Objective To review and summarize the latest development of the therapy for the Duchenne muscular dystrophy (DMD). Methods Therecentlypublished articles related to the therapies for DMD were extensively reviewed and briefly summarized. Results The therapeutic approaches for DMD included the gene therapy, the cell therapy, and the pharmacological therapy. The gene therapy and the cell therapy were focused on the treatment for the cause of DMD by the delivery of the missing gene, the modification of the mutated gene, and the transfer of the normal cells including the stem cells, while the pharmacological therapy dealt with the downstream events caused by the dystrophin gene defect, slowed down the pathologic progress of DMD, and improved the DMD patient’s life quality and life span, by medication and other factor treatments. Conclusion There is still no cure for DMD because of various difficulties in replacing or repairing thedefected gene and of the multifaceted nature of the severe symptoms. Therefore,it is imperative for us to find out a more effective treatment that can solve these problems.
Objective To observe the expressions of CXC chemokine receptor 4 (CXCR4) in muscle satell ite cells in situ of normal and cardiotoxin-intoxicated muscle tissues so as to further investigate the molecular mechanism involving inmuscle regeneration such as progressing muscular dystrophy (PMD) for seeking the way to cure muscle retrogression. Methods The muscle injured model of 12 C57 male mice was made by injecting cardiotoxin (5 μg per mouse) in left quadriceps femoris, their right quadriceps femoris was used as control without any injection. The histological, immunohistochemical analysis and RT-PCR were done to investigate the expression of CXCR4 in the quadriceps femoris in situ after 1 day, 4 days, 1 week, 2 weeks, 4 weeks and 6 weeks. Results HE staining results demonstrated that the muscle tissues experienced the process from muscle injury, repair to regeneration. The result of immunohistochemistry showed that the expressions of CXCR4 in injured muscle tissue were 1 955.6 ± 150.3, 2 223.2 ± 264.3, 2 317.6 ± 178.7, 3 066.5 ± 269.6, 1 770.9 ± 98.7 and 1 505.7 ± 107.1 at 1 day, 4 days, 1 week, 2 weeks, 4 weeks and 6 weeks after injection of cardiotoxin, there was significant difference when compared with normal muscle (640.3 ± 124.0, P lt; 0.001). The RT-PCR showed that the expressions of CXCR4 mRNA in injured muscle tissue were0.822 ± 0.013, 0.882 ± 0.025, 1.025 ± 0.028, 1.065 ± 0.041, 0.837 ± 0.011 and 0.777 ± 0.015 at 1 day, 4 days, 1 week, 2 weeks, 4 weeks and 6 weeks after injection of cardiotoxin, there was significant difference when compared with normal muscle (0.349 ± 0.006, P lt; 0.001). Conclusion CXCR4 may be the critical protein in the process of muscle impairment and reparation.
目的 通过检测异染色质蛋白1α（HP1α）在DNA损伤后的磷酸化状况，介绍一种用磷酸化标签(phos-tag)试剂检测磷酸化蛋白质的新方法。 方法 取雄雌C57小鼠交配后孕13.5 d胚胎，分离并原代培养小鼠胚胎成纤维细胞。对照组及实验组(6个损伤时间点)各取2个100 mm培养皿的细胞进行实验，实验组细胞用喜树碱进行DNA损伤；对照组用等量的二甲基亚砜处理。用掺入phos-tag的十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分离蛋白并转印，将膜用抗HP1α的抗体孵育，用偶联辣根过氧化物酶的抗体做二抗，通过成像系统检测蛋白。 结果 实验组存在一条与HP1α有明显不同迁移率的磷酸化HP1α条带，与对照组相比DNA损伤后磷酸化HP1α含量一过性增多。 结论 HP1α被DNA损伤诱导为磷酸化状态，提示其可能在DNA修复过程中扮演重要角色。 Phos-tag 蛋白质印迹法可采用普通抗体检测磷酸化的蛋白，是一种简便易行的检测未知磷酸化蛋白质的新方法。