T12. Six rats of each group were killed at 4 h after injury and the levels of free iron and malondialdehyde ( MDA) of the involved spinal cord segments were measured by bleomycin and thiobarbituric acid (TBA) assays separately. The recovery of hind limb function was assessed by Modified Tarlov 's scale and inclined plane method at 7 d,14 d and 21 d after SCI. The histological changes of the damaged spinal cord were also examined at 7 d after SCI. Results: After SCI, the levels of free iron and MDA were significantly increased in Groups B and D, while not in Group C. The Modified Tarlov 's score and the inclined plane angles were significantly decreased in Groups B, C and D. The histological findings were not improved. Conclusions: After SCI, quercetin can reduce the level of lipid peroxidation, but not improve recovery of function.     

Protective effect of deferoxamine on experimental spinal cord injury in rat

Objective

To observe the protective effect of deferoxamine on experimental spinal cord injury (SCI) in rats.

Methods

Sprague-Dawley rats were randomly divided into the following four groups. Control group: rats were performed laminectomy only; SCI group: rats were performed laminectomy with SCI; DFO group: rats were injected intraperitoneally a bolus of 100 mg/kg deferoxamine after SCI; vehicle group: rats were injected intraperitoneally 0.9% saline after SCI. The SCI of animal model was made by using a modified Allen's method on T₁₀. Six rats of each group were sacrificed at 4 h after injured, and the levels of free iron and malondialdehyde (MDA) of involved spinal cord segments were measured by bleomycin assay and the thiobarbituric acid (TBA) separately. The recovery of function was assessed by Modified Tarlov's scale and inclined plane method at 7, 14, 21 d after SCI. The histologic changes of the damaged spinal cord were also examined at 7 d after SCI.

Results

Following SCI, the levels of free iron and MDA were increased significantly and the Modified Tarlov's score and inclined plane angles decreased in SCI group and vehicle group. In DFO group, the levels of free iron and MDA were not increased, but the Modified Tarlov's score and inclined plane angles decreased, the histological findings were improved as well.

Conclusion

Deferoxamine can reduce the levels of free iron and lipid peroxidation, and improve the hind limb functional status of rats with spinal cord injury.     

Dose-dependent neuroprotective effects of melatonin on experimental spinal cord injury in rats

BACKGROUND: This report examines the dose-dependent effects of melatonin on early lipid peroxidation levels, ultrastructural changes, and neurological function in experimental spinal cord injury (SCI) by comparing them with therapeutic levels of methylprednisone in rats. METHODS: SCI was performed by an aneurysm clip placed extradurally at the level of T10. Rats were randomly divided into six groups of 10 rats each. Group 1 (sham) received only laminectomy; group 2 (control) received SCI; group 3 (placebo) received SCI and physiological saline; group 4 received methylprednisone (30 mg/kg); groups 5 and 6 received melatonin at doses of 50 or 100 mg/kg, respectively, after SCI. Rats were neurologically tested 24 hours after trauma. Spinal cord samples were harvested for both lipid peroxidation levels and ultrastructural histopathological evaluation. RESULTS: Neurological scores of rats were not different in SCI groups. Lipid peroxidation levels are significantly restricted only in methylprednisone group at 24 hours. Melatonin-treated groups showed more ultrastructural improvement on electron microscope studies when compared with methylprednisone group. However, the therapeutic effects of melatonin were mainly observed on white matter of spinal cord in ultrastructural investigation. There was significant difference between melatonin dose groups increasing with dose. CONCLUSIONS: Results showed that melatonin has no significant dose-dependent effects on early lipid peroxidation bur rather some neuroprotective effects on both axons and myelin sheaths of white matter in ultrastructural observations when compared with methylprednisone. These effects significantly augmented with dose increase.     

