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Title: [EXPERIMENTAL STUDIES ON EFFECTS OF SALIDROSIDE/COLLAGEN/ POLYCAPROLACTONE NERVE GUIDE CONDUITS FOR REPAIRING SCIATIC NERVE DEFECT IN RATS].
Author: Song X, Wei Y, Li G, Qin W, Wang W, Zhang X, Zhao H.
Journal: Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi; 2016 May 08; 30(5):634-640. PubMed ID: 29786309.
Abstract:
OBJECTIVE: To fabricate salidroside/collagen/polycaprolactone (PCL) nerve conduit composite and to investigate the effect of composite nerve conduits for repairing sciatic nerve defect. METHODS: The salidroside microspheres were prepared by W/O/W method, and the sustained release rate of microspheres was detected. The microspheres containing 10, 20, and 40 μg salidroside were mixed with collagen to prepare the nerve conduit core layer by freeze-drying method. The shell layer of collagen/PCL scaffold material was fabricated by electrospinning technology. The genipin cross-linked salidroside/collagen/PCL nerve conduit composite was prepared. The structure of nerve conduit was observed before and after cross-linked by scanning electron microscope. Thirty-eight Wistar rats were used to make the right sciatic nerve defect model of 15 mm in length, and randomly divided into groups A, B, C, D (n=9), and group E (n=2), then defect was repaired with the collagen/PCL conduit in group A, autologous nerve in group E, the 10, 20, and 40 μg/mL salidroside/collagen/PCL conduit in groups B, C, and D, respectively. The survival of rats was observed. The sciatic functional index (SFI) was evaluated at 1, 3, and 6 months after operation. At 6 months, the tissue of defect area was harvested for the general, electrophysiology, histological, and immunohistochemical[S-100 and peripheral myelin protein 0(P0)] staining observations. RESULTS: Salidroside microspheres showed burst release at 3 days, and then it tended to be stable at 13 days and lasted for 16 days, with a cumulative release rate of 76.59%. SEM showed that the disordered fiber of nerve conduit shell layer after crosslinking became conglutination, shrinkage, and density, and had void. The channels of core layer were clearly visible before and after crosslinking. The rats had no infection or death after operation. The SFI of group E was significantly higher than that of groups A, B, C, and D at 1, 3, and 6 months (P<0.05); it was significantly higher in groups B, C, and D than group A (P<0.05), but no significant difference was found among groups B, C, and D at 1 month (P>0.05); there was no significant difference in SFI among groups A, B, C, and D at 3 months (P>0.05); SFI was significantly higher in group C than groups A, B, and D and in groups A and B than group D (P<0.05), but no significant difference between groups A and B (P>0.05) at 6 months. In addition, no significant difference was shown among different time points in the other groups (P>0.05) except groups C and E at 1, 3, and 6 months (P<0.05). The general observation showed that good connection with the thick nerve in groups B and C, and connection with the fine nerves in groups A and D. The conduit materials obviously degraded. Nerve electrophysiological examination showed that the latency/conduction velocity of groups C and E were significantly lower than those of groups A, B, and D (P<0.05), but difference was not significant between groups C and E, and among groups A, B, and D (P>0.05). The histological observation showed that the nerve fiber tissue of groups B, C, and E was obviously more than that of groups A and D, and group C was similar to group E in the nerve fiber arrangement, and the core layer material of each group was completely degraded. Immunohistochemical staining showed that S-100 and P0 proteins expressed in all groups; and the expression level of groups B, C, and E was significantly higher than that of groups A and D, and gradually increased (P<0.05); difference in S-100 expression level was not significant between groups A and D (P>0.05), and P0 expression level of group A was significantly lower than that of group D (P<0.05). CONCLUSIONS: Salidroside/collagen/PCL nerve conduit can promote sciatic nerve defect repair. 目的: 构建红景天苷/胶原蛋白/聚己内酯（polycaprolactone，PCL）复合神经导管支架材料并桥接修复大鼠坐骨神经缺损，探讨其修复神经缺损效果。. 方法: 利用W/O/W方法制备红景天苷微球，检测其缓释率；然后取10、20、40 μg红景天苷微球分别与1 mL胶原蛋白混合，冷冻法制备神经导管芯层；静电纺丝技术构建胶原蛋白/PCL神经导管壳层；将芯层和壳层利用京尼平交联制备红景天苷微球/胶原蛋白/PCL复合神经导管。扫描电镜观察交联前后神经导管结构。将38只Wistar大鼠随机分为5组，其中A、B、C、D组各9只，E组2只。各组大鼠制备15 mm长坐骨神经缺损模型后，分别采用胶原蛋白/PCL复合导管（A组），10、20、40 μg/mL红景天苷/胶原蛋白/PCL复合神经导管（B、C、D组）以及自体神经（E组）桥接修复。观察各组大鼠存活情况；术后1、3、6个月行坐骨神经运动功能指数（sciatic functional index，SFI）评价；6个月后行大体观察、神经电生理检测，并取材行组织学、免疫组织化学染色[S-100和外周髓鞘蛋白0（peripheral myelin protein 0，P0）]观测。. 结果: 红景天苷微球于3 d出现突释，13 d后缓释趋于平稳，累计缓释率达76.59%，可持续缓释至16 d。扫描电镜观察示，神经导管壳层交联后，无序排列的纤维变得相互粘连、皱缩、致密且有空隙；芯层交联前后孔道均清晰可见。各组大鼠术后无感染及死亡。术后1、3、6个月，E组SFI显著高于A～D组（P＜0.05）；术后1个月，B、C、D组高于A组（P＜0.05），B、C、D组间差异无统计学意义（P＞0.05）；3个月，A～D组间比较差异均无统计学意义（P＞0.05）；6个月，C组高于A、B、D组（P＜0.05），A、B组高于D组（P＜0.05），A、B组间差异无统计学意义（P＞0.05）。除C、E组术后1、3、6个月SFI比较差异有统计学意义（P＜0.05）外，其余各组组内各时间点间比较差异均无统计学意义（P＞0.05）。术后6个月，大体观察示B、C组导管支架两端连接良好、神经较粗，A、D组近端连接神经较细；各组导管两端材料有明显降解。神经电生理检测示，C、E组潜伏期/传导速度显著低于A、B、D组（P＜0.05），C、E组间以及A、B、D组间比较差异均无统计学意义（P＞0.05）。组织学观察示，B、C、E组神经纤维组织明显多于A、D组，且C组神经纤维排列与E组相近，各导管组芯层材料完全降解。免疫组织化学染色示，各组均可见S-100及P0蛋白表达，B、C、E组两者表达水平均高于A、D组，且依次增强（P＜0.05）；A、D组S-100表达水平比较差异无统计学意义（P＞0.05），P0表达水平A组低于D组(P＜0.05)。. 结论: 红景天苷微球/胶原蛋白/PCL复合神经导管能促进大鼠坐骨神经损伤修复再生。.

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