认证: 洪正华 主任医师 台州医院 骨科
目的 探讨经后路椎体次全切除三柱重建治疗不稳定性胸、腰椎单发爆裂型骨折的临床疗效。方法 2005年1月至2009年3月, 采用该术式治疗不稳定性胸、腰椎单发爆裂型骨折患者30例,男22例,女8例;年龄17~58岁,平均36岁。手术采用后正中入路,切除伤椎的一侧椎板、椎弓根及关节突,创建后外侧通道,然后行椎体次全切,椎间植入钛网或人工骨笼,后路椎弓根内固定重建脊柱三柱的稳定性。随访时进行X线和CT检查,比较术前、术后和随访时的伤椎高度、Cobb角、椎管狭窄分级及植骨融合情况。结果 30例均获得随访,平均随访28个月(18~48个月)。手术后胸、腰椎生理曲度恢复满意,Cobb角及伤椎高度与术前相比得到明显改善;椎管狭窄分级,术前2级8例、3级22例,术后均为0级;神经功能明显恢复, 术后Frankel分级:A级1例、B级1例、C级3例、D级9例、E级16例。结论 经后路椎体次全切除及三柱重建治疗不稳定性胸、腰椎单发爆裂型骨折是安全、有效的方法,并且具备前后联合入路手术的优势,为治疗不稳定胸、腰椎单发爆裂型骨折提供一个理想的选择
Abstract. Erythropoietin (EPO) is a promising therapeutic agent used in a variety of spinal cord injuries. Therefore, identifying the specific molecular pathway mediating the neuronal protective effect of EPO after spinal cord injury (SCI) is of great value to the patients concerned. Platelet-derived growth factor (PDGF)-B is an important factor in the recovery of neurological function. We explored changes in the expression of PDGF-B in spinal cord injury rats after receiving EPO treatment. We used a weight-drop contusion SCI model, and EPO treatment group rats received single doses ofEPO (1,000 U/kg i.p.) immediately after the operation. Seven days after the operation, the results revealed a more rapid recovery as noted by the higher BBB scores, less disruption and more neuronal regeneration of the spinal cord in the EPO treatment group than that in the SCI group. PDGF-B expression also increased in the EPO treatment group compared to that in the SCI group (P<0.01). This study showed that PDGF-B plays a role in the neuronal protective effect of EPO on spinal cord injury in rats, which may help to explain the quick recovery after EPO treatment of spinal cord injury.
摘 要 目的 探讨促红细胞生成素(erythropoietin,EPO)在大鼠急性脊髓损伤后抑制凋亡相关蛋白caspase一3的表达。方法30只sD大鼠,随机分为假手术对照组、脊髓损伤组和脊髓损伤EPO治疗组。其中脊髓损伤组和EPO治疗组采用改良Allen S打击法制作脊髓损伤动物模型,假手术对照组同法显露脊髓,但不打击。EPO治疗组大鼠于术后lh腹腔一次性注射重组人促红细胞生成素(1O001U/kg),其余两组大鼠则腹腔注射等量生理盐水。术后24h,3组大鼠均麻醉处死,切取损伤段脊髓,用HE染色观察损伤脊髓组织病理变化,同时检测其凋亡相关蛋白caspase一3的表达。结果术后24h,HE染色发现该段脊髓出现大量囊腔,伴炎症细胞浸润和胶质细胞增生,神经元亦出现水肿以及部分溶解消失,而EPO治疗组上述病理变化程度较轻微。免疫组化结果发现,损伤组凋亡相关蛋白caspase一3的表达显著增加,EPO治疗组该蛋白表达亦比假手术组增加,但比脊髓损伤组大鼠表达减少,差别有显著性意义(P<0.01)。结论急性脊髓损伤后,损伤处脊髓发生明显的组织坏死和炎性反应,而EPO治疗能明显减轻上述反应,同时凋亡相关蛋白caspase一3的表达亦明显减少,而这可能是其脊髓损伤的保护机制之一。
Objectives: Erythropoietin (EPO) is a variety of tissue-protective functions, including spinal cord. This studyaimed to determine the neuron protective effect of erythropoietin on spinal cord injury (SCI) by assessing C/EBP-homologous protein (CHOP) in the development of a rat model of SCI.Methods: Sixty Sprague–Dawley rats were randomly assigned to three groups: sham-operation controlgroup, SCI group, and EPO treatment group. By using a weight-drop contusion SCI model, the rats in theSCI group and EPO treatment group were killed at 1 and 7 days subsequently. The Basso, Beattie, andBresnahan (BBB) scores were examined for locomotor function. Pathological changes were observed afterhematoxylin–eosin (H&E) staining. The expression of CHOP was determined by immunohistochemicalstaining and RT-PCR analysis.Results: BBB scores showed more quick recovery in the erythropoietin treatment group than that in the SCIgroup (P,0.01). Pathological changes also revealed a reduction in the volume of cavitations and moreneurons regeneration in the EPO treatment rats than that of the SCI rats. The