Effects of EPC-K1 on lipid peroxidation in experimental spinal cord injury

STUDY DESIGN: A study in which levels of lipid peroxidation were measured, the thiobarbituric acid-reactive substances were estimated in an experimental rat model, and the recovery was assessed. OBJECTIVE: To ascertain the occurrence of thiobarbituric acid-reactive substances in the damaged spinal cord, and to investigate the effectiveness of a hydroxyl radical scavenger EPC-K1, a phosphate diester linkage of vitamins E and C, in attenuating the severity of spinal cord injury. SUMMARY OF BACKGROUND DATA: Lipid peroxidation has been reported to play an important role in spinal cord injury. There is no report on the use of EPC-K1 to attenuate the severity of spinal cord injury in either animal or human studies. METHODS: Spinal cord injury was induced by placing a 25-g weight on T12, and the animals were divided into six groups. Group 1 (sham) received only laminectomy. Group 2 (control) received spinal cord injury. Group 3 received EPC-K1 5 minutes before injury. Group 4 received it 5 minutes after injury. Group 5 received it 3 hours after injury. Group 6 received it five times, respectively: at 5 minutes, then 1, 2, 3, and 4 hours after injury. The levels of thiobarbituric acid-reactive substances were measured in the spinal cord, and the recovery was assessed. RESULTS: The thiobarbituric acid-reactive substances content increased after injury, with two peaks, at 1 and 4 hours. Concentration at the 4-hour peak was lower in nitrogen mustard-induced leukocytopenia rats than in the control rats. The EPC-K1 injection reduced thiobarbituric acid-reactive substances content at 1 and 4 hours after injury in Group 3 (respectively, 34.3% and 42.7% vs. control) and only that at 4 hours in Group 6 (24.9% vs. control). Motor function recovery and histologic findings were better in these two groups than in Group 2. CONCLUSION: Repeated injection of EPC-K1 attenuated the severity of spinal cord injury.     

Erythropoietin improves oxidative stress following spinal cord trauma in rats

Spinal cord injury (SCI) is a very destructive process for both patients and society. Lipid peroxidation is the main cause of the further secondary damage which starts after mechanical destruction of tissues. Recent studies have shown that erythropoietin (EPO) has neuroprotective properties. In this study, we aimed to see the effect of EPO treatment after spinal cord injury on the oxidant and anti-oxidant enzyme systems and the relationship with the N-methyl-d-Aspartate (NMDA) blockage. Spinal cord injury was produced by epidural compression with a cerebral vascular clip that has a closing force of 40 g for 30 s after a limited multilevel laminectomy (T9-11). Experiment was done in 5 groups: Group1: Sham-operated untraumatised, Group 2: SCI untreated, Group 3: 150 i.u./kg EPO injected i.p. at the end of the first hour following the trauma. Group 4: NMDA receptor antagonist ketamine (100 mg/kg) i.p. Group 5: EPO + ketamine i.p. The experiments were finished after 12 h of the trauma. The spinal cords were excised for biochemical examinations.Anti-oxidant enzymes; catalase and reduced glutathione (GSH) levels increased and lipid peroxidation product, malonyldialdehyde (MDA) level decreased in EPO treated group when compared to the other groups. TNF-α levels decreased in EPO treated group. Application of ketamine before EPO treatment decreased effects of EPO. In conclusion, our results suggest that 150 i.u./kg i.p. EPO, a therapeutic dose in anaemic patients, applied after 1 h of spinal cord injury significantly attenuated the oxidative damage of spinal cord injuries in rats. This activity is abolished via ketamine pretreatment.     

Antioxidant actions and early ultrastructural findings of thiopental and propofol in experimental spinal cord injury

Thiopental and propofol are effective antioxidant agents. The current study was undertaken to examine the neuroprotective effects of a single intraperitoneal dose of thiopental and propofol. Effects of the drugs were evaluated by lipid peroxidation and ultrastructural findings. Fifty male Wistar rats were divided into five groups. Group 1 was the control group. Rats underwent laminectomy only, and nontraumatized spinal cord samples were obtained 1 hour after surgical intervention. All other rats sustained a 50-g/cm contusion injury by the weight drop technique. Group 2 rats underwent spinal cord injury alone, group 3 rats received 1 mL intralipid solution intraperitoneally immediately after trauma as the vehicle group, group 4 rats received a 15-mg/kg single dose of thiopental, and group 5 rats received a 40-mg/kg single dose of propofol intraperitoneally following the trauma. Samples from groups 2, 3, 4, and 5 were obtained 1 hour after injury. Lipid peroxidation was determined by measuring the concentration of malondialdehyde in the spinal cord tissue. The ultrastructure of the spinal cord was determined by electron microscopy. The contusion injury was associated with a rise in lipid peroxidation. Compared with the trauma group there was significant attenuation in lipid peroxidation of groups 4 and 5. Ultrastructural findings showed that the rats of group 4 sustained minor damage after spinal cord injury, but there was more evident damage in group 5 rats. These results indicate that thiopental decreases lipid peroxidation and improves ultrastructure, whereas propofol decreases lipid peroxidation without improving ultrastructure 1 hour after spinal cord injury in rats.     

