摘要
目的:观察热休克蛋白27(Hsp27)对大鼠臂丛神经根撕脱后脊髓运动神经元一氧化氮合酶(NOS)表达的影响。方法:Wistar大鼠60只,随机分为实验组和对照组。实验组动物分别以45℃预处理热处理15min,再置于42%维持20min,置室温恢复24h后,手术显微镜下进行脊髓C5~C8节段神经根撕脱术;对照组仅施行臂丛神经根撕脱术,两组分别于术后12h、1d、3d、5d、7d处死动物。各组取C5~C8节段脊髓,行Hsp27免疫组化、NADPH—d组化染色,结合自动图象分析系统对结果进行半定量分析。结果:①实验组在12h即有NOS大量表达,之后迅速回落;对照组伤后第5天开始大量出现NOS阳性。②两组Hsp27表达高峰均在热休克后1d,且实验组强于对照组。结论:臂丛神经根撕脱伤后Hsp27可能通过抑制NOS神经元来发挥其细胞保护作用。
AIM: To observe the effect of heat shock protein 27 (Hsp2?)on nitric oxide synthase (NOS) of spinal cord anterior horn after brachial plexus roots avulsion. METHODS: Sixty male adult Wistar rats were divided into control and experiment groups at random. The experiment group subjected to heat shock under 45℃ for 15 min, and maintained under 42℃ for 20 min subsequently. After recovering 24 h under the room temperature, the nerves of bra- chial plexus were avulsion with microhemostatic forcep. In a span from 12 h to 7 d, these animals were killed at different time. But the control group only received the surgery of the nerve roots of brachial plexus avulsion. The freeze sections of spinal cord were stained by NADPH-d histochemistry, HSP27 immunohistochemical. RESULTS: (1) In experi- ment group, the motoneuron began to express NOS abundantly at 12 h after avulsion (A =0.13525). Then the NOS- positive neurons declined quickly, but in control group, the motoneuron began to express NOS at the 5th day after lesion. (2) Hsp27 begin to show the peak at 1 d in experiment and control groups, but the experiment group were more strong than the control group. CONCLUSION: Hsp27 inhibited NOS of motoneuron after avulsion and brought into full play the cytoprotection.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2010年第7期709-711,共3页
Chinese Journal of Cellular and Molecular Immunology