中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2014年
15期
1189-1192
,共4页
申庆丰%田融%李辉南%徐天同%夏英鹏
申慶豐%田融%李輝南%徐天同%夏英鵬
신경봉%전융%리휘남%서천동%하영붕
脊髓损伤%氟%中毒
脊髓損傷%氟%中毒
척수손상%불%중독
Spinal cord injuries%Fluorine%Poisoning
目的 观察慢性氟中毒大鼠脊髓白质的损伤及其机制及短期脱氟治疗后脊髓白质损害的恢复情况.方法 120只Wistar大鼠随机分为4组,高氟组饮氟化水(200 mg/L);高氟对照组饮蒸馏水;脱氟组先饮氟化水(200 mg/L),12周后改为蒸馏水;脱氟对照组饮蒸馏水,实验期24周.分别于第4、8和12周测定4组大鼠尿氟含量,于第16、20、24周测定脱氟组和脱氟对照组尿氟含量,并在上述各个时间点应用BBB的评估标准及斜板试验分别对大鼠的脊髓功能进行行为学评估.12周时将高氟组和高氟对照组大鼠处死.脱氟组改饮蒸馏水,24周时将脱氟组及脱氟对照组大鼠处死,所有大鼠均取颈脊髓备电镜观察;取上胸髓行免疫组织化学染色观察MBP的表达;取下胸髓行免疫印迹检测MBP蛋白的含量.结果 大鼠饮高氟水8周后,高氟组大鼠BBB评分及斜板试验结果显著低于对照组[BBB评分(19.8±4.1)分比(17.0±3.9)分];斜板试验[(56.2±4.2)°比(60.1±4.0)°,P<0.01],脱氟组与高氟组相比未见明显改善;电镜检查发现高氟组大鼠脊髓白质呈慢性损害病理改变,脱氟组大鼠脊髓已经发生的慢性损害未见恢复;高氟组大鼠脊髓组织中MBP与高氟对照组比较表达显著降低;而脱氟组大鼠与高氟组MBP表达差异无统计学意义.结论 慢性氟中毒可以造成大鼠脊髓功能的损伤,与氟中毒造成脊髓白质脱髓鞘有关,短时间脱氟治疗后,该损伤不能恢复.
目的 觀察慢性氟中毒大鼠脊髓白質的損傷及其機製及短期脫氟治療後脊髓白質損害的恢複情況.方法 120隻Wistar大鼠隨機分為4組,高氟組飲氟化水(200 mg/L);高氟對照組飲蒸餾水;脫氟組先飲氟化水(200 mg/L),12週後改為蒸餾水;脫氟對照組飲蒸餾水,實驗期24週.分彆于第4、8和12週測定4組大鼠尿氟含量,于第16、20、24週測定脫氟組和脫氟對照組尿氟含量,併在上述各箇時間點應用BBB的評估標準及斜闆試驗分彆對大鼠的脊髓功能進行行為學評估.12週時將高氟組和高氟對照組大鼠處死.脫氟組改飲蒸餾水,24週時將脫氟組及脫氟對照組大鼠處死,所有大鼠均取頸脊髓備電鏡觀察;取上胸髓行免疫組織化學染色觀察MBP的錶達;取下胸髓行免疫印跡檢測MBP蛋白的含量.結果 大鼠飲高氟水8週後,高氟組大鼠BBB評分及斜闆試驗結果顯著低于對照組[BBB評分(19.8±4.1)分比(17.0±3.9)分];斜闆試驗[(56.2±4.2)°比(60.1±4.0)°,P<0.01],脫氟組與高氟組相比未見明顯改善;電鏡檢查髮現高氟組大鼠脊髓白質呈慢性損害病理改變,脫氟組大鼠脊髓已經髮生的慢性損害未見恢複;高氟組大鼠脊髓組織中MBP與高氟對照組比較錶達顯著降低;而脫氟組大鼠與高氟組MBP錶達差異無統計學意義.結論 慢性氟中毒可以造成大鼠脊髓功能的損傷,與氟中毒造成脊髓白質脫髓鞘有關,短時間脫氟治療後,該損傷不能恢複.
목적 관찰만성불중독대서척수백질적손상급기궤제급단기탈불치료후척수백질손해적회복정황.방법 120지Wistar대서수궤분위4조,고불조음불화수(200 mg/L);고불대조조음증류수;탈불조선음불화수(200 mg/L),12주후개위증류수;탈불대조조음증류수,실험기24주.분별우제4、8화12주측정4조대서뇨불함량,우제16、20、24주측정탈불조화탈불대조조뇨불함량,병재상술각개시간점응용BBB적평고표준급사판시험분별대대서적척수공능진행행위학평고.12주시장고불조화고불대조조대서처사.탈불조개음증류수,24주시장탈불조급탈불대조조대서처사,소유대서균취경척수비전경관찰;취상흉수행면역조직화학염색관찰MBP적표체;취하흉수행면역인적검측MBP단백적함량.결과 대서음고불수8주후,고불조대서BBB평분급사판시험결과현저저우대조조[BBB평분(19.8±4.1)분비(17.0±3.9)분];사판시험[(56.2±4.2)°비(60.1±4.0)°,P<0.01],탈불조여고불조상비미견명현개선;전경검사발현고불조대서척수백질정만성손해병리개변,탈불조대서척수이경발생적만성손해미견회복;고불조대서척수조직중MBP여고불대조조비교표체현저강저;이탈불조대서여고불조MBP표체차이무통계학의의.결론 만성불중독가이조성대서척수공능적손상,여불중독조성척수백질탈수초유관,단시간탈불치료후,해손상불능회복.
Objective To explore the injury mechanism for white matter of spinal cord and the improvement of function after defluoriation.Methods A total of 120 Wistar rats were separated randomly into 4 groups (n =30 each).High flouriod group received high concentration NaF water (200 mg/L) to establish fluorosis model; control group distilled water; deflourination group high concentration NaF water (200 mg/L) for 12 weeks and then distilled water for 12 weeks; defluorination control group.The urinary contents of fluoride were detected at Weeks 4,8 and 12.The first two groups were sacrificed at Week 12 while the other two groups at Week 24.The spinal cord functions were detected by BBB scale and incline plate test.Their cervical spinal cord tissues were collected and observed under electron microscope.The expression of myelin basic protein (MBP) in thoracic cord was detected by immunohistochemistry and Western blot.The comparison of measurement data was performed with F test and correlation analysis.Cytological changes of white matter in spinal cord were detected after chronic fluorosis.Results The spinal functions of high flouriod and deflourination groups were inferior to those of the control groups.But no difference existed among the groups.Pathological manifestations of chronic white matter injury of spinal cord could be found in high flouriod and deflourination groups.The MBP expression in spinal cord of fluorosis and deflurination groups decreased in comparison with those in control groups.But no difference existed among them.Conclusion White matter injury of spinal cord is present in chronic fluorosis rats.Defluoriation for a short time offers no recovery.