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本研究以兔坐骨神经挤压损伤为模型,通过光、电镜观察以及对前列腺素(PG)F_(2a)的放免测定,并结合乳兔背根神经节细胞体外培养等方法来研究PG对周围神经损伤后再生的影响及其合成抑制剂消炎痛的作用。放免测定结果显示,挤压伤后发生华勒氏变性的坐骨神经,PGF_(2a)含量随伤后时间延长呈梯度升高,而注射消炎痛的动物,PGF_(2a)则不升高或者降低。形态学观察结果显示,穿过神经挤压区再生的有髓神经纤维数目、直径、面积等,注射消炎痛的动物均大于注射生理盐水对照的动物。背根神经节分离细胞培养结果显示,在培养基中加入PGF_(2a),培养的神经细胞体积小,突起再生的数目少,RNA含量低;相反,在培养基中加入PG合成抑制剂消炎痛,培养神经细胞钵积大,突起再生的数目多,RNA含量高。同时扫描电镜观察到,各组培养神经细胞有不同的表面形态改变。 以上实验结果表明:(1)周围神经挤压损伤后华勒氏变性过程中产生了过量PG,抑制神经纤维的再生。(2)PG合成抑制剂消炎痛因能阻止神经损伤后PG的产生,故具有促进神经再生的作用。 文中讨论了神经损伤后过量PG产生的原因以及本实验结果的意义等问题。作者考虑:(1)周围神经损伤后,过量PG的产生为其修复和功能恢复缓慢的重要原因;(2)本实验研究在神经营养因素之外,找到一促进神经损
In this study, rabbit sciatic nerve crush injury as a model, through light and electron microscopy, as well as prostaglandin (PG) F_ (2a) radioimmunoassay, combined with rabbit dorsal root ganglion cells in vitro culture methods to study PG on the peripheral nerve Effect of regeneration after injury and the role of synthetic inhibitor indomethacin. The results of radioimmunoassay showed that the Wright’s degeneration sciatic nerve after crush injury showed that the content of PGF_ (2a) increased gradually with the prolongation of post-injury time, but the level of PGF_ (2a) did not increase or decreased in indomethacin-injected animals. Morphological observation showed that the number of myelinated nerve fibers regenerated through the nerve crush zone, the diameter, the area, and the like, the animals injected with indomethacin were larger than the animals injected with normal saline control. The results of cell culture in the dorsal root ganglion showed that PGF_ (2a) was added to the medium, the volume of the cultured neurons was small, the number of the regenerated neurons was small, and the RNA content was low. On the contrary, the PG synthesis inhibitor indomethacin , Cultivate the nerve cell bowl product, the number of protruding regeneration, RNA content is high. At the same time, it was observed by scanning electron microscopy that there were different morphological changes of nerve cells in each group. The above experimental results show that: (1) Excessive PG is produced in the process of Waller’s degeneration after crush injury of the peripheral nerve, which inhibits the regeneration of nerve fibers. (2) PG synthesis inhibitor indomethacin can prevent the generation of PG after nerve injury, it has the role of promoting nerve regeneration. In this paper, the reasons for excessive PG production after nerve injury and the significance of the experimental results are discussed. The authors consider: (1) peripheral nerve injury, the excessive production of PG is an important reason for its repair and functional recovery is slow; (2) In this study, in addition to neurotrophic factors to find a promotion of nerve damage