中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2012年
6期
418-422
,共5页
邹朝双%谢克勤%寇蕊蕊%高媛%宋福永
鄒朝雙%謝剋勤%寇蕊蕊%高媛%宋福永
추조쌍%사극근%구예예%고원%송복영
2,5-己二酮%神经组织%坐骨神经
2,5-己二酮%神經組織%坐骨神經
2,5-기이동%신경조직%좌골신경
2,5-hexanedione%Nerve tissue%Sciatic nerve
目的 研究2,5-己二酮(HD)对大鼠神经组织中低分子量神经丝(NF-L)降解的影响,探讨正己烷中毒性神经病发生的可能机制.方法 雄性Wistar大鼠50只随机分为1、2、3、4周染毒组和对照组,每组10只.经腹腔注射HD(400 mg/kg)染毒动物,剂量为,建立正己烷中毒性神经病模型.电子显微镜观察大鼠坐骨神经的超微结构变化,步态评分评价大鼠周围神经病症状的进展,免疫印迹法(Westem blot)检测坐骨神经和脊髓组织中NF-L降解率的变化.结果 HD染毒2周后,大鼠逐渐出现肌力降低、步态异常等表现,至染毒4周结束时大鼠呈现轻中度瘫痪,电子显微镜观察显示坐骨神经出现退行性病变.与对照组相比较,2、3、4周染毒组大鼠坐骨神经上清和沉淀组分中NF-L降解率均呈进行性下降,其中上清NF-L降解率分别下降25.8％、70.4％和69.7％,沉淀中NF-L降解率分别下降14.7％、64.6％和67.3％,差异均有统计学意义(P＜0.01).在脊髓组织中,与对照组相比较,1周染毒组脊髓上清中NF-I,降解率下降33.87％,4周染毒组脊髓上清中NF-L降解率升高16.2％,1、2周染毒组脊髓沉淀中NF-L降解率分别下降46.3％和13.0％,差异均有统计学意义(P＜0.01).结论 HD染毒显著抑制了坐骨神经中NF-L的降解,这可能与正己烷中毒性神经病轴突中NF变性堆积有关.
目的 研究2,5-己二酮(HD)對大鼠神經組織中低分子量神經絲(NF-L)降解的影響,探討正己烷中毒性神經病髮生的可能機製.方法 雄性Wistar大鼠50隻隨機分為1、2、3、4週染毒組和對照組,每組10隻.經腹腔註射HD(400 mg/kg)染毒動物,劑量為,建立正己烷中毒性神經病模型.電子顯微鏡觀察大鼠坐骨神經的超微結構變化,步態評分評價大鼠週圍神經病癥狀的進展,免疫印跡法(Westem blot)檢測坐骨神經和脊髓組織中NF-L降解率的變化.結果 HD染毒2週後,大鼠逐漸齣現肌力降低、步態異常等錶現,至染毒4週結束時大鼠呈現輕中度癱瘓,電子顯微鏡觀察顯示坐骨神經齣現退行性病變.與對照組相比較,2、3、4週染毒組大鼠坐骨神經上清和沉澱組分中NF-L降解率均呈進行性下降,其中上清NF-L降解率分彆下降25.8％、70.4％和69.7％,沉澱中NF-L降解率分彆下降14.7％、64.6％和67.3％,差異均有統計學意義(P＜0.01).在脊髓組織中,與對照組相比較,1週染毒組脊髓上清中NF-I,降解率下降33.87％,4週染毒組脊髓上清中NF-L降解率升高16.2％,1、2週染毒組脊髓沉澱中NF-L降解率分彆下降46.3％和13.0％,差異均有統計學意義(P＜0.01).結論 HD染毒顯著抑製瞭坐骨神經中NF-L的降解,這可能與正己烷中毒性神經病軸突中NF變性堆積有關.
목적 연구2,5-기이동(HD)대대서신경조직중저분자량신경사(NF-L)강해적영향,탐토정기완중독성신경병발생적가능궤제.방법 웅성Wistar대서50지수궤분위1、2、3、4주염독조화대조조,매조10지.경복강주사HD(400 mg/kg)염독동물,제량위,건립정기완중독성신경병모형.전자현미경관찰대서좌골신경적초미결구변화,보태평분평개대서주위신경병증상적진전,면역인적법(Westem blot)검측좌골신경화척수조직중NF-L강해솔적변화.결과 HD염독2주후,대서축점출현기력강저、보태이상등표현,지염독4주결속시대서정현경중도탄탄,전자현미경관찰현시좌골신경출현퇴행성병변.여대조조상비교,2、3、4주염독조대서좌골신경상청화침정조분중NF-L강해솔균정진행성하강,기중상청NF-L강해솔분별하강25.8％、70.4％화69.7％,침정중NF-L강해솔분별하강14.7％、64.6％화67.3％,차이균유통계학의의(P＜0.01).재척수조직중,여대조조상비교,1주염독조척수상청중NF-I,강해솔하강33.87％,4주염독조척수상청중NF-L강해솔승고16.2％,1、2주염독조척수침정중NF-L강해솔분별하강46.3％화13.0％,차이균유통계학의의(P＜0.01).결론 HD염독현저억제료좌골신경중NF-L적강해,저가능여정기완중독성신경병축돌중NF변성퇴적유관.
Objective To investigate the effect of 2,5-hexanedione (HD) on degradation of lowmolecular-weight neurofilaments (NF-L) in nervous tissue of rats,and to explore the molecular mechanism of nhexane neuropathy.Methods Fifty male Wistar rats were randomly divided into one-week poisoning group (n=10),two-week poisoning group (n=10),three-week poisoning group (n=10),four-week poisoning group (n=10),and control group (n=10).In the four poisoning groups,a rat model of n-hexane neuropathy was established by intraperitoneal injection of HD (400 mg/kg/d).The change in the sciatic nerve ultrastructure of each rat was observed under an electron microscope.The progression of HD-induced peripheral neuropathy was evaluated using a gait scooring system.The degradation rates of NF-L in the sciatic nerve and spinal cord of each rat were measured by Western Blotting.Results The rats showed decrease in muscle strength and abnormal gait after two weeks of HD poisoning and mild or moderate paralysis after four weeks of HD poisoning.The sciatic nerve showed degenerative change,according to electron microscope observation.Compared with the control group,the two-week poisoning group,three-week poisoning group,and four-week poisoning group had the NF-L degradation rates decreased by 25.8%,70.4%,and 69.7%,respectively,in the supernatant fraction of sciatic nerve,and by 14.7%,64.6%,and 67.3%,respectively,in the sediment fraction of sciatic nerve,all showing a significant difference (P＜0.01).Compared with the control group,the one-week poisoning group had the NF-L degradation rate decreased by 33.87% in the supernatant fraction of spinal cord,the four-week poisoning group had the NF-L degradation rate increased by 16.2% in the supernatant fraction of spinal cord,and the one-week poisoning group and two-week poisoning group had the NF-L degradation rates decreased by 46.3% and 13.0% in the sediment fraction of spinal cord,all showing a significant difference (P＜0.01).Conclusion HD poisoning significantly inhibits NF-L degradation in the sciatic nerve,which may be associated with NF degeneration and accumulation in the axons of patients with n-hexane neuropathy.
