中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2010年
41期
7770-7774
,共5页
罗春山%田晓滨%汪雷%李波%彭智%周焯家%简月奎%赵伟峰
囉春山%田曉濱%汪雷%李波%彭智%週焯傢%簡月奎%趙偉峰
라춘산%전효빈%왕뢰%리파%팽지%주작가%간월규%조위봉
汉防己甲素%急性脊髓损伤%凋亡%bcl-2%bax%甲基强的松龙
漢防己甲素%急性脊髓損傷%凋亡%bcl-2%bax%甲基彊的鬆龍
한방기갑소%급성척수손상%조망%bcl-2%bax%갑기강적송룡
背景:研究证实汉防己甲素对急性脊髓损伤有保护作用,但其具体机制尚不清楚.目的:观察汉防己甲素对急性脊髓损伤大鼠的神经保护作用,并从细胞凋亡通路探讨其作用机制.方法:将100只成年大鼠随机分为4组.采用加速压迫型Allen's打击法制备脊髓损伤模型.甲强龙组和汉防己甲素组分别于造模前和造模后24,48 h经尾静脉注射甲基强的松龙和汉防己甲素.假手术组与模型组注射等量生理盐水.造模后8 h,1,3,7,14 d采用BBB评分评估大鼠的运动功能,苏木精-伊红染色观察损伤脊髓组织的形态改变,免疫组织化学染色检测bcl-2和bax的表达.结果与结论:伤后7,14 d,甲强龙组和汉防己甲素组大鼠的BBB评分显著高于模型组(P<0.05),各时间点甲强龙组和汉防己甲素组间BBB评分差异无显著性意义(P>0.05).伤后3~7 d,脊髓组织损伤最为严重,甲强龙组和汉防己甲素组的损伤程度较模型组轻,同时bax表达较模型组少,而bcl-2表达较模型组多(P<0.01).说明汉防己甲素可通过增加bcl-2表达、降低bax表达,抑制急性脊髓损伤大鼠神经细胞凋亡,促进大鼠运动功能恢复,其作用不逊于甲基强的松龙.
揹景:研究證實漢防己甲素對急性脊髓損傷有保護作用,但其具體機製尚不清楚.目的:觀察漢防己甲素對急性脊髓損傷大鼠的神經保護作用,併從細胞凋亡通路探討其作用機製.方法:將100隻成年大鼠隨機分為4組.採用加速壓迫型Allen's打擊法製備脊髓損傷模型.甲彊龍組和漢防己甲素組分彆于造模前和造模後24,48 h經尾靜脈註射甲基彊的鬆龍和漢防己甲素.假手術組與模型組註射等量生理鹽水.造模後8 h,1,3,7,14 d採用BBB評分評估大鼠的運動功能,囌木精-伊紅染色觀察損傷脊髓組織的形態改變,免疫組織化學染色檢測bcl-2和bax的錶達.結果與結論:傷後7,14 d,甲彊龍組和漢防己甲素組大鼠的BBB評分顯著高于模型組(P<0.05),各時間點甲彊龍組和漢防己甲素組間BBB評分差異無顯著性意義(P>0.05).傷後3~7 d,脊髓組織損傷最為嚴重,甲彊龍組和漢防己甲素組的損傷程度較模型組輕,同時bax錶達較模型組少,而bcl-2錶達較模型組多(P<0.01).說明漢防己甲素可通過增加bcl-2錶達、降低bax錶達,抑製急性脊髓損傷大鼠神經細胞凋亡,促進大鼠運動功能恢複,其作用不遜于甲基彊的鬆龍.
배경:연구증실한방기갑소대급성척수손상유보호작용,단기구체궤제상불청초.목적:관찰한방기갑소대급성척수손상대서적신경보호작용,병종세포조망통로탐토기작용궤제.방법:장100지성년대서수궤분위4조.채용가속압박형Allen's타격법제비척수손상모형.갑강룡조화한방기갑소조분별우조모전화조모후24,48 h경미정맥주사갑기강적송룡화한방기갑소.가수술조여모형조주사등량생리염수.조모후8 h,1,3,7,14 d채용BBB평분평고대서적운동공능,소목정-이홍염색관찰손상척수조직적형태개변,면역조직화학염색검측bcl-2화bax적표체.결과여결론:상후7,14 d,갑강룡조화한방기갑소조대서적BBB평분현저고우모형조(P<0.05),각시간점갑강룡조화한방기갑소조간BBB평분차이무현저성의의(P>0.05).상후3~7 d,척수조직손상최위엄중,갑강룡조화한방기갑소조적손상정도교모형조경,동시bax표체교모형조소,이bcl-2표체교모형조다(P<0.01).설명한방기갑소가통과증가bcl-2표체、강저bax표체,억제급성척수손상대서신경세포조망,촉진대서운동공능회복,기작용불손우갑기강적송룡.
BACKGROUND:Studies have demonstrated that tetrandrine has protection on acute spinal cord injury,but the specific mechanism remains poorly understood.OBJECTIVE:To study the protection of tetrandrine on rat acute spinal cord injury and to study its mechanism from apoptosis pathway.METHODS:A total of 100 rats were randomly divided into 4 groups.All rats were prepared for spinal cord injury models using modified Allen method except that in the sham-surgery group.Methylprednisolone and tetrandrine was injected into rats in the methylprednisolone and tetrandrine groups by tail intravenous injection prior to and at 24,48 hours after model preparation.The same volume of physiological saline was injected in the sham-surgery and model groups.Basso-BeatUe-Bresnahan(BBB score)was recorded at 8 hours,1,3,7 and 14 days after model preparation.The morphological changes of spinal cord injury sites were observed by hematoxylin-eosin staining and the expressions of bcl-2 and bax were determined by immunohistochemistry.RESULTS AND CONCLUSION:The BBB score of methylpradnisolone and tetrandrine groups were significantly higher than that model group at 7 and 14 days(P<0.05),but there were no significant difference between the methylprednisolone group and tetrandrine group(P>0.05).Hematoxylin-eosin staining showed that the spinal cord injured severely at 3-7 days,the injury degree in the methylpradnisolone group and tetrandrine group was slighter than that of the model group,with smaller bax expression and greater bcl-2 expression(P<0.01).The findings demonstrated that,tetrandrine is able to protect neurons from apoptosis and promote the nerve function recovery by inhibiting the expression of Bax and promoting the expression of Bcl-2.Its effect is not inferior to methylprednisolone.