pentazocine阻断人胎儿肌肉培养的肌肉发生。

G Meola, E Scarpini, L Manfredi, C Mariani, G Scarlato
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引用次数: 2

摘要

对已发表病例报告的批判性回顾表明,戊唑嗪可能通过局部肌毒性以外的机制诱导肌肉变化。Pentazocine-肌病的肌毒性机制仍不确定,因此进行了组织培养研究,以调查肌病与Pentazocine之间的密切关系。研究了戊唑嗪对人胎肌培养中肌发生程度的影响。相对比研究、光镜和肌发生的定量评估(计算入肌管的细胞核数量并以细胞核总数的百分比表示)显示,戊唑嗪处理的培养物完全阻断了肌发生,d -阿拉伯氟脲基胞嘧啶(Ara-C)-戊唑嗪处理的培养物存在延迟融合过程。然而,目前的初步数据表明,肌肉干细胞可能参与了Pentazocine诱导的神经肌肉综合征中骨骼肌被纤维组织取代的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pentazocine-blocked myogenesis in human foetal muscle cultures.

A critical review of the published cases reports suggests that the muscle changes could be induced by Pentazocine by mechanisms other than local myotoxicity. The mechanism of myotoxicity in Pentazocine-myopathy remains uncertain and for this reason a tissue culture study was performed in order to investigate the close relationship between myopathy and Pentazocine. The effects of Pentazocine on the extent of myogenesis in human foetal muscle cultures were investigated. The phase contrast study, the light microscopy the quantitative assessment of myogenesis (the number of nuclei incorporated into myotubes were counted and expressed as a percentage of the total number of nuclei) showed a complete block of myogenesis in Pentazocine treated culture and a delayed fusion process was present in D-arabinofuranosylcytosine (Ara-C)-Pentazocine-treated cultures. The present preliminary data, however, suggest that muscle stem cells could participate in the replacement of skeletal muscle by fibrous tissue in neuromuscular syndrome induced by Pentazocine.

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