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目的探讨脊髓继发性损伤的病理生理机制及三七总皂苷的防治作用机制。方法以大鼠为脊髓损伤模型,采用免疫细胞化学及组织化学方法按2、6、12、24h 时相点观察空白组、假手术组、溶媒对照组、三七总皂苷组脊髓组织 c-fos、热应激蛋白70、一氧化氮合酶阳性神经元的表达变化。结果 c-fos 原癌基因、热应激蛋白70、一氧化氮合酶在脊髓损伤的不同时相表达有差异。结论 c-fos 原癌基因、热应激蛋白70、一氧化氮合酶可能参与了脊髓继发性损伤的病理生理过程,三七总皂苷可能通过对 c-fos 原癌基因、热应激蛋白70、一氧化氮合酶的影响对脊髓神经组织起保护作用。
Objective To investigate the pathophysiological mechanism of secondary spinal cord injury and the mechanism of action of Panax notoginseng saponins. Methods Rat spinal cord injury models were immunocytochemistry and histochemical methods at 2, 6, 12 and 24 hours of observation of the blank group, sham operation group, vehicle control group, Panax notoginseng group spinal c-fos , Heat stress protein 70, nitric oxide synthase positive neurons. Results The expression of c-fos proto-oncogene, heat stress protein 70 and nitric oxide synthase were different at different time points of spinal cord injury. Conclusions The c-fos proto-oncogene, heat stress protein 70 and nitric oxide synthase may be involved in the pathophysiological process of secondary spinal cord injury. Panax notoginseng saponins may play an important role in the pathogenesis of spinal cord injury. 70, the impact of nitric oxide synthase on the spinal cord nerve tissue play a protective effect.