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BACKGROUND:After spinal cord injury, endogenous neural stem cells are activated to proliferate and migrate to repair damaged tissue. As a clinical medicine, methylprednisolone shows a lot of functions, but its effects on endogenous neural stem cells are still unknown.
OBJECTIVE:To explore the effects of methylprednisolone on the proliferation and migration of endogenous neural stem cells after spinal cord injury.
METHODS:Seventy-five Sprague-Dawley rats were used to make animal models of T10 complete paraplegia using Allen’s method, and randomized into methylprednisolone, normal saline and model groups. Rats in these three groups were given intraperitoneal injection of 1 g/L methylprednisolone solution at a dose of 30 mg/kg for 10 minutes and at a dose of 5.4 mg/kg/h for 23 hours, given intraperitoneal injection of normal saline at the same dose and given no treatment, respectively. Neurological and motor functions were assessed by somatosensory evoked potential and Basso Beattie Bresnahan scores at 7, 14, 21, 28 days after spinal cord injury. BrdU and Nestin staining of the injured spinal cord segment was conducted.
RESULTS AND CONCLUSION:A large amount of BrdU- and Nestin-positive cells were visible in all the groups, and the number of these cells reached the peach at 14 days after spinal cord injury. Methylprednisolone was found to inhibit BrdU-, Nestin- or double-positive cells, indicating methylprednisolone can inhibit the proliferation and migration of endogenous neural stem cells. The results of Basso Beattie Bresnahan scores showed no notable improvement in the motor function of the limbs. Methylprednisolone also showed no significant effects on the motor evoked potential latency, but promoted nerve conduction recovery. All these findings indicate that methylprednisolone has some hindering effects on spinal cord repair by inhibiting the proliferation and migration of endogenous neural stem cells after spinal cord injury. 相似文献
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目的:探讨纳米羟基磷灰石/聚酰胺66/富血小板血浆(n-HA/PA66/PRP)复合物修复兔股骨中段骨缺损的疗效。方法新西兰大白兔共40只,切除左股骨中段1 cm 连同骨膜的骨质造成骨缺损模型后随机分为两组,实验组植入 n-HA/PA66/PRP 复合物后予以钢板固定;对照组植入 n-HA/PA66后予以钢板固定。术后2、4、8、12周每时间点处死5只兔子,进行 X 线片、大体标本观察、组织学、免疫组织化学染色等观察股骨骨缺损愈合情况。结果术后所有动物无感染、死亡及植入物脱落,大体标本及组织学结果显示术后2周内实验组开始有新生骨组织,随着时间的延长,实验组新骨生长速度和数量明显优于对照组;术后12周 Lane-Sandhu 法 X 线片评分显示实验组(6.80±2.05)分,对照组(4.20±1.30)分,二者比较差异有统计学意义(P <0.05);免疫组织化学染色结果显示实验组血管内皮细胞生长因子表达强度在术后第2、4周时与对照组比较,差异有统计学意义(P <0.05),在术后第8、12周时与对照组比较差异无统计学意义(P >0.05)。结论n-HA/PA66/PRP 复合物具有促进骨质愈合的作用,尤其在早期修复骨缺损的效果优于 n-HA/PA66。 相似文献
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