慢病毒介导的脑红蛋白体内基因转染对兔损伤脊髓的作用

【摘要】　目的：观察慢病毒介导脑红蛋白（Ngb）体内基因转染兔损伤的脊髓组织后对后肢运动功能的影响,探讨其作用机制。方法：用球囊压迫法制成兔脊髓损伤（ＳＣＩ）模型96只,随机分为对照组（A组）、生理盐水组（B组）、空载体组（C组）和Ngb慢病毒组（D组）,每组动物24只,A组SCI后无治疗;B组SCI后向脊髓内注射生理盐水;C组SCI后向脊髓内注射空病毒;D组SCI后向脊髓内注射Ngb重组慢病毒。各组分别在1、3、7、14、21d采用BBB运动功能评分系统检测兔后肢运动功能情况;观察损伤脊髓组织内标记荧光的表达;Real-time PCR和Western blot检测Ngb mRNA及其相应蛋白的表达情况,生化方法检测丙二醛（MDA）和一氧化氮（NO）水平。结果：损伤后14d和21d,D组BBB评分明显高于其他3组（P<0.05）,但A、B及C组之间比较无差异（P＞0.05）;C组和D组兔损伤部位脊髓组织均有GFP表达的绿色荧光信号;损伤后7d、14d和21d,D组的Ngb表达与其他3组比较明显增强（P<0.05）;损伤后7d、14d和21d,D组损伤脊髓组织中MDA、NO含量明显低于其他3组（P<0.05）。结论：慢病毒介导脑红蛋白（Ngb）体内基因转染可使Ngb高表达,可能是通过减轻继发性SCI,从而促进SCI后后肢运动功能的恢复。     

Acute phase effects of ATP-MgCl<Subscript>2</Subscript> on experimental spinal cord injury

The purpose of this study was to study the acute phase effects of adenosine triphosphate (ATP)-MgCl₂ on experimental spinal cord clip compression injury. Spinal cord clip compression injury was performed on 36 albino Wistar rats. The rats were divided into five groups. T4–T8 total laminectomy was performed on all rats. Group 1: sham-operated group. Group 2: clip compression group. In group 3, ATP-MgCl₂ (100 μmol/kg) was given 2 min before the "clip compression injury." In group 4, ATP-MgCl₂ (100 μmol/kg) was given 5 min after the clip compression injury. In group 5, ATP MgC1₂ (100 μmol/kg) was administered 8 h after the injury. The spinal cords were excised for a length of 2 cm and deep frozen at –76°C. Tissue malondialdehyde (MDA) levels were used to determine the effects of ATP-MgCl₂ on spinal cord lipid peroxidation. In the groups in which ATP MgCl₂ was administered after the clip compression injury (groups 4 and 5), the decrease in spinal cord MDA levels was statistically significant when compared with those of the injury group (group 2). Although MDA levels of group 4 were lower than those of group 5, this difference was not statistically significant. Administration of the ATP-MgCl₂ before the clip compression injury (in group 3) did not have a statistically significant effect on lipid peroxidation when compared with the injury group (group 2). In this study, we found that ATP-MgCl₂ has decreased lipid peroxidation in spinal cord injury and protected the spinal cord from secondary injury after the trauma. We concluded that ATP-MgCl₂ may be used in the treatment of spinal cord injuries in conjunction with the other treatment modalities, but further investigations are mandatory. Electronic Publication     

Effect of methylprednisolone, tirilazad mesylate and vitamin E on lipid peroxidation after experimental spinal cord injury

