Objective: To explore the effect of tripterygium glycoside (TG) on the skeletal muscle atrophy and apoptosis after nerve allograft.
Methods: Twenty Wistar male rats were adopted as donors, weighing 200-250 g, and the sciatic nerves were harvested. Fifty SD male rats were adopted as recipients, weighing 200-250 g. Fifty SD rats were made the models of 10 mm right sciatic nerve defect randomly divided into five groups (n=10): group A, group B, group C, group D and group E. groups A and B received fresh nerve allograft, groups C and D received sciatic nerve allograft pretreated with TG, and group E received autograft. The SD rats were given medicine for 5 weeks from the second day after the transplantation: groups A and E were given physiological saline, groups B and D TG 5 mg/(kg x d), and group C TG 2.5 mg/(kg x d). At 3 and 6 weeks, respectively, after nerve transplantation, general observation was performed; the structure of skeletal muscles was observed by HE staining; the diameter of skeletal muscles was analyzed with Image-Pro Plus v5.2; the ultrastructure of skeletal muscles was observed by TEM; the expressions of Bax and Bcl-2 were detected by immunohistochemical staining; and the apoptosis of skeletal muscles was detected by TUNEL.
Results: All rats survived to the end of the experiment. In general observation, the skeletal muscles of SD rates atrophied to different degrees 3 weeks after operation. The muscular atrophy in group A was more serious at 6 weeks, and that in the other groups improved. The wet weight, fiber diameter and expression of Bcl-2 in group A were significantly lower than those in groups B, C, D and E (P < 0.01); those in groups B, C and D were lower than those in group E (P < 0.05); and there were no significant differences among groups B, C and D (P > 0.05). The apoptosis index and expression of Bax in group A were significantly higher than those in groups B, C, D and E (P < 0.01); those in groups B, C and D were higher than in group E (P < 0.05); and there were no significant differences among groups B, C and D (P > 0.05). Three weeks after nerve allograft, under the light microscope, the muscle fibers became thin; under the TEM, the sarcoplasmic reticulum was expanded. Six weeks after nerve allograft, under the light microscope, the gap of the muscle fibers in group A was found to broaden and connective tissue hyperplasia occurred obviously; under the TEM, sarcomere damage, serious silk dissolution and fragmentary Z lines were seen in group A, but the myofibrils were arranged tidily in the other groups, and the light band, dark band and sarcomere were clear.
Conclusion: TG can decrease the skeletal muscle atrophy and apoptosis after nerve allograft. The donor's nerve that is pretreated with TG can reduce the dosage of immunosuppressant for the recipient after allograft.