摘要
背景:舒芬太尼具有组织保护作用,但对神经系统损伤的修复作用及可能机制的报道甚少。目的:探讨舒芬太尼预处理对脊髓损伤的保护作用及可能机制。方法:通过脊髓钳夹损伤法建立脊髓损伤模型小鼠,腹腔注射舒芬太尼6,3μg/kg预处理干预。结果与结论:(1)Western blot、酶联免疫吸附法、TUNEL检测结果:舒芬太尼6μg/kg预处理可以显著抑制小鼠脊髓组织TLR4、核因子κBp65以及cleaved-caspase-3蛋白的表达(P<0.05),并显著抑制脊髓组织炎性因子肿瘤坏死因子α和白细胞介素1β蛋白的表达(P<0.05),显著减轻脊髓组织中神经元的凋亡(P<0.05);(2)神经功能:舒芬太尼6μg/kg预处理可以显著改善脊髓损伤后第14天的神经功能评分(P<0.05)。(3)结果证实:舒芬太尼6μg/kg预处理对脊髓损伤小鼠可以发挥显著的神经保护作用,其机制可能与抑制TLR4/核因子κB信号通路相关。
BACKGROUND： Sufentanil exerts protective effects on tissues, but its roles in the repair of nervous system injury and the underlying mechanism are still unknown. OBJECTIVE： To explore the protective effect of sufentanil preconditioning in the repair of spinal cord injuries and the underlying mechanism. METHODS： Mouse models of spinal cord injuries were prepared through clipping spinal cord followed by intraperitoneal injection of 3 and 6 μg/kg sufentanil, respectively. RESULTS AND CONCLUISON：（1） Western blotting, ELISA and TUNEL assays showed that 6 μg/kg sufentanil significantly down-regulated the protein expression levels of TLR4, nuclear factor-κBp65, cleaved-caspase 3, tumor necrosis factor-α and interlenkin-1β in the spinal cord of mice（P 0.05）; at the same time, the number of apoptotic neurons was significantly decreased（P 0.05）.（2） Furthermore, high-dose sufentanil preconditioning significantly ameliorated the recovery of limb function at 14 days after injury（P 0.05）.（3） These results administrate that the neuroprotection provided by 6 μg/kg sufentanil preconditioning for spinal cord injuries in mice maybe related to the TLR4/nuclear factor-κB signaling pathway inactivation.
出处
《中国组织工程研究》
CAS
北大核心
2016年第40期5966-5972,共7页
Chinese Journal of Tissue Engineering Research
