首页|肌注心脏毒素后小鼠肌肉生长相关基因表达变化研究

肌注心脏毒素后小鼠肌肉生长相关基因表达变化研究

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本研究以雄性C57BL/6小鼠为实验动物,利用心脏毒素(cardiotoxin,CTX)处理构建肌肉损伤模型,采用组织切片HE染色方法分析肌肉组织的结构变化;以未经处理的实验动物为对照组,运用实时定量PCR(RT-qPCR)技术检测肌肉损伤组中肌肉分化基因、肌肉生长发育相关信号通路基因的表达情况。结果表明:在小鼠胫骨前肌一次性注射50 μL CTX(1 g/L),4d后可引起肌肉损伤,肌肉显微结构明显被破坏,胫骨前肌质量与长度比值显著降低;与对照组相比,MyOD1、MyOG、MYH1、MYH2等肌肉分化相关基因和AMPK、Notch、AKT、PI3K、mTOR等信号通路的标志基因(PRKAA1、NOTCH1、AKT、PI3K、mTOR)在CTX处理模型组胫骨前肌组织的表达显著下降。本研究成功构建小鼠肌肉损伤模型,检测了肌细胞分化相关基因和肌肉生长发育相关信号通路基因在肌肉损伤后的表达变化情况,为肌肉再生的分子调控机制研究和开发肌肉损伤治疗方法提供一定的理论基础。
Expression Profiling of Related Genes of Muscle Growth in Mice After Intramuscular Cardiotoxin Injection
In this study,male C57BL/6 mice were used as experimental animals to establish muscle injury model by cardiotoxin(CTX)injection.Structural alterations of skeletal muscle were observed by the HE staining,and the expressions profiling of related genes of skeletal muscle growth and differentiation were detected by real-time quantitative PCR(RT-qPCR),the untreated mice were used as the control.The results revealed that there was significant muscle histologic alteration and tibialis anterior muscle weight-to-length ratio was decreased by the single injection of 50 μL CTX(1 g/L)into the mouse tibialis anterior muscle after 4 days.The expression of related genes for muscle differentiation,MyOD1,MyOG,MYH1,MYH2,AMPK,and mTOR signaling pathway marker genes(PRKAA1,NOTCH1,AKT,PI3K,mTOR)in the tibialis anterior muscle decreased significantly compared with those of the untreated group.This study successfully established the mouse muscle injury model after intramuscular Cardiotoxin injection by morphological examination and detection of related genes expression.The research provided a theoretical basis for molecular regulatory mechanisms for muscle regeneration and treatment methods for muscle injury.

muscle injurydamaging modelmuscle growthgene expression

陈春、张瑞门、蒙丽娜、杨燕燕、吴超权、冯万有

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广西壮族自治区药品检验研究院药理室,广西南宁 530029

广西大学动物科学技术学院,广西南宁 530004

南宁师范大学环境与生命科学学院,广西南宁 530001

肌肉损伤 损伤模型 肌肉生长 基因表达

2024

广西师范大学学报(自然科学版)
广西师范大学

广西师范大学学报(自然科学版)

CSTPCD北大核心
影响因子:0.448
ISSN:1001-6600
年,卷(期):2024.42(6)