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首页> 外文期刊>Journal of orthopaedic research >How muscles recover from paresis and atrophy after intramuscular injection of botulinum toxin A: Study in juvenile rats.
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How muscles recover from paresis and atrophy after intramuscular injection of botulinum toxin A: Study in juvenile rats.

机译：肌肉注射肉毒杆菌毒素A后肌肉如何从轻瘫和萎缩中恢复：在未成年大鼠中的研究。

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Botulinum toxin A (BoNT-A) is a potent biological toxin widely used for the management of skeletal muscle spasticity or dynamic joint contracture. Intramuscular injection of BoNT-A causes muscle denervation, paresis, and atrophy. This clinical effect of botulinum toxin A lasts 3 to 6 months, and injected muscle eventually regains muscle mass and recovers muscle function. The goal of the present study was to characterize the molecular and cellular mechanisms leading to neuromuscular junction (NMJ) regeneration and skeletal muscle functional recovery after BoNT-A injection. Fifty-six 1-month-old Sprague-Dawley rats were used. Botulinum toxin A was injected into the left gastrocnemius muscle at a dosage of 6 units/kg body weight. An equivalent volume of saline was injected into the right gastrocnemius muscle to serve as control. The gastrocnemius muscle samples were harvested from both hind limbs at 3 days, 7 days, 15 days, 30 days, 60 days, 90 days, 180 days, and 360 days after administration of toxin. In addition, the gastrocnemius muscles from 1-month-old rats with no injections were harvested to serve as uninjected control group. Muscle samples were processed and mRNA was extracted. Real-time polymerase chain reaction (PCR) and gene microarray technology were used to identify key molecules involved in NMJ stabilization and muscle functional recovery. More than 28,000 rat genes were analyzed and approximately 9000 genes are expressed in the rat gastrocnemius muscle. Seven days following BoNT-A injection, 105 genes were upregulated and 59 genes were downregulated. Key molecules involved in neuromuscular junction (NMJ) stabilization and muscle functional recovery were identified and their time course of gene expression following BoNT-A injection were characterized. This animal study demonstrates that following intramuscular injection of BoNT-A, there is a sequence of cellular events that eventually leads to NMJ stabilization, remodeling, and myogenesis and muscle functional recovery. This recovery process is divided into two stages (aneural and neural) and that the IGF-1 signaling pathway play a central role in the process.
机译：肉毒杆菌毒素A（BoNT-A）是一种有效的生物毒素，广泛用于管理骨骼肌痉挛或动态关节挛缩。肌内注射BoNT-A会引起肌肉神经支配，轻瘫和萎缩。肉毒杆菌毒素A的这种临床作用持续3到6个月，注射的肌肉最终会恢复肌肉质量并恢复肌肉功能。本研究的目的是表征BoNT-A注射后导致神经肌肉接头（NMJ）再生和骨骼肌功能恢复的分子和细胞机制。使用了56只1个月大的Sprague-Dawley大鼠。将肉毒杆菌毒素A以6单位/ kg体重的剂量注射到左腓肠肌中。将等量的生理盐水注入右腓肠肌，以作为对照。施用毒素后3天，7天，15天，30天，60天，90天，180天和360天从两个后肢收获腓肠肌样品。另外，收获未注射的1个月大大鼠的腓肠肌，作为未注射的对照组。处理肌肉样品并提取mRNA。实时聚合酶链反应（PCR）和基因芯片技术用于鉴定与NMJ稳定和肌肉功能恢复有关的关键分子。分析了超过28,000个大鼠基因，并且在大鼠腓肠肌中表达了大约9000个基因。 BoNT-A注射后7天，105个基因被上调而59个基因被下调。确定了参与神经肌肉接头（NMJ）稳定和肌肉功能恢复的关键分子，并表征了BoNT-A注射后其基因表达的时程。这项动物研究表明，肌肉内注射BoNT-A后，会发生一系列细胞事件，这些事件最终导致NMJ稳定，重塑以及肌生成和肌肉功能恢复。该恢复过程分为两个阶段（神经和神经），而IGF-1信号通路在该过程中起着核心作用。

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