中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
18期
2861-2866
,共6页
孙延卿%陈雄生%曹东%朱巍%贾连顺
孫延卿%陳雄生%曹東%硃巍%賈連順
손연경%진웅생%조동%주외%가련순
实验动物%组织构建%组织构建基础实验%氢盐水%脊髓损伤%缺血再灌注%运动神经元%凋亡%抗氧化%腹腔注射%模型%运动功能%保护
實驗動物%組織構建%組織構建基礎實驗%氫鹽水%脊髓損傷%缺血再灌註%運動神經元%凋亡%抗氧化%腹腔註射%模型%運動功能%保護
실험동물%조직구건%조직구건기출실험%경염수%척수손상%결혈재관주%운동신경원%조망%항양화%복강주사%모형%운동공능%보호
hydrogen%spinal cord injuries%reperfusion injury%apoptosis%oxidation-reduction
背景：脊髓缺血再灌注损伤是一种严重的继发性脊髓损伤，其损伤机制是多因素综合作用的结果，其治疗上也有多种措施，但治疗效果不甚理想。<br> 目的：探讨氢盐水对脊髓缺血再灌注损伤兔模型运动神经元的保护作用及机制。<br> 方法：采用ZIVIN法制备脊髓缺血再灌注损伤兔模型，并采用氢盐水治疗(设为氢盐水组)，同时设模型组和假手术组为对照。<br> 结果与结论：氢盐水组兔后肢运动功能Tarlov评分于再灌注后6，12，24，72 h明显优于模型组(P<0.01)。再灌注后72 h，与模型组相比，氢盐水组丙二醛浓度降低(P<0.05)，过氧化氢酶活性升高(P<0.05)。苏木精-伊红染色显示，假手术组脊髓前角运动神经元细胞结构完整，模型组脊髓前角大量运动神经元细胞坏死，胞浆内颗粒变性和空泡变性。氢盐水组脊髓前角运动神经元细胞结构基本完整，仅有少量运动神经元细胞空泡变性。原位末端标记染色显示，假手术组未见运动神经元细胞凋亡；模型组见大量凋亡的运动神经元及大量炎性细胞浸润；氢盐水组见脊髓前角少量凋亡的运动神经元及少量炎性细胞浸润。结果证实，氢盐水可抑制兔缺血再灌注损伤脊髓运动神经元的凋亡，其机制与其抗氧化作用有关。
揹景：脊髓缺血再灌註損傷是一種嚴重的繼髮性脊髓損傷，其損傷機製是多因素綜閤作用的結果，其治療上也有多種措施，但治療效果不甚理想。<br> 目的：探討氫鹽水對脊髓缺血再灌註損傷兔模型運動神經元的保護作用及機製。<br> 方法：採用ZIVIN法製備脊髓缺血再灌註損傷兔模型，併採用氫鹽水治療(設為氫鹽水組)，同時設模型組和假手術組為對照。<br> 結果與結論：氫鹽水組兔後肢運動功能Tarlov評分于再灌註後6，12，24，72 h明顯優于模型組(P<0.01)。再灌註後72 h，與模型組相比，氫鹽水組丙二醛濃度降低(P<0.05)，過氧化氫酶活性升高(P<0.05)。囌木精-伊紅染色顯示，假手術組脊髓前角運動神經元細胞結構完整，模型組脊髓前角大量運動神經元細胞壞死，胞漿內顆粒變性和空泡變性。氫鹽水組脊髓前角運動神經元細胞結構基本完整，僅有少量運動神經元細胞空泡變性。原位末耑標記染色顯示，假手術組未見運動神經元細胞凋亡；模型組見大量凋亡的運動神經元及大量炎性細胞浸潤；氫鹽水組見脊髓前角少量凋亡的運動神經元及少量炎性細胞浸潤。結果證實，氫鹽水可抑製兔缺血再灌註損傷脊髓運動神經元的凋亡，其機製與其抗氧化作用有關。
배경：척수결혈재관주손상시일충엄중적계발성척수손상，기손상궤제시다인소종합작용적결과，기치료상야유다충조시，단치료효과불심이상。<br> 목적：탐토경염수대척수결혈재관주손상토모형운동신경원적보호작용급궤제。<br> 방법：채용ZIVIN법제비척수결혈재관주손상토모형，병채용경염수치료(설위경염수조)，동시설모형조화가수술조위대조。<br> 결과여결론：경염수조토후지운동공능Tarlov평분우재관주후6，12，24，72 h명현우우모형조(P<0.01)。재관주후72 h，여모형조상비，경염수조병이철농도강저(P<0.05)，과양화경매활성승고(P<0.05)。소목정-이홍염색현시，가수술조척수전각운동신경원세포결구완정，모형조척수전각대량운동신경원세포배사，포장내과립변성화공포변성。경염수조척수전각운동신경원세포결구기본완정，부유소량운동신경원세포공포변성。원위말단표기염색현시，가수술조미견운동신경원세포조망；모형조견대량조망적운동신경원급대량염성세포침윤；경염수조견척수전각소량조망적운동신경원급소량염성세포침윤。결과증실，경염수가억제토결혈재관주손상척수운동신경원적조망，기궤제여기항양화작용유관。
BACKGROUND:Spinal cord ischemia-reperfusion injury is a serious secondary injury of the spinal cord. Multifactor could contribute to the mechanism of this injury, and many therapeutic measures emerge, but the therapeutic effect is not ideal. <br> OBJECTIVE:To investigate the protective effects and mechanism of hydrogen-rich saline on spinal cord ischemia-reperfusion injury in rabbits. <br> METHODS:ZIVIN method was adopted to prepare the model of spinal cord ischemia-reperfusion injury. The rabbit models were randomly divided into model group, sham operation group, and hydrogen-rich saline group. <br> RESULTS AND CONCLUSION:Improved Tarlov scores for the evaluation of motor function were significantly increased in hydrogen-rich saline group compared with the model group at 6, 12, 24, 72 hours after reperfusion (P<0.01). The contents of malondialdehyde were significantly lower (P<0.05), while catalase activity was significantly higher (P<0.05) in hydrogen-rich saline group than that in model group at 72 hours after reperfusion. Hematoxylin-eosin staining revealed that, spinal cord anterior-horn motor neurons maintained intact structure in sham operation group;more necrotic spinal cord anterior-horn motor neurons were found in model group, and granular-vacuolar degeneration occurred in the endochylema. In hydrogen-rich saline group, the structure of spinal cord anterior-horn motor neurons was basical y intact, only a smal amount of spinal cord anterior-horn motor neurons appeared vacuolar degeneration. TUNEL staining showed no apoptotic spinal cord anterior-horn motor neurons in sham operation group. Many inflammatory cel s and apoptotic neurons were found in model group. There were few inflammatory cel s and apoptotic neurons in hydrogen-rich saline group. Hydrogen-rich saline can prevent the apoptosis of spinal cord anterior-horn motor neurons in rabbits with spinal cord ischemia-reperfusion injury, and the underlying mechanism is associated with antioxidative effect.