Effect of methylprednisolone (MP), tirilazad mesylate (TM) and vitamin E on lipid peroxidation (LP) was evaluated in an experimental model of spinal cord compression injury in anesthetized rats. Forty rats, divided randomly into four groups, were injured by compressing on the spinal cord at Th 3 for 1 min. Bolus injections of saline solution, MP (30 mg/kg bolus and 5.4 mg/kg/h), TM (10 mg/kg four times per day), or vitamin E (30 mg/ kg four times per day) were begun 1 h after the spinal cord injury (SCI). Twenty-four hours after treatment, the rats were killed, and malondialdehyde (MDA), a LP product, was measured in the spinal cord tissues. Rats treated with MP, TM and vitamin E had significantly decreased MDA levels (P<0.01) than rats in the control group. The lowest MDA levels were found in the TM group. These results suggest that MP, TM and vitamin E may have a protective effect against SCI in rats by its antioxidant effect.     

内皮素受体拮抗剂对损伤脊髓早期保护作用

目的评价非选择性内皮素(ET)受体拮抗剂PD145065对损伤脊髓的保护作用,证实ET参与脊髓损伤(SCI)后继发损伤的假设并探讨其作用机制。方法压迫法致伤大鼠脊髓(50g,1min)。损伤前10min鞘内注射PD145065或生理盐水,观察脊髓血流(SCBF)、丙二醛(MDA)、细胞内钙(［Ca2+］i)、伊文思兰(EB)及水含量变化。结果伤区SCBF在伤后5min即有明显下降,为基线的(75.23±9.21)%,2h降为(57.06±7.35)%;伤区邻近血流下降较慢,伤后30min降为(79.82±7.98)%。伤区及邻近区伤后4h?SCBF都未恢复。伤段脊髓组织中MDA、［Ca2+］i、EB和水含量均高于假手术组(P＜0.05)。PD145065明显改善了伤区SCBF,消除了伤区邻近段SCBF的下降。PD145065预处理组脊髓中MDA、［Ca2+］i、EB和水含量均低于生理盐水组(P＜0.05)。结论PD145065对损伤脊髓早期有明显保护作用,ET及其受体可能通过多种途径参与SCI后的继发损伤。临床应用ET受体拮抗剂对SCI可能有治疗作用。     

硬膜内局部灌注甲强龙对兔急性脊髓损伤后血清SOD、MDA的影响

目的探讨硬膜内局部灌注甲强龙(MP)对兔脊髓损伤(SCI)后血清超氧化物歧化酶(SOD)、丙二醛(MDA)的浓度的影响。方法将54只白兔随机分为3组,每组18只,Ⅰ组为不完全SCI+局部灌注MP,Ⅱ组为不完全SCI+局部灌注生理盐水(NS),Ⅲ组为对照组。用改良Allen法造成Ⅰ、Ⅱ组不完全SCI模型,硬膜内置管,检测血清中SOD、MDA的变化情况,同时进行改良Tarlov评分测评及病理组织学观察。结果Ⅱ组血清中的MDA升高,SOD浓度下降,与Ⅲ组比较差异有统计学意义(P<0.05)。与Ⅱ组比较,Ⅰ组能明显降低SCI后血清中MDA含量,提高SOD浓度,差异有统计学意义(P<0.05)。结论 SCI后硬膜内局部灌注MP能够降低血清MDA含量,提高SOD浓度,在一定程度上阻止继发性损伤的发展。     

Neuroprotective effect of magnesium on lipid peroxidation and axonal function after experimental spinal cord injury.

STUDY DESIGN: An experimental study examining the neuroprotective effect of magnesium on axonal function and lipid peroxidation in a rat model of acute traumatic spinal cord injury. OBJECTIVE: To determine the effectiveness of postinjury treatment with magnesium on evoked potentials and lipid peroxidation after spinal cord injury (SCI). SETTING: Pamukkale University, Denizli, Turkey. METHODS: Spinal cord injury occurred in 30 rats with an aneurysm clip at T9 and the rats were randomly assigned to undergo subcutaneous administration of one of the following at 1 h after injury: (1) Physiological saline (n = 10); (2) MgSO4, 300 mg/kg (n = 10) and (3) MgSO4, 600 mg/kg (n = 10). Spinal somatosensory evoked potentials (SSEPs) were recorded before injury, 30 min after injury and 3 h after injections. Rats were killed 24 h after the injury, and malondialdehyde (MDA) levels were measured. RESULTS: Following SCI, there were significant decreases in the amplitudes of P1 and N1 (P<0.001) and only high-dose magnesium improved the SSEPs (P<0.01). On the other hand, there was significant difference in lipid peroxide content between high-dose magnesium treated group and both of saline treated and low-dose magnesium treated groups (P<0.01). CONCLUSION: These results suggest that magnesium has a dose-dependent neuroprotective effect on SSEPs and lipid peroxidation after experimental spinal cord injury.     

