| Objective: To apply nerve casting-jointing to repair rat sciatic nerve injury, observe the sciatic nerve function recovery and explore whether the nerve casting-jointing repair can promote the expression of rat spinal cord ventral horn glial fibers acidic protein(GFAP).Methods: Materials: 78 healthy adult male SD rats with weight of 200-250g; Neurotube nerve socketed pipe; immunohistochemical staining kits, rabbit against human GFAP polyclonal antibody, TUNEL kit and 34 X-ray double binocular operating microscope. Methods:(1) Abdomen anesthesia is conducted on 72 healthy adult SD rats with 0.5 m L chloral hydrate at concentration of 100 g/L. Posterior median incision is made; Valero and other model preparation methods are referred; the right sciatic nerve is exposed under aseptic conditions; sciatic nerve below 8 mm of the bottom of ischial tuberosity is clipped with 17 cm curved clamps vascular clamp tip(clamp to buckle, for 30 s) and sciatic nerve severe clamps injury model is created. Sciatic nerve clamps injury model are established with clamping method and then they are randomly divided into Neurotube neural casing-joining repair group(group A) and control group(group B), with 36 ones in each group; the remaining 6 ones are set as blank group(group C), without any processing;(2) after the establishment of model, Group A immediately receive Neurotube neural casing-joining repair(Neurotube neural casing-joining the hidden sciatic nerve injury is cut open and suture is conducted with the epineurium), and group B is not processed. one rat from blank group respectively 6 rats from experimental group and control group are randomly taken out respectively after 1, 3, 7, 14, 21, 28 days of the repairing; then after the anesthesia fixation, L 4~6 segmental spinal cord about 1 cm is taken out, embed with paraffin and sliced; two slices are selected for each dyeing of each rat.Results: The right hind legs of control group rats appear different degree of edema, autophagy, coxal muscle atrophy and motion dysfunction, such as inconsistent movement of front and hind legs and the gravity offset of body center. Compared with control group, experimental group shows these symptoms relatively later, with relatively lighter severity and can improve earlier. For control group rats, their right leg movement function recovers at different degrees after about three weeks, while that of the experimental group improves after one or two weeks. For blank group rats, under the light microscope, cytoplasm presents clear yellowish brown astrocyte, more soma protuberance, relatively small circular or elliptic nucleus and less chromatin. Postoperative astrocyte soma is big and soma bumps branch are much and bulky. According to the results of statistics, the expression of glial fibers acidic protein(GFAP) of experimental group and control group begin to rise from the first day of repairing, and reach the peak at the 14 th day; the expression quantity of GFAP of the experimental group is significantly higher than that of the control group(P< 0.01); the expression of GFAP of control group only continues to the 14 th day, and basically returns to normal level at the 28 th day; the expression level of GFAP of experimental group is still high at the 28 th day. Under the light microscope, the positive expression of anterior horn neurons cells before the apoptosis of spinal cord is in the nucleus and is featured by tan cell nucleus are; thick and dense mottled chromatin, nucleus pycnosis, cell shrinkage and fracture. On the first day of the repairing, the control group and experimental group appear TUNEL staining positive cells, which reach the peak at the 14 th day and decrease significantly at the 21 st day. Apoptotic cells of experimental group decrease more significantly than that of the control group(P< 0.05 or P < 0.01).Conclusion: Nerve casing-joining repair can promote expression of GFAP of rat ventricornu and is advantageous to the repair of nerve injury. |
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