中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2010年
7期
970-971
,共2页
魏福堂%张学昌%徐志久%黄洪%夏春林
魏福堂%張學昌%徐誌久%黃洪%夏春林
위복당%장학창%서지구%황홍%하춘림
硫氧还蛋白%脊髓损伤%Nogo-A%再生%轴突
硫氧還蛋白%脊髓損傷%Nogo-A%再生%軸突
류양환단백%척수손상%Nogo-A%재생%축돌
Thioredoxin%Spinal cord injury%Nogo-A%Regenaration%Axon
目的 观察经硬膜外注入硫氧还蛋白(Trx)对大鼠急性脊髓损伤(ASCI)后脊髓组织中Nogo-A表达的影响,探讨其对脊髓损伤的保护作用.方法 成年Wister大鼠56只,分为假手术组(A组,n=8)、损伤对照组(B组,n=24)和Trx治疗组(C组,n=24).B、c组用改良Allen's法以30 g/cm致伤大鼠T8脊髓制作损伤模型,同时在蛛网膜下腔置管,C组术后即刻和随后每天1次按0.75mg/kg从硬膜下导管推入硫氧还蛋白,B组在相同时问点给予等量生理盐水;A组打开椎板后蛛网膜下腔置管,不损伤脊髓,不给药.在术后3、7、14 d分别对其进行后肢运动功能BBB评分(n=8),评分完毕即处死动物,取受损节段脊髓组织行免疫组织化学观察脊髓组织中Nogo-A阳性细胞的表达,同时计数阳性细胞.结果 各时间点B组大鼠BBB评分均显著低于A组(P<0.01),伤后7、14 d时C组评分显著高于B组(P<0.05或0.01).B组在术后7与14日Nogo-A表达均显著高于A组(P<0.01);C组在伤后7、14 d的表达量显著低于B组,差异有统计学意义(P<0.05).结论 大鼠急性脊髓损伤后Nogo-A显著升高,Trx能明显抑制Nogo-A的表达,可能促进轴突的再生.
目的 觀察經硬膜外註入硫氧還蛋白(Trx)對大鼠急性脊髓損傷(ASCI)後脊髓組織中Nogo-A錶達的影響,探討其對脊髓損傷的保護作用.方法 成年Wister大鼠56隻,分為假手術組(A組,n=8)、損傷對照組(B組,n=24)和Trx治療組(C組,n=24).B、c組用改良Allen's法以30 g/cm緻傷大鼠T8脊髓製作損傷模型,同時在蛛網膜下腔置管,C組術後即刻和隨後每天1次按0.75mg/kg從硬膜下導管推入硫氧還蛋白,B組在相同時問點給予等量生理鹽水;A組打開椎闆後蛛網膜下腔置管,不損傷脊髓,不給藥.在術後3、7、14 d分彆對其進行後肢運動功能BBB評分(n=8),評分完畢即處死動物,取受損節段脊髓組織行免疫組織化學觀察脊髓組織中Nogo-A暘性細胞的錶達,同時計數暘性細胞.結果 各時間點B組大鼠BBB評分均顯著低于A組(P<0.01),傷後7、14 d時C組評分顯著高于B組(P<0.05或0.01).B組在術後7與14日Nogo-A錶達均顯著高于A組(P<0.01);C組在傷後7、14 d的錶達量顯著低于B組,差異有統計學意義(P<0.05).結論 大鼠急性脊髓損傷後Nogo-A顯著升高,Trx能明顯抑製Nogo-A的錶達,可能促進軸突的再生.
목적 관찰경경막외주입류양환단백(Trx)대대서급성척수손상(ASCI)후척수조직중Nogo-A표체적영향,탐토기대척수손상적보호작용.방법 성년Wister대서56지,분위가수술조(A조,n=8)、손상대조조(B조,n=24)화Trx치료조(C조,n=24).B、c조용개량Allen's법이30 g/cm치상대서T8척수제작손상모형,동시재주망막하강치관,C조술후즉각화수후매천1차안0.75mg/kg종경막하도관추입류양환단백,B조재상동시문점급여등량생리염수;A조타개추판후주망막하강치관,불손상척수,불급약.재술후3、7、14 d분별대기진행후지운동공능BBB평분(n=8),평분완필즉처사동물,취수손절단척수조직행면역조직화학관찰척수조직중Nogo-A양성세포적표체,동시계수양성세포.결과 각시간점B조대서BBB평분균현저저우A조(P<0.01),상후7、14 d시C조평분현저고우B조(P<0.05혹0.01).B조재술후7여14일Nogo-A표체균현저고우A조(P<0.01);C조재상후7、14 d적표체량현저저우B조,차이유통계학의의(P<0.05).결론 대서급성척수손상후Nogo-A현저승고,Trx능명현억제Nogo-A적표체,가능촉진축돌적재생.
Objective To observe the effects of thioredoxin (Trx) perfused through subarachnoid space on Nogo-A after acute spinal cord injury (ASCI) in rats and to probe into protective effects of Trx on ASCI. Methods Fifty-six rats were randomly divided into 3 groups: sham group (group A, n=8 ) , SCI group (group B,n =24) and Trx group (group C,n =24). The ASCI model was induced using the modified Allen technique in groups B and C. A thin plastic tube was placed in subarachnoid space below the injury level for perfusion. Rats in group C received Trx (0.75 mg/kg) from the tube everyday after injury, those in group B received the equal volume of normal saline at the same time as control, and those in group A only received vertebral laminectomy and tube placement in subarachnoid space. The BBB score was recorded at the 3rd, 7th and 14th day postinjury (n=8), then the rats were sacrificed and the injured spinal cord was taken out. Immunohistochemistry was used to detect the expression of Nogo-A and positive cells were counted at the 3rd, 7th and 14th day. Results The BBB score in group B was significantly lower than that in group A at each time point (P <0.01) , but the score in group C was significantly higher than that in group B (P<0.05 or 0.01) at the 7th and 14th day postinjury. The number of positive cells was significantly more in group B than in group A at the 7th and 14th day postoperatively (P<0.01). The number of positive cells was significantly more in group C than in group B at the 7th and 14th day postoperatively (P<0.05). Conclusion The expression of Nogo-A is notably increased in injured spinal cord. Trx can inhibit the expression of Nogo-A protein obviously, which can promote the regeneration of axon after ASCI possibly.