Lisboa Marcelo José Santiago, De Oliveira Lima Marília Fabiana, Stabille Sandra Regina, Zanoni Jacqueline Nelisis, Gagliardo Karina Martinez, Souto Melyna Soares, Souza Renivaldo, Da Silva Jodonai Barbosa, De Almeida Yokomizo Sônia Regina, Liberti Edson Aparecido, Clebis Naianne Kelly
Laboratório de Microscopia Celular e Tecidual, Programa de Pós-graduação em Biologia Estrutural e Funcional, Departamento de Morfologia, Universidade Federal do Rio Grande do Norte, Natal, RN, Brazil.
Departamento de Ciências Morfofisiológicas, Universidade Estadual de Maringá, Maringá, PR, Brazil.
Auton Neurosci. 2017 Jul;205:57-66. doi: 10.1016/j.autneu.2017.05.001. Epub 2017 May 17.
The Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by the absence of dystrophin protein, causing severe myopathy from increases of oxidative stress. Injuries of intestinal muscle can compromise the myenteric plexus. This study aimed to evaluate the disorders occurred in the muscular layer and in the acetylcholinesterase myenteric neurons (ACHE-r) of ileum of mdx mice, and the effects of supplementation with ascorbic acid (AA) in both components. 30 male mice C57BL/10, and 30 male mice C57BL/10Mdx were separated according to the age and treatment (n=10/group): 30-days-old control group (C30); 30-days-old dystrophic group (D30); 60-days-old control group (C60); 60-days-old dystrophic group (D60); 60-days-old control group supplemented with AA (CS60); and 60-days-old dystrophic group supplemented with AA (DS60). The animals were euthanized and the ileum was collected and processed. Semi-serial sections were stained by Masson's trichrome, and acetylcholinesterase histochemical technique in whole-mounts preparations to identify the myenteric neurons. The muscular layer thickness and the area of smooth muscle of ileum were lower in dystrophic groups, especially in D30 group. The DS60 group showed the muscular layer thickness similar to C60. The density of ACHE-r neurons of myenteric plexus of ileum was lower in D30 animals; however, it was similar in animals of 60-days-old without treatment (C60 and D60) and, higher in DS60. The cell body profile area of ACHE-r neurons was similar in C30-D30 and C60-D60; however, it was higher in DS60. DMD caused damage to the ileum's musculature and myenteric plexus, and the AA prevented the ACHE-r neuronal loss.
杜氏肌营养不良症（DMD）是一种遗传性疾病，其特征是缺乏肌营养不良蛋白，由于氧化应激增加导致严重的肌病。肠道肌肉损伤会损害肌间神经丛。本研究旨在评估mdx小鼠回肠肌层和乙酰胆碱酯酶肌间神经元（ACHE-r）中发生的紊乱，以及补充抗坏血酸（AA）对这两个成分的影响。根据年龄和治疗方法将30只雄性C57BL/10小鼠和30只雄性C57BL/10Mdx小鼠分开（每组n = 10）：30日龄对照组（C30）；30日龄营养不良组（D30）；60日龄对照组（C60）；60日龄营养不良组（D60）；补充AA的60日龄对照组（CS60）；以及补充AA的60日龄营养不良组（DS60）。对动物实施安乐死后，收集并处理回肠。制作半连续切片，用Masson三色染色法染色，并在整装制剂中采用乙酰胆碱酯酶组织化学技术来识别肌间神经元。营养不良组回肠的肌层厚度和平滑肌面积较低，尤其是D30组。DS60组的肌层厚度与C60组相似。D30组动物回肠肌间神经丛的ACHE-r神经元密度较低；然而，在60日龄未经治疗的动物（C60和D60）中该密度相似，而在DS60组中较高。C30-D30组和C60-D60组中ACHE-r神经元的细胞体轮廓面积相似；然而，DS60组中的该面积更大。DMD对回肠的肌肉组织和肌间神经丛造成损害，而AA可防止ACHE-r神经元丢失。
