Objective To explore the effect of tri pterygium 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 of10 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 sal ine, groups B and D TG 5 mg/ (kg·d), and group C TG 2.5 mg/ (kg·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 lt; 0.01)；those in groups B, C and D were lower than those in group E (P lt; 0.05); and there were no significant differences among groups B, C and D (P gt; 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 lt; 0.01)；those in groups B, C and D were higher than in groupE (Plt; 0.05); and there were no significant differences among groups B, C and D (P gt; 0.05). Three weeks after nerve allograft, under the l ight microscope, the muscle fibers became thin; under the TEM, the sarcoplasmic reticulum was expanded. Six weeks after nerve allograft, under the l ight 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 l ines were seen in group A, but the myofibrils were arranged tidily in the other groups, and the l ight 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.
Objective To observe whether the motor nerve babysitter could improve the delayed nerve anastomosisand promote the functional recovery. Methods Sixteen SD rats weighing 200-250 g were randomly divided into 2 groups.In group A, the left musculocutaneous nerve was transected to make the model of biceps brachii denervation and anastomosed to its proximal end 6 weeks later; In group B, the musculocutaneous nerve was transected and the distal end was coapted to the purely motor medial pectoral nerve immediately (nerve babysitter) and the musculocutaneous nerve was separated from the medial pectoral nerve, and reanastomosed to its proximal end 6 weeks later. In the animal model, the left l imbs served as experimental sides, the right l imbs as control sides. After 6 and 12 weeks of the second surgery, behavioral test (grooming test) was performed and the degree of the biceps brachii atrophy was observed, the latent period and the ampl itude of the maximun action potentials of the biceps brachii were detected, the wet muscle weight, muscle fiber cross-section area and the activity of Na+-K+-ATPase of the biceps brachii were measured. Results After 4 weeks of the second surgery, grooming behavior was found in group B, while few grooming behavior was seen in group A till 6 weeks after the secondary surgery. After 6 weeks of the second surgery, the recovery rate of the latent period and the ampl itude, the wet muscle weight, muscle fiber cross-section area and the enzymatic activity of Na+-K+-ATPase of the biceps brachii in group A was 187.25% ± 1.97%, 46.25% ± 4.63%, 55.14% ± 1.99%, 49.97% ± 1.71%, and 65.81% ± 2.24%, respectively, which was significantly different from that in group B (155.96% ± 3.02%, 51.21% ± 2.13%, 74.18% ± 1.82%, 55.05% ± 1.64% and 71.08% ± 1.53%, respectively, P lt; 0.05). After 12 weeks of the second surgery, the recovery rate of the latent period and ampl itude, the wet muscle weight, muscle fiber cross-section area andthe enzymatic activity of Na+-K+- ATPase of the biceps brachii in group A was 145.36% ± 3.27%, 51.84% ± 5.02%, 77.92% ± 1.73%, 61.04% ± 2.68% and 71.94% ± 1.65%, respectively, which was significantly different from that in group B (129.83% ± 8.36%, 75.22% ± 2.78%, 84.51% ± 1.34%, 78.75% ± 3.69% and 84.86% ± 1.81%, respectively, P lt; 0.05). Conclusion Motor nerve babysitting could reduce muscular damage after denervation, improve the effect of delayed nerve repair and promote the functional recovery of musculocutaneous nerve.
Objective To summarize the recent progress in research on the mechanism of denerved skeletal muscle atrophy. Methods The recently-publ ished l iteratures at home and abroad on denerved skeletal muscle atrophy were reviewedand summarized. Results The mechanism of denerved skeletal muscle atrophy was very complex. At present, the studyof the mechanism was based on the changes in histology, cytology and molecules. Fiber thinning and disorderly arrangement of denerved skeletal muscles were observed and apoptotic bodies were detected. Apoptosis-promoting genes expressed upregulatedly and apoptosis-restraining genes expressed down-regulatedly. Muscle satell ite cells increased after denervation, but then they decreased and disappeared because they could not differentiate to mature muscle fibers. The structural change of cytomiscrosome and down-regulation of metabol ism-related enzymes induced cell metabol ism disorder. Conclusion The histological change of skeletal muscle fibers, the change of the number of muscle satell ite cells and differentiation, the structural change of cytomiscrosome and the change of apoptosis-related and metabol ism-related gene expressions contribute to denerved skeletal muscle atrophy.