低剂量他克莫司治疗大鼠急性脊髓损伤的实验研究

目的：探讨低剂量他克莫司（tacrolimus，又名FK506）对大鼠急性脊髓损伤是否具有神经保护作用。方法：雄性Wistar大鼠72只，随机分为假手术组（12只）、损伤组（30只）和FK506治疗组（30只）。采用Allen’s打击法致伤大鼠T10脊髓，假手术组仅做椎板切除术。FK506治疗组在脊髓损伤后5min一次性经尾静脉注射FK5060．3mg／kg，其余两组以相同方法给予等量生理盐水。致伤后30min、6h、24h、48h、72h取伤段脊髓组织行病理观察及原位末端标记法（TUNEL）检测神经细胞凋亡，伤后1、3、7、14、21d行脊髓功能BBB评分和斜板实验。结果：伤后3、7、14、21d，FK506治疗组斜板实验和BBB评分明显优于损伤组，两组间比较差异有显著性（P〈0．05）；伤后各时间点FK506治疗组脊髓损伤区出血坏死较损伤组轻；伤后6、24、48、72h神经细胞凋亡FK506治疗组较损伤组明显减少，两组间比较差异有显著性（P〈0．05）。结论：在大鼠急性脊髓损伤后早期应用低剂量他克莫司（0．3mg/kg）治疗对神经具有保护作用，可减少神经细胞凋亡，减轻脊髓继发性损伤，促进脊髓功能恢复。     

Effectiveness of FK506 on lipid peroxidation in the spinal cord following experimental traumatic injury

STUDY DESIGN: An in vivo study in Wistar albino rats with injured spinal cord. SETTING: Department of Neurosurgery, Biochemistry and Pathology, Gazi University, Ankara, Turkey. OBJECTIVES: The aim of this study was to investigate and compare the effects of FK506 an immunosupressive agent with methylprednisolone (MP) on lipid peroxidation (LP) in injured spinal cord tissue. METHOD: A total of 28 adult healthy Wistar albino rats were subjected to traumatic spinal cord injuries (SCI) by using an aneurysmal clip compression technique, and they were divided into four groups. The G1 group (n=8) received FK506 (1 mg/kg); the G2 group (n=8) received FK506 (1 mg/kg) and MP (30 mg/kg); the G3 group (n=6) received only MP (30 mg/kg); and the G4 group (n=6) received no medication. The injured spinal cord tissue was studied by means of lipid peroxides, malondialdehyde (MDA), with thiobarbituric acid reaction and additionally the FK506 (G1); the MP (G3) groups were studied for histopathologic alterations 72 h after SCI with eight separate animals. RESULTS: Although LP values of G1, G2, G3 showed no statistical difference between intergroup analyses (P=0.547), a histopathological examination revealed that in the group that received MP, the oedema pattern was more significant than the group that received FK506. Another interesting finding was the presence of polymorphonuclear leucocytes in the MP group, whereas no infiltration was found in the FK506 group. CONCLUSION: Analysis of the results indicated that FK506 is a valuable pharmacological agent that could be used to decrease the LP and polymorphonuclear leucocyte infiltration and inflamatory reactions in the injured spinal cord tissue.     

猪胸腰段脊髓火器伤后早期血糖变化

目的建立家猪胸腰段脊髓火器伤模型和改良Allens打击伤后全瘫模型,观察伤后早期血糖的变化。方法将实验动物随机分为两组,其中火器伤(G)组6只,在全麻状态下制作胸腰段(L1,2)脊髓火器伤模型;打击伤(C)组6只,L1节段脊髓行改良Allen’s打击。各组动物分别于伤前、伤后0.5、1、2、4h检测血糖。结果两组动物在伤后4h内均出现高血糖,以伤后0.5h最高,而伤后1～4h逐渐降低。G组血糖的升高幅度较C组显著(P<0.01)。结论由于火器伤后血糖升高幅度较大,故脊髓火器伤后早期应慎用葡萄糖液。     

Association of riluzole and dantrolene improves significant recovery after acute spinal cord injury in rats

Background Context

Damage to the spinal cord can result in irreversible impairment or complete loss of motor, sensory, and autonomic functions. Riluzole and dantrolene have been shown to provide neuroprotection by reducing neuronal apoptosis after brain and spinal cord injury (SCI) in several animal models of neurologic disorders. As these drugs protect the injured spinal cord through different mechanisms, we investigated the cumulative effects of riluzole and dantrolene.