number of CHOP positive cellsin the SCI group on day 1 and 7 days after SCI increased compared with the erythropoietin treatment groupand sham-operation control group (P,0.01). CHOP mRNA folds in sham-operation control rat from 1 to7 days showed the same trend.Conclusions: Endoplasmic reticulum (ER) stress was triggered at the early stage of SCI. Increasedexpression of CHOP can be found in the injured segment of the spinal cord after injury. EPO treatmentcould prevent pathological alterations from severe spinal cord injury by reducing expression of CHOP.Keywords: Spinal cord injury, Endoplasmic reticulum stress, C/EBP-homologous protein, Erythropoietin
Zhenghua Hong, Haixiao Chen, Huaxing Hong, Lie Lin and Zhangfu WangDepartment of Orthopaedics, Taizhou Hospital of Zhejiang Province, Taizhou, ChinaObjectives: Spinal cord injury (SCI) is associated with high morbidity and mortality worldwide,especially in patients with diabetes mellitus. Thrombospondin 1 (TSP-1) is a mutual activator andcan cause neuron injury during hyperglycemia. We investigated the role of TSP-1 in a model ofdiabetic rats in the development of SCI.Methods: Thirty Sprague–Dawley female rats were divided into three groups (SCI group, SCI zdiabetes group and sham-operated group) at random. Ten rats were intraperitoneally injectedwith streptozocin (60 mg/kg) to induce diabetes; the remaining 20 rats received an injection of0.9% saline as SCI group and the third group was sham-operated group. Four weeks later, tenrats in the SCI group and ten diabetic rats were subjected to SCI using an impactor, and the shamoperatedgroup was also followed at the same time course without SCI. These animals werekilled at 12 hours after SCI for immunochemistry and Western blot analysis of the injured sectionfor the expression of TSP-1 protein. Morphological changes of spinal cord in three groups alsowere observed through hematoxylin–eosin staining. All data were analysed by t-test.Results: The data of weight and blood sugar indicated no significant difference in all three groupsbefore animal model induction. Four weeks after the induction of diabetes, the differencesbetween the SCI and SCI z diabetes groups in weight and blood sugar were distinct.Immunochemistry and Western blot analysis showed increased TSP-1 expression in SCI groupwhen compared with the sham-operated group rat but less than the SCIzdiabetes group(p,0.01). The pathological alterations, such as central core lesion with a spare peripheral rim oftissue, and variable cyst formations and gliosis were very apparent in the damaged spinal cordarea in the SCI group and especially in the SCIzdiabetes group.Discussion: Our work provides experimental evidence that the elevated expression of TSP-1 canbe detected in the injured segment of the spinal cord at 12 hours after injury in diabetic rats. Itmay contribute to severe damage in diabetic rats after SCI. [Neurol Res 2009; 31: 878–882]Keywords: Thrombospondin 1; spinal cord injury; diabetes mellitus
患 患者、女、62岁,已婚 5前因车祸致胸腰背外伤疼痛,当时诊为胸12骨折行保守治疗,卧床休息10天后,就起床活动,未行支具等治疗。5年来胸腰背有不同程度的疼痛,出现驼背逐渐加重,并行走困难,每次行走500m左右就感到累及出汗,3年前出现不能平卧,因家庭经济困难一直未行治疗。 否认有低热、盗汗史,否认有结核病史。 患者走入病房,身高142cm 胸腰部后凸畸形明显,局部无明显的压痛 四肢肌力无殊,感觉无明显的异常。 四肢腱反射无殊,病理征未引出。 血常规、血生化等常规检查无明显异常。 结核抗体阴性,肿瘤相关因子均为阴性。双能骨密度测定为:-0.8(-1.0~-2.0骨量减少)。一期行后路胸12截骨后凸矫形术