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
49期
7914-7918
,共5页
傅智轶%刘兴振%吴玉杰%朱彤%金文杰
傅智軼%劉興振%吳玉傑%硃彤%金文傑
부지질%류흥진%오옥걸%주동%금문걸
实验动物%组织工程%马尾神经综合征%硫化氢%氧化应激%神经保护
實驗動物%組織工程%馬尾神經綜閤徵%硫化氫%氧化應激%神經保護
실험동물%조직공정%마미신경종합정%류화경%양화응격%신경보호
hydrogen sulfide%malondialdehyde%glutathione
背景:研究发现内源性硫化氢可以作为一种新型气体信号分子,具有重要的信号传递功能和生物调节作用。目的:研究硫化氢对急性马尾神经损伤大鼠的神经保护作用。方法:将72只SD大鼠随机均分为3组,实验组、模型组咬除L4椎板,将长10 mm、厚1.0 mm、宽1.0 mm的硅胶条植入大鼠L5和L6椎管内,建立大鼠马尾神经压迫损伤模型;假手术组仅咬除L4椎板,未植入硅胶条;实验组造模前1 h腹腔注射20μmol/kg的NaHS,模型组与假手术组腹腔注射等量生理盐水。造模后12,24,48,72 h检测马尾神经组织中丙二醛和谷胱甘肽水平,同时在48 h取材进行苏木精-伊红染色和TUNEL染色。结果与结论:苏木精-伊红染色显示,假手术组马尾神经纤维致密有序,髓鞘完整,轴突无肿胀;模型组马尾神经纤维松散,脱髓鞘改变,部分轴突及髓鞘肿胀;实验组马尾神经纤维紧密,少量轴突肿胀、脱髓鞘改变。TUNEL染色显示,假手术组中脊髓和背根神经节组织中阳性细胞数量较少,模型组脊髓和背根神经节中可见大量阳性细胞,实验组阳性细胞数量显著低于模型组。假手术组、实验组丙二醛水平低于模型组(P <0.05, P <0.01),谷胱甘肽水平高于模型组(P <0.05,P <0.01)。表明硫化氢可以降低氧化应激反应,保护急性损伤大鼠马尾神经。
揹景:研究髮現內源性硫化氫可以作為一種新型氣體信號分子,具有重要的信號傳遞功能和生物調節作用。目的:研究硫化氫對急性馬尾神經損傷大鼠的神經保護作用。方法:將72隻SD大鼠隨機均分為3組,實驗組、模型組咬除L4椎闆,將長10 mm、厚1.0 mm、寬1.0 mm的硅膠條植入大鼠L5和L6椎管內,建立大鼠馬尾神經壓迫損傷模型;假手術組僅咬除L4椎闆,未植入硅膠條;實驗組造模前1 h腹腔註射20μmol/kg的NaHS,模型組與假手術組腹腔註射等量生理鹽水。造模後12,24,48,72 h檢測馬尾神經組織中丙二醛和穀胱甘肽水平,同時在48 h取材進行囌木精-伊紅染色和TUNEL染色。結果與結論:囌木精-伊紅染色顯示,假手術組馬尾神經纖維緻密有序,髓鞘完整,軸突無腫脹;模型組馬尾神經纖維鬆散,脫髓鞘改變,部分軸突及髓鞘腫脹;實驗組馬尾神經纖維緊密,少量軸突腫脹、脫髓鞘改變。TUNEL染色顯示,假手術組中脊髓和揹根神經節組織中暘性細胞數量較少,模型組脊髓和揹根神經節中可見大量暘性細胞,實驗組暘性細胞數量顯著低于模型組。假手術組、實驗組丙二醛水平低于模型組(P <0.05, P <0.01),穀胱甘肽水平高于模型組(P <0.05,P <0.01)。錶明硫化氫可以降低氧化應激反應,保護急性損傷大鼠馬尾神經。
배경:연구발현내원성류화경가이작위일충신형기체신호분자,구유중요적신호전체공능화생물조절작용。목적:연구류화경대급성마미신경손상대서적신경보호작용。방법:장72지SD대서수궤균분위3조,실험조、모형조교제L4추판,장장10 mm、후1.0 mm、관1.0 mm적규효조식입대서L5화L6추관내,건립대서마미신경압박손상모형;가수술조부교제L4추판,미식입규효조;실험조조모전1 h복강주사20μmol/kg적NaHS,모형조여가수술조복강주사등량생리염수。조모후12,24,48,72 h검측마미신경조직중병이철화곡광감태수평,동시재48 h취재진행소목정-이홍염색화TUNEL염색。결과여결론:소목정-이홍염색현시,가수술조마미신경섬유치밀유서,수초완정,축돌무종창;모형조마미신경섬유송산,탈수초개변,부분축돌급수초종창;실험조마미신경섬유긴밀,소량축돌종창、탈수초개변。TUNEL염색현시,가수술조중척수화배근신경절조직중양성세포수량교소,모형조척수화배근신경절중가견대량양성세포,실험조양성세포수량현저저우모형조。가수술조、실험조병이철수평저우모형조(P <0.05, P <0.01),곡광감태수평고우모형조(P <0.05,P <0.01)。표명류화경가이강저양화응격반응,보호급성손상대서마미신경。
BACKGROUND:Endogenous hydrogen sulfide can be used as a new gaseous signaling molecule, and has important signal transfer function and biological regulation effects. OBJECTIVE:To study the neuroprotective effects of hydrogen sulfide in rats with acute cauda equina syndrome. METHODS: The 72 Sprague-Dawley rats were randomly assigned to three groups. Experimental group, model group: laminectomy was performed at the lumbar 4 (L4) level of the vertebra, and a piece of silicone (10 mm long, 1 mm thick, and 1 mm wide) was placed under the laminae of the L5-6 vertebra to produce the animal model of cauda equina syndrome. Sham surgery group: a simple laminectomy was performed in L4, but silicone was not implanted. In the experimental group, 20 μmol/kg NaHS was injected intraperitonealy at 1 hour before model establishment. Model and sham surgery groups: an equal volume of saline was injected intraperitonealy. At 12, 24, 48 and 72 hours after model establishment, malonaldehyde and glutathione levels in cauda equina nerve tissue were detected. Simultaneously, hematoxylin-eosin staining and TUNEL staining were performed at 48 hours. RESULTS AND CONCLUSION:Hematoxylin-eosin staining demonstrated that cauda equina nerve tissue was dense and regular, with complete myelin sheath, no axon sweling in the sham surgery group. Cauda equina nerve tissue was sparse, with the presence of demyelination, and partial axons and myelin sheath sweling in the model group. Cauda equina nerve tissue was tight, with axonal sweling and demyelination in the experimental group. TUNEL staining demonstrated that the number of positive cels was less in the spinal cord and dorsal root ganglia in the sham surgery group. Abundant positive cels were detected in the spinal cord and dorsal root ganglia in the model group. The number of positive cels was significantly lower in the experimental group than that in the model group. Malonaldehyde levels were lower in the sham surgery and experimental groups than in the model group (P < 0.05, P < 0.01), but glutathione levels were higher than model group (P < 0.05,P < 0.01). These results indicated that hydrogen sulfide could decrease oxidative stress and protect cauda equina nerve in rats with acute cauda equina syndrome.