The effect of duration of compression on lipid peroxidation after experimental spinal cord injury

The present study was performed to evaluate the effect of duration of acute spinal cord compression on tissue lipid peroxidation in rats. A clip compression method (1) was used to produce acute spinal cord injury. Rats were divided into 3 groups, each consisting of 10. At 1 hour after trauma all rats were sacrificed, and MDA content of the injured spinal cord segment was measured. The tissue MDA contents were 3.922 μmolMDA/gww in group 1 (control), 10.192 μmol MDA/gww in group 2 (30 seconds compression), and 12.147 μmolMDA/gww in group 3 (60 seconds compression). These results demonstrate that the length of duration of compression significantly enhances lipid peroxidation. Our study supported the view that persisting compression may cause progression of secondary mechanisms which may irreversibly eliminate any potential for recovery.     

Methylprednisolone reduces spinal cord injury in rats without affecting tumor necrosis factor-alpha production

Methylprednisolone (MPS) is the only therapeutic agent currently available for traumatic spinal cord injury (SCI). However, little is known about its therapeutic mechanisms. We have demonstrated that tumor necrosis factor-alpha (TNF-alpha) plays a critical role in posttraumatic SCI in rats. Since MPS has been shown to inhibit TNF-alpha production in vitro, it is possible that MPS can reduce SCI by inhibiting TNF-alpha production. To examine this possibility, we investigated the effect of MPS on TNF-alpha production in injured segments of rat spinal cord. Leukocytopenia and high-dose intravenous administration of MPS markedly reduced the motor disturbances observed following spinal cord trauma. Both treatments also reduced the intramedullary hemorrhages observed histologically 24 hr posttrauma. Leukocytopenia significantly reduced tissue levels of both TNF-alpha mRNA and TNF-alpha, 1 and 4 hr posttrauma, respectively, and it also inhibited the accumulation of leukocytes in the injured segments 3 hr posttrauma, while MPS had no effects. Lipid peroxidation and vascular permeability at the site of spinal cord lesion were both significantly increased over time after the induction of SCI, peaking 3 hr posttrauma. These events were significantly reduced in animals with leukocytopenia and in those given anti-P-selectin monoclonal antibody compared to sham-operated animals. Administration of MPS significantly inhibited both the increase in lipid peroxidation and the vascular permeability. These findings suggested that MPS reduces the severity of SCI, not by inhibiting the production of TNF-alpha at the site of spinal cord trauma, but by inhibiting activated leukocyte induced lipid peroxidation of the endothelial cell membrane. This suggests that MPS may attenuate spinal cord ischemia by inhibiting the increase in endothelial permeability at the site of spinal cord injury.     

大剂量甲基强的松龙对大鼠急性脊髓半切损伤的早期神经保护作用

目的研究大剂量甲基强的松龙（methylprednisolone,MP）对大鼠急性脊髓半切损伤的早期神经保护作用。方法 50只SD大鼠随机取10只仅行椎板切除,作为对照组。其余40只随机分为2组,脊髓半切损伤组及MP治疗组各20只。各组动物再随机平分为2个小组,分别在脊髓半切损伤后1d、7d进行BBB法神经功能评分、脊髓组织形态学观察、神经中丝（neurofilament NF）和胶质纤维酸性蛋白（glial fibrillary acidic protein,GFAP）免疫组化测定。结果脊髓半切损伤后立即使用大剂量MP明显提高了伤后7d时MP治疗组的BBB评分;对损伤脊髓的组织形态学有明显改善;明显提高了NF的表达,抑制了GFAP的表达。结论早期大剂量使用MP对大鼠急性脊髓半切损伤有神经保护作用。