L. Rodella, G. Bonaspetti, R. Rezzani, E. Borsani, R. Fenu, U. Pazzaglia, R. Bianchi
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引用次数: 0
摘要
当成人骨骼肌失神经时,其终板退行性变,其乙酰胆碱酯酶(AChE)活性逐渐降低。然而,如果将神经近端段与远端段缝合,或者将神经植入以前的无神经肌肉中,轴突会在不同的时间内再生并重建新的终板。这段时间取决于神经切割和再植之间的时间,这表明退行性过程与再生密切相关。环孢素- a (CsA)在神经再生中有重要作用,但在神经退行性变中的作用尚不清楚。我们用乙酰胆碱酯酶组织化学方法评估了CsA对大鼠腓肠肌去神经支配实验模型终板退变的影响。15 mg/kg/天剂量的CsA未引起正常大鼠肌肉终板的定量或定性改变。此外,我们的研究结果表明,CsA减少了大鼠无神经肌肉的终板退变和损失。
Cyclosporine‐A delays the end‐plate degeneration in denerved rat muscles
When an adult skeletal muscle is denervated, its end-plates degenerate and their acethylcholinesterase (AChE) activity gradually decreases. However, if the proximal segment of the nerve is sutured to the distal segment, or if the nerve is implanted in a previous denerved muscle the axons regenerate and reconstitute new end-plates over a variable period. This period depends on the time passed between the nerve cutting and the reimplantation suggesting that the degenerative processes are closely correlated to regeneration. It has been shown that cyclosporine-A (CsA) is useful in nerve regeneration but their role in nerve degeneration is not well understand. We evaluated, using AChE histochemistry, the effects of CsA, on the degeneration of the end-plates in an experimental model of gastrocnemius muscle denervation in the rat. CsA at a dose of 15 mg/kg/day did not cause any quantitative or qualitative alterations in the end-plates on normal rat muscles. Moreover, our findings showed that CsA reduced the end-plate degeneration and loss in the denerved rat muscles.